Step 1 Complicated Concepts Thread

[TheSeanieB]

ASK AND ANSWER TOUGH QUESTIONS RELATED TO STEP 1.

Starting with me:
physiologic chloride shift - When CO2 diffuses into a RBC, it quickly converts with H2O to H+ and HCO3- so that CO2 will continue to passively diffuse into the RBC. The HCO3- is then excreted into the plasma by a Cl-/HCO3- exchanger. When the RBC enters the pulmonary capillaries, the process reverses. HCO3- is taken up by exchange for a Cl-. It combines with H+ to creates CO2 +H2O. The CO2 then diffuses out of the RBC and ultimately into the alveoli. This process allows for maximal CO2 excretion by a RBC.

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[Akarat]

Ok that makes sense. I'm pretty sure the question using a paper cut was a horrible example, but it got me thinking. Thank you.

Maybe you already know this, but are you familiar with the concept of primary hemostasis vs secondary hemostasis?

Primary hemostasis is achieved by the formation of a platelet plug. Secondary hemostasis is achieved by the formation of a fibrin clot.

If you overdose on an anti-coagulant, you'll severely inhibit the secondary hemostasis process. Therefore, if you cut yourself, you will have a normal bleeding time because a platelet plug can form. However, when the platelet plug dissolves some time afterwards, you don't have a sufficient enough fibrin clot. Therefore, you will start bleeding again.

Edit: Jamiu22 explained the process in more detail in the post before mine.

 

[coolforschool]

Ok your original explanation was way too simplified and I know all of that, but thank you for the effort. (seriously, not being sarcastic)

So why is there excessive bleeding when someone ODs on anticoagulant yet there is no difference in "bleeding time".

The reason I ask this is I had a vignette on a question where the lady had Warfarin + a 450 inhibitor. She gets a papercut and can't stop bleeding, yet her bleeding time is normal. Now having done bleeding times on patients I know if you bleed excessively from a paper cut you're going to bleed more from the lancet with a bleeding time but clearly that's not what the USMLE wants

Haha. This is what makes me a bad teacher. I think my explanations make so much sense but then people are still confused.

 

[loveoforganic2]

***NBME 3 spoiler***

This question really annoyed me....



Which of the following is the rationale for advising a decrease in dietary intake of NaCl in patients with hepatic disease who develop edema?
a. Edema fluid has a high concentration of Cl
b.Glomerular filtration rate is increased
c. Injured hepatocytes are more permeable to Na
d. Secondary hyperaldosteronism is present
e. serum globulin concentration is increased


Why is the answer D? I figured that with liver disease you have impaired production of angiotensinogen. So how could you have hyperaldosteronism? I put B, thinking that a loss of albumin would cause an increase GFR would affect the macula densa somehow and related that to NaCl

I get that the loss of albumin and body water is causing renin release, but figured that liver dz would lower angiotensinogen and not result in a rise in aldosterone...I guess that is not the case

P.S...dude you need to change your avatar lol. It is distracting the hell out of me

Edema => Shift of fluid from vascular to extravascular space => volume depletion => RAAS activation => Edema

My understanding, though I get angiostensinogen is a hepatic product

 

[Pinkleton]

Guy on DIT just said that TNF-a is important for the formation of granulomas. I thought that this was due to the IFN-gamma/IL-12 loop. Maybe TNF helps maintain it, hence drugs like etanercept causing granuloma breakdown?

 

[SLC]

Guy on DIT just said that TNF-a is important for the formation of granulomas. I thought that this was due to the IFN-gamma/IL-12 loop. Maybe TNF helps maintain it, hence drugs like etanercept causing granuloma breakdown?

TH1 cells secrete the IFN-gamma, which gets the macrophages in a tizzy.

Then the Macrophages secrete TNF-alpha from the macrophages induces/maintains the granuloma.

Yes, that's why you get reactivation of granuloma contained TB with Etanercept.

 

[MLT2MT2DO]

***NBME 3 spoiler***

This question really annoyed me....



Which of the following is the rationale for advising a decrease in dietary intake of NaCl in patients with hepatic disease who develop edema?
a. Edema fluid has a high concentration of Cl
b.Glomerular filtration rate is increased
c. Injured hepatocytes are more permeable to Na
d. Secondary hyperaldosteronism is present
e. serum globulin concentration is increased


Why is the answer D? I figured that with liver disease you have impaired production of angiotensinogen. So how could you have hyperaldosteronism? I put B, thinking that a loss of albumin would cause an increase GFR would affect the macula densa somehow and related that to NaCl

Just got a Uworld question on this.

Edema leads to increased ACE by the lungs, leads to further activation of the RAA system. Was surprised to find it was this simple.

 

[MLT2MT2DO]

I had the same confusion earlier... and everything Jonari said is accurate, let me at least take a stab at it from another perspective....

Whenever you bleed, the process to stop the wound bleed and healing occurs in two different steps...

the first step is a temporary hemostatic plug...which is strictly done by platelet aggregation. All this does is to put something on that wound to stop the bleeding - this is the bleeding time and note that we haven't talked about the coagulation cascade in this process. this temporary plug is not strong so a light touch on the wound would cause it to rebleed.

the second step in healing the wound is coagulation.... and in this step all the coagulation cascade is activated to eventually deposit more fibrin on temporary plug to make them stronger... this usually occurs much later and since the bleeding was already controlled, you can't measure this with bleeding time (that part was taking care off by platelets) - tis why the only way you can test for coagulation factor deficiency is PT or PTT (depending on which factor you think is deficient)...

Now, when you think of bleeding time... the would is usually small and the temp plug could do the job... but if the wound is a lot bigger, it makes it really hard for the platelets to stop bleeding.. folks with factor VIII deficiency (hemophilia) have bleeding issues mainly because once they get a cut, depending on how large the wound is - the temp plug may not be sufficient especially for this folks... this is same thing with warfarin overdose... they will bleed a lot more than regular folks with an injury... reason why surgery on hemophiliac's a lot more complicated.

Another perl
1. Platelet issue - superficial bleeds
2. Coagulation factor issue - Rebleeding issue; or bleeding into joints (hemarthrosis) from mechanical wear and tear and lack of factors..


I know that was verbose...and you may already know that, lol....but just in case it helps.

Maybe you already know this, but are you familiar with the concept of primary hemostasis vs secondary hemostasis?

Primary hemostasis is achieved by the formation of a platelet plug. Secondary hemostasis is achieved by the formation of a fibrin clot.

If you overdose on an anti-coagulant, you'll severely inhibit the secondary hemostasis process. Therefore, if you cut yourself, you will have a normal bleeding time because a platelet plug can form. However, when the platelet plug dissolves some time afterwards, you don't have a sufficient enough fibrin clot. Therefore, you will start bleeding again.

Edit: Jamiu22 explained the process in more detail in the post before mine.

Haha. This is what makes me a bad teacher. I think my explanations make so much sense but then people are still confused.

Thank you all. My question was really much more superficial than the pathophys/physiology of it all, though I must admit the big bleed vs small bleed was a good refresher that I had forgotten.

The "a person bleeds more but for the normal amount of time" description by pinkleton really cleared it up.

 

[tiedyeddog]

Ok, are these type I or type III hypersensitivity? FA says type 1 test is "skin test" whole type III is IF.

How is this different from a PPD? Isn't ppd type III? Is it because of the time course?

Ok 1 more question: is the ppd reaction an arthus reaction?

 

[tiedyeddog]

I had the same confusion earlier... and everything Jonari said is accurate, let me at least take a stab at it from another perspective....

Whenever you bleed, the process to stop the wound bleed and healing occurs in two different steps...

the first step is a temporary hemostatic plug...which is strictly done by platelet aggregation. All this does is to put something on that wound to stop the bleeding - this is the bleeding time and note that we haven't talked about the coagulation cascade in this process. this temporary plug is not strong so a light touch on the wound would cause it to rebleed.

the second step in healing the wound is coagulation.... and in this step all the coagulation cascade is activated to eventually deposit more fibrin on temporary plug to make them stronger... this usually occurs much later and since the bleeding was already controlled, you can't measure this with bleeding time (that part was taking care off by platelets) - tis why the only way you can test for coagulation factor deficiency is PT or PTT (depending on which factor you think is deficient)...

Now, when you think of bleeding time... the would is usually small and the temp plug could do the job... but if the wound is a lot bigger, it makes it really hard for the platelets to stop bleeding.. folks with factor VIII deficiency (hemophilia) have bleeding issues mainly because once they get a cut, depending on how large the wound is - the temp plug may not be sufficient especially for this folks... this is same thing with warfarin overdose... they will bleed a lot more than regular folks with an injury... reason why surgery on hemophiliac's a lot more complicated.

Another perl
1. Platelet issue - superficial bleeds
2. Coagulation factor issue - Rebleeding issue; or bleeding into joints (hemarthrosis) from mechanical wear and tear and lack of factors..


I know that was verbose...and you may already know that, lol....but just in case it helps.

Jaimu, this is an excellent explanation, great work!

 

[MLT2MT2DO]

Ok, are these type I or type III hypersensitivity? FA says type 1 test is "skin test" whole type III is IF.

How is this different from a PPD? Isn't ppd type III? Is it because of the time course?

Ok 1 more question: is the ppd reaction an arthus reaction?

Ppd is a type 4 my friend, it's the only one that directly involves Tcells and why you sometimes see a negative ppd on an HIV patient with TB.
An arthus reaction is type 3 reaction it is deposits of AB/AG complexes, though it shows a skin reaction it is due to deposits (much like SLE deposits or other type 3) in the vasculature that leads to a skin reaction.
The above reaction is a type 1, those look like classical "wheals" to me. The accumulation of fluid due to mast cells releasing histamine and other inflammatory mediators which screws with your starling equation due to an increase of KD of the vessels.

 

[tiedyeddog]

Ppd is a type 4 my friend, it's the only one that directly involves Tcells and why you sometimes see a negative ppd on an HIV patient with TB.
An arthus reaction is type 3 reaction it is deposits of AB/AG complexes, though it shows a skin reaction it is due to deposits (much like SLE deposits or other type 3) in the vasculature that leads to a skin reaction.
The above reaction is a type 1, those look like classical "wheals" to me. The accumulation of fluid due to mast cells releasing histamine and other inflammatory mediators which screws with your starling equation due to an increase of KD of the vessels.

So, basically type I, III, and IV skin reactions all look the same to the naked eye? Probably can't tell them apart on sight alone?

 

[Jamiu22]

Ppd is a type 4 my friend, it's the only one that directly involves Tcells and why you sometimes see a negative ppd on an HIV patient with TB.
An arthus reaction is type 3 reaction it is deposits of AB/AG complexes, though it shows a skin reaction it is due to deposits (much like SLE deposits or other type 3) in the vasculature that leads to a skin reaction.
The above reaction is a type 1, those look like classical "wheals" to me. The accumulation of fluid due to mast cells releasing histamine and other inflammatory mediators which screws with your starling equation due to an increase of KD of the vessels.

Yup, got it right....that's RAST testing (had one done about 2yrs ago when my PCP couldn't figure out what I was allergic to.... def type 1

 

[tiedyeddog]

You guys might think this is cool.

I was wondering why in IgA selective immunodeficiency you have a heterophile antibody that causes false + pregnancy tests due. Turns out the lack of IgA probably allows more antigens introduced mucosally into the systemic circulation, causing IgM and IgG antibodies to form against HcG that is exposed to people via muscosa.

The heterophile false + looks like this:

http://jcem.endojournals.org/content/88/7/3069/F1.large.jpg

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1809437/

 

[Akr]

Thanks for this thread everyone!!

Here's something that's bugging me, hopefully someone can explain? Murmurs of mitral valve prolapse vs. mitral regurg (which can be caused by prolapse among other things)... First Aid says that mitral REGURG murmur is enhanced by increased TPR (e.g. squatting), which I get. But mitral PROLAPSE murmurs instead are enhanced by decreased venous return (e.g. standing up).

Can't wrap my head around what the decreased venous return has to do with a prolapse murmur, and why it's so different from regurg murmurs in the first place.

 

[MLT2MT2DO]

So, basically type I, III, and IV skin reactions all look the same to the naked eye? Probably can't tell them apart on sight alone?

Type 1 and IV does....Type III not at all it's nasty looking

 

[tiedyeddog]

Type 1 and IV does....Type III not at all it's nasty looking

ok, thanks man, you're awesome.

 

[coolforschool]

Thanks for this thread everyone!!

Here's something that's bugging me, hopefully someone can explain? Murmurs of mitral valve prolapse vs. mitral regurg (which can be caused by prolapse among other things)... First Aid says that mitral REGURG murmur is enhanced by increased TPR (e.g. squatting), which I get. But mitral PROLAPSE murmurs instead are enhanced by decreased venous return (e.g. standing up).

Can't wrap my head around what the decreased venous return has to do with a prolapse murmur, and why it's so different from regurg murmurs in the first place.

Mitral regurg = holosystolic murmur, so what's happening is that during systole, you're trying to push blood out of the aorta, but some of it gets pushed into the left atrium because of the weakness of the mitral valves, hence the regurgitation. Imagine if you increased the TPR; you get more resistance from the aorta, so more blood gets pushed into the left atrium = murmur intensity increases.

Mitral valve prolapse = mid-systolic click due to ballooning of the mitral valves into the left atrium (from redundant, overly big mitral valves). These big valves can't close properly, so imagine if you have a lower preload (less blood) --> these redundant valves will flop around even more --> louder murmur. If you increase the preload (more blood), you actually facilitate the closing of these valves because you're able to fill those redundant valves up (like a parachute filled up with air), so they don't cause as much noise --> decreased murmur.

Maybe not entirely correct, but that's how I think of it. Perhaps someone else can add some insight to this.

 

[Akr]

Mitral valve prolapse = mid-systolic click due to ballooning of the mitral valves into the left atrium (from redundant, overly big mitral valves). These big valves can't close properly, so imagine if you have a lower preload (less blood) --> these redundant valves will flop around even more --> louder murmur. If you increase the preload (more blood), you actually facilitate the closing of these valves because you're able to fill those redundant valves up (like a parachute filled up with air), so they don't cause as much noise --> decreased murmur.

Maybe not entirely correct, but that's how I think of it. Perhaps someone else can add some insight to this.

Thanks, that helps a lot!! I never thought of it as floppy balloony valves that are too big for their job, but it makes sense now

 

[tiedyeddog]

Mitral regurg = holosystolic murmur, so what's happening is that during systole, you're trying to push blood out of the aorta, but some of it gets pushed into the left atrium because of the weakness of the mitral valves, hence the regurgitation. Imagine if you increased the TPR; you get more resistance from the aorta, so more blood gets pushed into the left atrium = murmur intensity increases.

Mitral valve prolapse = mid-systolic click due to ballooning of the mitral valves into the left atrium (from redundant, overly big mitral valves). These big valves can't close properly, so imagine if you have a lower preload (less blood) --> these redundant valves will flop around even more --> louder murmur. If you increase the preload (more blood), you actually facilitate the closing of these valves because you're able to fill those redundant valves up (like a parachute filled up with air), so they don't cause as much noise --> decreased murmur.

Maybe not entirely correct, but that's how I think of it. Perhaps someone else can add some insight to this.

I have also always been confused by this, excellent description! thanks a million.

 

[Jamiu22]

Effect modification vs Confounding Bias. Anybody really get this, or have a good example that could distinguish them?

 

[issey]

Difference between lacunar vs charcot bouchard? I have no idea what the difference is since every book says "hypertension" as a cause for both

 

[SLC]

Difference between lacunar vs charcot bouchard? I have no idea what the difference is since every book says "hypertension" as a cause for both

Charcot-Bouchard=aneurysm from chronic HTN: lipohyalinosis-->aneurysm of small intercerebral arterioles. Rupture is a major cause of death in chronic untreated (or poorly treated) HTN.

Lacunar infarcts=hypertension causes acute and chronic ischemia at small cerebral arterioles, leading to thrombosis-->fibrinoid necrosis. Often relatively asymptomatic, or minor symptoms like some memory loss etc.

At least that's my understanding.

 

[Akarat]

Effect modification vs Confounding Bias. Anybody really get this, or have a good example that could distinguish them?

I lack examples, but I have essentially distilled it down to this:

Both Confounding Bias and Effect Modification can be detected by risk stratification.

During the post-stratification analysis (i.e., after you run the study with risk stratification and subsequent analysis of the data):

Confounding factor:

• p value > 0.05
• Relative risk is approximately equal to or is equal to 1

Therefore, a confounding factor is a factor that seems to have an effect but really does not.

Effect modification:

• p value < 0.05
• Relative risk is not approximately equal to or is not equal to 1

Therefore, an effect modification is a factor that seems to have an effect, and indeed does.

This is how I have come to understand it. UWorld's explanation isn't, in my opinion, very good.

 

[addo]

nvm

 

[Akarat]

Difference between lacunar vs charcot bouchard? I have no idea what the difference is since every book says "hypertension" as a cause for both

Lacunar infarcts are small infarcts in the basal ganglia and white matter. The mechanism is due to chronic hypertension that then predisposes the small, penetrating arterioles to arteriolosclerosis. Therefore, this is ischemia from a cut off blood supply that then leads to an infarct.

Charcot-Bouchard pseudoaneurysms are small infarcts in the basal ganglia and internal capsule. The mechanism is due to chronic hypertension that then causes rupture of the pseudoaneurysms. Therefore, this causes intracerebral hemorrhage.

Bottom line: Lacunar infarct is non-hemorrhagic whereas Charcot-Bouchard pseudoaneurysm is hemorrhagic.

 

[sharklasers]

Charcot-Bouchard=aneurysm from chronic HTN: lipohyalinosis-->aneurysm of small intercerebral arterioles. Rupture is a major cause of death in chronic untreated (or poorly treated) HTN.

Lacunar infarcts=hypertension causes acute and chronic ischemia at small cerebral arterioles, leading to thrombosis-->fibrinoid necrosis. Often relatively asymptomatic, or minor symptoms like some memory loss etc.

At least that's my understanding.

any way to tell these apart on imaging?

also, im sure hypertensive encephalopathy is completely different, but i always get these confused on uworld images. mind explaining?

Thanks!!

 

[SLC]

Effect modification vs Confounding Bias. Anybody really get this, or have a good example that could distinguish them?

Effect modifier is like a 3rd variable that alters the interaction between the independent and dependent variable.

Confounding bias is something that's related to both, and can be mistaken as being causal because of that.

Example of effect modifier could be smoking in relation to hyperlipidemia and atherosclerosis. Smoking will accelerate the development of atherosclerosis in patients with hyperlipidemia. It modifies the effect by increasing it, in this case.

Example of Confounding Bias is Grey Hair and risk of Stroke. Older adults have more grey hair, and they have more strokes, but that doesn't mean that grey hair causes strokes. Though a poorly designed study might come to that conclusion because older age is associated with both grey hair and strokes.

Hope that helps.

 

[SLC]

any way to tell these apart on imaging?

also, im sure hypertensive encephalopathy is completely different, but i always get these confused on uworld images. mind explaining?

Thanks!!

I'm not sure about imaging, my best estimate would be to do it based on location, my Path professor (and the Phoenix, AZ Med-Examiner) says that 75% of hypertensive intercerebral hemorrhage occurs at the basal-ganlia/thalamus; 15% in the pons; and 10% in the cerebellum. He also says that Charcot-Bouchard Aneurysm occurs in a very similar geographic distribution, which argues for a relationship between the two.

Also, Charcot-Bouchard aneurysm would rupture, causing intracerebral bleeding, while lacunar infarcts would cause small areas of ischemia rather than hemorrhage. I'm guessing on CT you'd see areas light up for CBA-rupture, and you'd see dark areas for lacunar infarct since ischemia produces darkening.

But that last part is purely my speculation at work. I'm not even sure if lacunar infarct would show up on CT all that well.

Just remember that ruptured Charcot Bouchard Aneurysms will cause intercerebral hemorrhage, and are a major cause of death when they occur. I'd think if this came up on a question, the patient presentation alone would be enough to make an informed decision (minor forgetfulness vs. severe neuro defecit/death).

 

[loveoforganic2]

So, basically type I, III, and IV skin reactions all look the same to the naked eye? Probably can't tell them apart on sight alone?

I think one big differentiator for type III from type I is the appearance and from type IV is the onset (much quicker). We kind of skimmed over wth an arthus rxn was in immuno though

 

[Jamiu22]

I lack examples, but I have essentially distilled it down to this:

Both Confounding Bias and Effect Modification can be detected by risk stratification.

During the post-stratification analysis (i.e., after you run the study with risk stratification and subsequent analysis of the data):

Confounding factor:

• p value > 0.05
• Relative risk is approximately equal to or is equal to 1

Therefore, a confounding factor is a factor that seems to have an effect but really does not.

Effect modification:

• p value < 0.05
• Relative risk is not approximately equal to or is not equal to 1

Therefore, an effect modification is a factor that seems to have an effect, and indeed does.

This is how I have come to understand it. UWorld's explanation isn't, in my opinion, very good.

Effect modifier is like a 3rd variable that alters the interaction between the independent and dependent variable.

Confounding bias is something that's related to both, and can be mistaken as being causal because of that.

Example of effect modifier could be smoking in relation to hyperlipidemia and atherosclerosis. Smoking will accelerate the development of atherosclerosis in patients with hyperlipidemia. It modifies the effect by increasing it, in this case.

Example of Confounding Bias is Grey Hair and risk of Stroke. Older adults have more grey hair, and they have more strokes, but that doesn't mean that grey hair causes strokes. Though a poorly designed study might come to that conclusion because older age is associated with both grey hair and strokes.

Hope that helps.

Guys... thanks a lot for this...exactly what I was looking for!

 

[Pinkleton]

***Another NBME 3 spoiler****










A 73-year-old man is brought to the emergency department because of excruciating low back pain that began while he was painting his garage 1 day ago. He visits the physician every 6 months for monitoring of hypertension well controlled with a diuretic. An x-ray of the spine shows several osteoblastic lesions in the vertebrae. Which of the following is the most likely diagnosis?
A) Malignant lymphoma
B) Metastatic lung carcinoma
C) Metastatic prostate carcinoma
D) Multiple myeloma
E) Osteosarcoma

Apparently the answer is C. I was thinking of that but then I chose D instead because the stem said he goes to the physician every 6 months so I figure he has been getting prostate exams!

Thoughts? I'm trying to hone in on how NBME wants us to think, since it is very different than UWORLD

 

[dbeast]

Ok geniuses, who's ready to get a little abstract?

I had asked a question in this thread about polysaccharide capsule vaccines (for example pneumovax), and how it only produces IgM antibodies... I believe the consensus was that a protein component of a vaccine was necessary for class switching.

So, here we go: Would pneumovax theoretically have full effect on a patient with Hyper-IgM immunodeficiency? Considering they're lacking a good part of the rest of their immune system, this seems like quite a good idea for them. If we collectively win the National Medal of Science over this, I'll split it with you guys.

 

[MLT2MT2DO]

Effect modifier is like a 3rd variable that alters the interaction between the independent and dependent variable.

Confounding bias is something that's related to both, and can be mistaken as being causal because of that.

Example of effect modifier could be smoking in relation to hyperlipidemia and atherosclerosis. Smoking will accelerate the development of atherosclerosis in patients with hyperlipidemia. It modifies the effect by increasing it, in this case.

Example of Confounding Bias is Grey Hair and risk of Stroke. Older adults have more grey hair, and they have more strokes, but that doesn't mean that grey hair causes strokes. Though a poorly designed study might come to that conclusion because older age is associated with both grey hair and strokes.

Hope that helps.

So in the second study age would be an effect modifier?

 

[SLC]

So in the second study age would be an effect modifier?

Yes. In whatever way old age makes atrial-fibrillation, and therefore thrombotic strokes, more likely.

 

[coolforschool]

***Another NBME 3 spoiler****










A 73-year-old man is brought to the emergency department because of excruciating low back pain that began while he was painting his garage 1 day ago. He visits the physician every 6 months for monitoring of hypertension well controlled with a diuretic. An x-ray of the spine shows several osteoblastic lesions in the vertebrae. Which of the following is the most likely diagnosis?
A) Malignant lymphoma
B) Metastatic lung carcinoma
C) Metastatic prostate carcinoma
D) Multiple myeloma
E) Osteosarcoma

Apparently the answer is C. I was thinking of that but then I chose D instead because the stem said he goes to the physician every 6 months so I figure he has been getting prostate exams!

Thoughts? I'm trying to hone in on how NBME wants us to think, since it is very different than UWORLD

I think the big thing is that metastatic prostatic carcinoma usually involves osteoblastic lesions whereas multiple myeloma involves osteolytic lesions. I agree though. It seems like the NBMEs have a lot more gimme questions that aren't trying to be tricky (even though we don't know that).

 

[SLC]

I think the big thing is that metastatic prostatic carcinoma usually involves osteoblastic lesions whereas multiple myeloma involves osteolytic lesions. I agree though. It seems like the NBMEs have a lot more gimme questions that aren't trying to be tricky (even though we don't know that).

This is the crux of it. Osteoblastic vs. Osteolytic.

Sad that it's really that simple.

 

[Pinkleton]

Thankz dudez. When I read osteoblastic lesion I thought they were referring to the fact that osteoblasts overexpress RANK-L which causes multiple myleoma

 

[coolforschool]

Thankz dudez. When I read osteoblastic lesion I thought they were referring to the fact that osteoblasts overexpress RANK-L which causes multiple myleoma

It's all right, man. One time the stem described a man whose prostate was symmetrically enlarged without nodularity. I picked something other than BPH.

 

[Jamiu22]

It's all right, man. One time the stem described a man whose prostate was symmetrically enlarged without nodularity. I picked something other than BPH.

I know where that question is from..... I baffled over that question for a while....saying in my head "it can't be that easy"

 

[JP2740]

I cannot get my head fully around reaction formation v.s. sublimation. halp

 

[addo]

I cannot get my head fully around reaction formation v.s. sublimation. halp

reaction formation is doing the opposite of what you really feel... like acting like a jerk to the girl you like. this is an immature defense mechanism

Sublimation is a mature defense mechanism and it is taking negative tendencies or feelings into good and socially acceptable actions. The classic example is the person with aggressive tendencies becoming a surgeon.

 

[coolforschool]

I cannot get my head fully around reaction formation v.s. sublimation. halp

Reaction formation: having a feeling and then doing the complete opposite of that feeling, like being gay and then speaking out against gay rights (amirite, senators?), or having a high sex drive and then joining a monastery.

Sublimation: redirecting "bad" feelings into something good. Your dad beats you, so you take out your anger by joining football (socially acceptable place to be aggressive).

Pretty bad examples, but I'm about to go to sleep. I'm sure someone can define those terms better.

 

[coolforschool]

On that note, can someone explain to me displacement vs. projection? I could never wrap my head around the difference between those two for some reason.

 

[SLC]

On that note, can someone explain to me displacement vs. projection? I could never wrap my head around the difference between those two for some reason.

Projection is when you "Project" your undesirable or unacceptable thoughts/feelings onto someone else. Like when you do poorly at school and you convince yourself that the person at the head of the class really isn't doing that well.

Displacement is the classic "taking it out on someone else". You had a rough day, so you come home and yell at your kids for no apparent reason.

 

[addo]

On that note, can someone explain to me displacement vs. projection? I could never wrap my head around the difference between those two for some reason.

displacement is taking it out on someone who has nothing to do with your frustrations... for example, a man yelling at his wife, and then the wife yelling at the kid and the kid taking it out on the sister

projection is projecting your own unacceptable feelings into someone else. For example some angry person may accuse other people of being hostile or antagonistic when they are really not.

 

[coolforschool]

Projection is when you "Project" your undesirable or unacceptable thoughts/feelings onto someone else. Like when you do poorly at school and you convince yourself that the person at the head of the class really isn't doing that well.

Displacement is the classic "taking it out on someone else". You had a rough day, so you come home and yell at your kids for no apparent reason.

displacement is taking it out on someone who has nothing to do with your frustrations... for example, a man yelling at his wife, and then the wife yelling at the kid and the kid taking it out on the sister

projection is projecting your own unacceptable feelings into someone else. For example some angry person may accuse other people of being hostile or antagonistic when they are really not.

Haha. The colloquial terms really make this stuff much easier to understand. Thanks, guys.

 

[Pinkleton]

I remember reading a good example differentiating projection from displacement. It's a good reminder that projection doesn't always have to appear "negative".

A married man sees an attractive woman when he's out with some friends and thinks about having sex with her. If he goes home to his wife (who was also out with her friends) and thinks that she may have cheated on him, that is projection. If instead he goes home and has sex with his wife, that is displacement

 

[JP2740]

I remember reading a good example differentiating projection from displacement. It's a good reminder that projection doesn't always have to appear "negative".

A married man sees an attractive woman when he's out with some friends and thinks about having sex with her. If he goes home to his wife (who was also out with her friends) and thinks that she may have cheated on him, that is projection. If instead he goes home and has sex with his wife, that is displacement

That doesn't sound like displacement, sounds way more mature like sublimation lol. Wanting to cheat but fuarking his wife instead. Good man. Good strong mature defense

 

[addo]

That doesn't sound like displacement, sounds way more mature like sublimation lol. Wanting to cheat but fuarking his wife instead. Good man. Good strong mature defense

haha, I agree.

 

[Pinkleton]

Haha but I think the point is, he is thinking of the other woman while doing it

Maybe it would be sublimation if he went down on her lol