USMLE OFFICIAL NBME 20 - Questions & Answers - Explanations & Discussions ?

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MegaKleos

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So let's continue the trend of this forum and discuss the doubts of the test. I intend on taking this as soon as it is out. Please post below if you wish to discuss and let's get together and solve our doubts.

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A 50 yr old woman is brought to the emergency department by her husband because he found her in a semi comatose state with an empty bottle next to her. The bottle had contained a sodium salt of drug with central nervous system effects. Alkalization of her urine will cause the greatest absoulute increase in elimination of the unmetabolized drug if it has which of the following pharmacokinetic profile?
Pka protein binding in plasma vol of distribution
6.0 20 1
6.0 98 1
6.0 98 10
10 20 1
10 20 10
10 98 10
ans a
i know that a weak
acid needs alkalinization of urine but i dont get the vol of distribution and protein binding in plasma. please explain
 
On the question with 34 year old HIV positive man who had enlarged abdominal lymph nodes following antiretroviral therapy, how do we know this is due to CD4+ T lymphocytes ? Thanks in advance!

Lymph node enlargement in due to proliferation of the immune cells that are fighting the infection. In this case it is Mycobacterium avium intracellulare which like all mycobacteria is cleared through cell-mediated immune response which is mediated by CD4+ T cells.

Also the patient just started anti-retrovirals which would increase his CD4+ count.
 
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A 50 yr old woman is brought to the emergency department by her husband because he found her in a semi comatose state with an empty bottle next to her. The bottle had contained a sodium salt of drug with central nervous system effects. Alkalization of her urine will cause the greatest absoulute increase in elimination of the unmetabolized drug if it has which of the following pharmacokinetic profile?
Pka protein binding in plasma vol of distribution
6.0 20 1
6.0 98 1
6.0 98 10
10 20 1
10 20 10
10 98 10
ans a
i know that a weak
acid needs alkalinization of urine but i dont get the vol of distribution and protein binding in plasma. please explain

In order for a drug to be cleared by the kidney, it must first be filtered in the glomeruli. Drugs with a high VD have more in tissue that are not available to filtered by the kidney. Drugs with high protein binding won't be filtered either.
 
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pt with severe cellular rejection, was on maximal immunosuppression. 2 weeks later pt develops lymphadenopathy and hepatospleenomegaly. Histo of lymphnodes shows the presence of monomorphous population of b lymphocytes. Which of the following is likely present on further evaluation

adenovirus antigen
cytomegalovirus
ebv
herpes simplex
hiv genome
parvovirus antigen
why is the ans ebv, ebv infects only t lymphocytes right?
 
pt with severe cellular rejection, was on maximal immunosuppression. 2 weeks later pt develops lymphadenopathy and hepatospleenomegaly. Histo of lymphnodes shows the presence of monomorphous population of b lymphocytes. Which of the following is likely present on further evaluation

adenovirus antigen
cytomegalovirus
ebv
herpes simplex
hiv genome
parvovirus antigen
why is the ans ebv, ebv infects only t lymphocytes right?

EBV infects B cells. The reactive T cells seen on smear are 'normal' CD8+ T cells reacting to the virus infected cells.
 
Drug that alternates platelets function and providing direct arteriolar vasodilation?
Abciximab, aspirin, cilostazol, clopidogrel, nifidepine
Ans cilostazol. Why not clopidogrel?
 
Which of the following changes in the cardiovascular system occurs with normal aging?
Ans increased basal systolic pressure. Why not coronary atherosclerosis
 
An 83 yr old man is brought to the emergency department after being found at home bed ridden and confused. He takes no medication. Temp is 35.6, pulsr is 100, bp is 85?50. bp is unchanged after intravenous infusion of 1 liter of isotonic saline.
Cardiac output- high
Pulmonary capillary wedge pressure low
Systermic vascular resistance- low

Ans early septic shock. I agree with it but why not gi bleeding. Does hypotension improve with administration of saline in gi bleed?
 
A 92 yr old women develops large purpuric lesions over the dorsa of both forearms and hands. The lesions occur in the absence of trauma. Her platelet count is normal. Explanation of her purpura?
Ans dermal collagen atrophy. Why not platelet dysfunction? Is it because with platelet dysfunction atleast minor trauma is required to produce purpura.
 
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A 70yr old women is transferred to a rehabilitative service 2 days after operative repair of a fracture of the right femur. She weighs 65 kgs. Findings on physical and mental status examinations are unremarkable. Which of the following is the most important predictor of success in the rehabilitation of this patient
Ans- activity level before fracture
Other options age, postop hb conc. S.ca and s. vit d
why not post op hb conc
 
Lymph node enlargement in due to proliferation of the immune cells that are fighting the infection. In this case it is Mycobacterium avium intracellulare which like all mycobacteria is cleared through cell-mediated immune response which is mediated by CD4+ T cells.

Also the patient just started anti-retrovirals which would increase his CD4+ count.

Makes perfect sense now. Thank you!
 
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Could someone explain this one? Sketchy Micro and Google say IgG? Also IgG is the only one that would cross the placenta?
262761
 
Hi everyone! I have (quite a few) questions from NBME 20 that I can't seem to figure out. If anyone is able to help, I'd really appreciate it!

  1. 32 yo woman who fell from a ladder. Why is arterial laceration is the right answer?

  2. 55 yo man diagnosed with hypertension. Given an ACE inhibitor, plasma renin activity increases more. Why is the answer renal artery stenosis?

  3. 47 yo woman with increasing cough, shortness of breath, exposure to parakeets. CXR shows reticulogranular changes and biopsy has lymphocytes and granulomas. Does this person have Chlamydia psittaci pneumonia or something else?

  4. 50 yo woman who overdosed. Question is about pharmacokinetics. Can someone explain the relationship between protein binding in plasma and volume of distribution at steady state?

  5. 4 yo boy with fever, abdominal pain, bloody stools. How do you know that this is Shigella and not E. coli? I’ve only ever seen methylene blue stains mentioned in the context of E. coli.

  6. 19 yo college student brought into ED due to chest pain and difficulty breathing. Why is subcutaneous crepitus the right answer?

  7. 66 yo man brought to ED after MVA. Picture of kidney and histo slide. What are the picture and histo slide showing?

  8. Female newborn with respiratory distress. X-ray is given. What condition is this, and what are you supposed to see on the x-ray?

  9. 36 yo woman with 1 month history of joint pain. CT is given. What are you supposed to see on the CT, and why is the answer splenomegaly?

  10. 12 yo girl with with CBFA1 gene mutation. What condition is this?

  11. Newborn male with decreased T4. Why is the answer thyroid hormone-binding globulin deficiency?

  12. 70 yo woman with right femur fracture. Is this indirectly asking about peak bone density?

  13. 6-week-old female newborn with bilious vomit. Why is the answer annular pancreas?

  14. 23 yo woman with DIC. History of splenectomy. How do you know that Strep pneumo is the right answer? Is it just because she has a history of splenectomy?

  15. 56 yo woman with shortness of breath. Iatrogenic chylothorax. Why is the answer central line via the left internal jugular vein?

  16. This question gives you a sequence from beta globin gene and asks about a G->A mutation. What are they asking and how are you supposed to solve this problem?

  17. 16 yo student with uncontrollable sleepiness. Why is the answer direct transition from wakefulness to REM? Is it because they have narcolepsy?

  18. 53 yo woman with 1 year history of abdominal pain. Picture of stool sample is given. What in the history suggests that this is Schistosoma mansoni?

Here you go: NBME Answers and Explanations
 
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60 yr old man who smoked 1 pack for 30 yrs comes in w/ 6 week history of cough and bloody sputum. also 6 lb weight gain in last 8 weeks. CT shows pulmonary lesion, labs show sodium 122 mEq/L. BP 165/101 mmhg. Lab abnormality related to lesion...
Asks increase/decrease in Urine Na+ and Serum Osmolality.
Answer is increase urine Na+ and decrease Serum osmolality.

Can someone plz explain why?
 
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Could someone explain this one? Sketchy Micro and Google say IgG? Also IgG is the only one that would cross the placenta? View attachment 262761
Maternal IgG from maternal toxoplasma infection would cross the placenta, so that doesn't rule IN toxoplasma in the baby. Since IgM cannot cross the placenta you can infer that it was generated in the baby, which means the baby would for sure have it.
 
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Maternal IgG from maternal toxoplasma infection would cross the placenta, so that doesn't rule IN toxoplasma in the baby. Since IgM cannot cross the placenta you can infer that it was generated in the baby, which means the baby would for sure have it.

Got ya! That makes more sense.
262767
 
60 yr old man who smoked 1 pack for 30 yrs comes in w/ 6 week history of cough and bloody sputum. also 6 lb weight gain in last 8 weeks. CT shows pulmonary lesion, labs show sodium 122 mEq/L. BP 165/101 mmhg. Lab abnormality related to lesion...
Asks increase/decrease in Urine Na+ and Serum Osmolality.
Answer is increase urine Na+ and decrease Serum osmolality.

Can someone plz explain why?

He has small cell carcinoma which is associated with paraneoplastic syndromes like SIADH. SIADH causes decreased serum osmolality because of the water retention and increase in urine sodium because the body responds to the inc. water retention with ANP/BNP which increases the sodium excretion. It ends up making a euvolemic hyponatremia.
 
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He has small cell carcinoma which is associated with paraneoplastic syndromes like SIADH. SIADH causes decreased serum osmolality because of the water retention and increase in urine sodium because the body responds to the inc. water retention with ANP/BNP which increases the sodium excretion. It ends up making a euvolemic hyponatremia.
Thank you!!
 
Which of the following changes in the cardiovascular system occurs with normal aging?
Ans increased basal systolic pressure. Why not coronary atherosclerosis

Atherosclerosis is a pathological process, not a normal one. As we age the compliance in our arteries decreases, hence an increase in systolic pressure.
60 yr old man who smoked 1 pack for 30 yrs comes in w/ 6 week history of cough and bloody sputum. also 6 lb weight gain in last 8 weeks. CT shows pulmonary lesion, labs show sodium 122 mEq/L. BP 165/101 mmhg. Lab abnormality related to lesion...
Asks increase/decrease in Urine Na+ and Serum Osmolality.
Answer is increase urine Na+ and decrease Serum osmolality.

Can someone plz explain why?
Thank you!!

Anytime you see a sodium that low you should instantly think SIADH according to Goljan.
 
Can anyone explain why the answer is not B?
low oxygen content in arteries can cause vasodilation and that can increase intracranial pressure?

Annotation 2019-05-18 141829.png
 
So question 50 on the 3rd block. Could anyone explain why the answer is "Antidepressant therapy?" I put low calorie diet, but when I looked back at it during review, it looks like the question presented a patient with depression, and just threw a bunch of labs at me to throw me off.

Any input?
 
So question 50 on the 3rd block. Could anyone explain why the answer is "Antidepressant therapy?" I put low calorie diet, but when I looked back at it during review, it looks like the question presented a patient with depression, and just threw a bunch of labs at me to throw me off.

Any input?
In this clinical vignette, labs are normal except bp and the patient is depressed, so the most likely risk factor for patient mortality is suicide.
 
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"Intention-to-treat" means that you analyze the data solely based on the groups they were assigned to in the beginning of the study.
 
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An 83 yr old man is brought to the emergency department after being found at home bed ridden and confused. He takes no medication. Temp is 35.6, pulsr is 100, bp is 85?50. bp is unchanged after intravenous infusion of 1 liter of isotonic saline.
Cardiac output- high
Pulmonary capillary wedge pressure low
Systermic vascular resistance- low

Ans early septic shock. I agree with it but why not gi bleeding. Does hypotension improve with administration of saline in gi bleed?

Hypovolemic shock is characterized by low CO (because there's not enough volume) and high SVR (to compensate).
High CO and Low SVR are consistent with septic shock, even though they try to confuse you with the normal temp.
 
A 65 year old woman dies 6 months after onset of severe headaches. Brain is shown at autopsy, which is the most likely cell of origin of the neoplasm?
---I put Astrocyte, as the picture showed a big ass midline tumor that looked like it crossed into both frontal lobes, but the answer said meningeal?

A 3-year old boy has a 1-month history of pale skin. Basically the blood smear shows spherocytosis. Now I know spherocytosis is typically Autosomal dominant, but the question stem stated that the patient has "no family history of major medical illness," which made me put homozygous mutation for ankyrin gene. Should I have just ignored that part? I researched a bit and found that spherocytosis can be autosomal recessive, and I would find it high unlikely that no one else in the family suffered from spherocytosis if this was the AD type
 
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A 3-year old boy has a 1-month history of pale skin. Basically the blood smear shows spherocytosis. Now I know spherocytosis is typically Autosomal dominant, but the question stem stated that the patient has "no family history of major medical illness," which made me put homozygous mutation for ankyrin gene. Should I have just ignored that part? I researched a bit and found that spherocytosis can be autosomal recessive, and I would find it high unlikely that no one else in the family suffered from spherocytosis if this was the AD type

I read somewhere that hereditary spherocytosis can be asymptomatic; maybe that's why there was no history? Or, maybe it's not classified as a "major medical illness", but that would be stretching it a bit
 
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2 y/o undergoes resection of R kidney. L is normal. What structural adaptation happened? Why is it increase in glomerular size and not increase in number of glomeruli? Since kidney is not a permanent structure, can't it undergo both hyperplasia and hypertrophy?

The only mild answer explanation I can find is that according to Pathoma, in unilateral renal agenesis, the existing kidney undergoes hypertrophy.
 
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70 yr old man with cerebral infarction 8 yrs ago, The question is neurologic deficits most likely present? But my question is about the photograph, is that a cerebral peduncle infarction at the right side?
BUMP. I had the same issue! I said right dysmetria. I could not for the life of me figure out that lesion, because if it was the right spastic hemiplegia, it probs wouldn't be a midbrain issue, right?
 
1) Can someone explain why a left axis deviation would be associated w/ coarctation of the aorta? Is it because the LV overload will lead to hypertrophy of the LV and thus left axis deviation?
- Yep

2) In someone diagnosed w/ Fanconi syndrome, is there a reason why hypophosphatemia would be more likely to show up in a serum study than hypokalemia? I would assume that due to the massive luminal concentration of Na+ from lack of PCT reabsorption (and associated water) that Na+ will be reabsorbed in the more distal nephron w/ further loss of K+.

3) If you guys remember the vignette featuring a pregnant woman w/ fever and kidney pain and a histology picture of obstructive uropathy, what is the picture showing? Normal tubules?
- Intact tubules w/ inflammatory infiltrate

4) This is just a math problem, but if you have a pt who has an autosomal dominant disease and a family Hx for that disease on her father's side, what's the likelihood of her potential kids getting a cancer that affects those w/ that autosomal dominant disease ~100% of the time.

I'm very confused here since you don't get any info on the potential father. The answer was 50%, but wouldn't that assume the father was homozygous for the recessive trait? If the future father also had the disease (what if they meet at a support group for ppl w/ the condition), then the likelihood of her kids getting the cancer is much higher. I must be missing something here?
- Just assume the most likely scenario of a homozygous recessive father.

Edit: Some kind ppl answered some of these q's for me on another site, so I'll add their answers here in case others were also wondering. I'm still somewhat unsure about the Fanconi syndrome one since RTA type II is also associated w/ hypokalemia and it at least makes sense to be that more K+ would be dumped later to reabsorb Na+ and H2O, but clearly that's not what's happening.
I think it's because phosphate is a specific PCT-associated ion, while K+ is more of a distal nephron-associated ion? Correct me if I'm wrong
 
Hello everyone, i just took and reviewed the answers to NBME 20. I have a few questions that I am still not sure about. Any help will be appreciated, thank you in advance.

section 3, question 25: the question stem describes a pt with chest pain for the past hour. The pt has a history of HTN and type 2 diabetes. The pts vitals are pulse:120, RR:24, BP:98/60. The pt has JVD and crackles are heard in the lungs. The question asks what ECG changes will you see in this pt?
  • The correct answer is ST segment elevation.
  • Another answer choice is QT interval shortening. Can someone explain to me why this pts QT interval is not shortened. My understanding of the QT interval is that it is inversely related to HR. this pt is tachycardic thus will have a short QT interval.

Section 3 question 6: the question stem describes a pt which a hemoglobin concentration of 18.5 and then shows a peripheral blood smear.
  • What is in that blood smear which points to COPD?

Section 4 question 15: a 17YO girl with right sides weakness, slurred speech, elevated pyruvate and lactate and has a NADH dehydrogenase deficiency.
  • The question shows a pedigree and asks what is the mode of inheritance? The answer is mitochondrial.
  • My question is, why are mothers not passing on the disease to all their children. One mother passed on the disease to 2 of her 3 children while another mother passed it on to 1 of her 2 children.

Section 4 question 20: a 36YO pt with decreased urinary output for 3 days was diagnosed with bilateral hydronephrosis. The pts BP is 150/96, pulse is 112, Na: 138, K: 5.9, HCO3: 22, creatinine: 5
  • Bilateral nephrostomy tubes were placed
  • The question asks which will happen to the pts urine output and urine K?
  • I understand that his urine output will increase. What I don’t understand is why is urine K will increase also. If the nephron is secreting K then it must be reabsorbing Na which will worsen the HTN
For the COPD one sect3/q6, he would be hypoxic so increased EPO and thus increased RBC's/Hct. That's how I reasoned it.
 
For the mitochondrial one, look up heteroplasmy in first aid. It basically mosaicism for mitochondrial DNA.
 
A 77 yr old has difficulty fastening buttons, weakness in intrinsic muscles of hands, loss of sensation in little fingers. What is the cause?

A. Chronic lunate subluxation w/ Median N compression.
B. Compression of radial N. in spiral groove.
C. Compression of ulnar N. in carpal tunnel
D. C7-T1 foraminal stenosis.

Why D? And what did you do to rule out the others?
D is the only thing that would be bilateral. They only reason I caught that was because they said little fingerS.
 
265702



how to tell from this question stem that the hernia is indirect vs direct?... groin doesn't necessarily mean scrotum?
 
why does a kidney have inc in size of glomeruli and not number? is this hypertrophy and not hyperplasia? why is this?
Hey! So I had the same question and ended up emailing a pathologist about it. He sent me this from a journal paper:

"Compensatory renal hypertrophy is known to occur after the removal of one kidney in the adult. Nephrogenesis is complete before birth in the human, ... so enlargement (hypertrophy) of the remaining kidney cannot involve the formation of new nephrons. Whether compensatory renal hypertrophy, including compensatory nephrogenesis, can occur in utero, when the placenta is a major regulator of the fetal fluid and electrolyte balance, is unknown. The size of the one functional kidney in human fetuses with either unilateral renal agenesis or contralateral multicystic dysplastic kidney has been found to be larger than normal, suggesting compensatory growth has occurred. However, there are no valid studies of nephron number in such human fetuses."

tl;dr since kidney is already fully made in utero, you can't make new nephrons/glomeruli.
 
please can someone explain this;
23 year old woman with fever DIC hypotension.
Hx: splenectomy after trauma. Which bacteria is cause of sepsis?

I know that strep pneuomoniae is common with splenectomized patient and they need vaccination against strep to prevent infection but I think sepsis and DIC common with gram negative septicemia. So It confused me and I choosed E. coli.

Is DIC also common with gr + bacterial sepsis?
For the sepsis part as you said encapsulated infection is common in splenic dysfunction cuz the sinusoids and red pulp have a huge amount of the B cells necessary for opsonizing polysaccharides of encapsulated organisms. And apparently S pneumonia is the culprit of like 40-60 % of post splenectomy sepsis cases. Also neat fact I just saw that seams testable dog bites in asplenics ●Capnocytophaga spp – C. canimorsus and, less commonly, C. cynodegmi
For this DIC anything promoting a high immune/inflammatory response can be the cause so it can and does happen frequently with blood borne infections esp sepsis. Can happen with fungal and parasitic blood infections as well like babes is. Also apparently the rate DIC in sepsis in gram + is similar to that of gram negative.
 
Thanks so much for the reply! I was trying to be pretty vague about the questions but the 2nd one was in a woman who had a HTN and T2DM and was only listed to be on HCTZ. She came in with a 3 month history of a thin milky discharge and the question asked for the responsible mechanism. The correct answer was drug effect.

Bonus add on question: Why is the chance for HLA match between siblings in organ donation 25%?

In 2017 FA, Endocrinology section has a diagram showing that Renal failure increases Prolactin via decreased elimination.
Now we know that Hyperglycemia is one of the side Effects of HTZ. As this patient is already chronically Diabetic and because of the added hyperglycemia, She might have prematurely developed Diabetic glomerulo-nephropathy (which is the most common cause of End stage renal disease in U.S) leading to Renal failure and hence increased prolactin leading to cause her symptoms. I am not sure 100% but this is the only relation I could derive.
 
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My bad! I didn't go back to look at the picture so mixed up L and R. On the left side, you see where he had the infarction 7 years ago and the tissue is now dead and gone. Right side is normal. As this slice is above the decussation, an issue on the left side will produce right sided hemiparesis, like you said. Here's a pic of a normal stained around the same level from the internet.

View attachment 257674

I understand the logic but why is dysmetria not an option?
 
A 65 year old woman dies 6 months after onset of severe headaches. Brain is shown at autopsy, which is the most likely cell of origin of the neoplasm?
---I put Astrocyte, as the picture showed a big ass midline tumor that looked like it crossed into both frontal lobes, but the answer said meningeal?

I think because the tumor is on the surface of the brain, meningeal origin is of important. Astrocyte would be within the substance.
 
In this clinical vignette, labs are normal except bp and the patient is depressed, so the most likely risk factor for patient mortality is suicide.

That and I read some papers yesterday that a patient with history of depression and MI, by giving antidepressaant therapy you can reduce the risk of future infarct.
 
Part 1: I used the equation: (freq. autosomal recessive)^2 +2(AR)(AD)+ (freq. autosomal dominant)=1
To get the freq. of a single allele: Square root of (1/1600) =.025, then
Part 2: (.8+.2)=1 which is provided. You are looking at the heterozygote frequency (2pq)
so again p(^2) +2pq + q(^2) =1 ... plug it in... so you will be doing the square root of .8 and .2 which is about .9 and .4 then you must do (.9*.4*2) and get about .8

So now you take the answer from part 1 and 2 and
(.025 x .8 x .2) = .004 =1/25

Please someone tell me if this is wrong.. but this was my thought process..

This process is actually wrong. Starting by mentioning that 0.004 is not equal to 1/25 but to 1/250. I'll try to explain it in an easy way:
Starting from the formula: 1=p+q;
If we square it (elevate it to the power of 2) we get:
1=p(^2) + 2pq + q(^2)

We should now the following facts: p(^2) = homozygote normal; 2pq = carrier state, aka heterozygote; q(^2) = homozygote mutated.
We are asked for the amount of carriers with a mutation by deletion which we've been told is 80%. So:
q(^2) = 1/1600; q = 1/40 = 0.025
p=1-q; p = 39/40 = 0.975 (for practicality we can round it up to 1)

Then: 2pq = 2 x (1) x 0.025 = 0.05 or also 2 x (1) x (1/40) = 1/20 (This is the amount of carriers)
Multiply by 80% (0.8): 0.05 x 0.8 = 0.04 or 1/20 x .8 = 1/25

I hope this helps someone, I actually got it wrong on the test and was so frustrated that had to find the easiest way for me to understand and apply the formula.
 
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