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 +0  (nbme18#41)

Is this Guillain barre though? I felt it was Acute inflammatory demyelinating polyradiculopathy, discussed on page 512 FA 2019.

There is no relation to C jejuni here nor does the patient have any other relations to infection such as eating something or etc.


 +1  (nbme18#25)

This patient has a dry tap, which is seen in myelofibrosis and aplastic anemia. The abnormal RBC are most likely dacrocytes (teardrop cells).

AML would have auer rods and many circulating myeloblasts, but nor abnormal RBC.

CML, defined by the t[9;22] Philadelphia chromosome, will have many mature and maturing granulocytes, with a low LAP because this is not a leukemoid reaction.

Dysmyelopoietic syndrome is the same as a myselodysplastic syndrome, which are a group of cancers with immature RBC in the bone marrow that do not become mature. https://en.wikipedia.org/wiki/Myelodysplastic_syndrome

Essential thrombocythemia (which is not essential polycythemia) is just a rare cancer with high platelets, which presents with abnormal blood clotting, leading to thrombosis, strokes, and PE.

Polycythemia vera has very large RBC mass and low EPO due to negative feedback. It is due to a JAK2 mutation and also has high WBC and platelets. Our patient is anemic.

https://www.youtube.com/usmlelive


 +0  (nbme18#25)

his patient has a dry tap, which is seen in myelofibrosis and aplastic anemia. The abnormal RBC are most likely dacrocytes (teardrop cells).

AML would have auer rods and many circulating myeloblasts, but nor abnormal RBC.

CML, defined by the t[9;22] Philadelphia chromosome, will have many mature and maturing granulocytes, with a low LAP because this is not a leukemoid reaction.

Dysmyelopoietic syndrome is the same as a myselodysplastic syndrome, which are a group of cancers with immature RBC in the bone marrow that do not become mature. https://en.wikipedia.org/wiki/Myelodysplastic_syndrome

Essential thrombocythemia (which is not essential polycythemia) is just a rare cancer with high platelets, which presents with abnormal blood clotting, leading to thrombosis, strokes, and PE.

Polycythemia vera has very large RBC mass and low EPO due to negative feedback. It is due to a JAK2 mutation and also has high WBC and platelets. Our patient is anemic.

https://www.youtube.com/usmlelive


 +0  (nbme18#25)

This patient has a dry tap, which is seen in myelofibrosis and aplastic anemia. The abnormal RBC are most likely dacrocytes (teardrop cells).

AML would have auer rods and many circulating myeloblasts, but nor abnormal RBC. CML, defined by the t[9;22] Philadelphia chromosome, will have many mature and maturing granulocytes, with a low LAP because this is not a leukemoid reaction. Dysmyelopoietic syndrome is the same as a myselodysplastic syndrome, which are a group of cancers with immature RBC in the bone marrow that do not become mature. https://en.wikipedia.org/wiki/Myelodysplastic_syndrome Essential thrombocythemia (which is not essential polycythemia) is just a rare cancer with high platelets, which presents with abnormal blood clotting, leading to thrombosis, strokes, and PE. Polycythemia vera (pg 466) has very large RBC mass and low EPO due to negative feedback. It is due to a JAK2 mutation and also has high WBC and platelets. Our patient is anemic.

https://www.youtube.com/usmlelive


 +1  (nbme21#38)

Just remember "Taxes stabilize society." FA2019 Page 433


 +1  (nbme21#6)

The stem is describing primary adrenal insufficiency, or Addison's.

ACTH is being over-produced to stimulate the adrenals to produce cortisol, but they can't respond, either due to atrophy or destruction (TB, autoimmune: DR4, etc.) The first 13 amino acids of ACTH can be cleaved to form α-MSH, which stimulates melanocytes, causing hyperpigmentation. Cortisol helps with BP and his is low.

Patients also have low aldosterone. Low Na and high K is a sign of hypoaldosteronism. Patients retain H and lose HCO3. Losing HCO3 causes Cl- retention in the PCT. This all leads to metabolic acidosis. Loss of cortisol causes anorexia, hypoglycemia, and a low BP as seen in this patient.


 +1  (nbme21#37)

The Lineweaver Burk Plot is mainly interpreted by its X and Y intercepts. The question states that giving B6 increases the activity to normal levels, which means the activity should be the same as the normal. Hence, their Y intercept should be the same, so we are between choices B and C. A and D do not have the same Y intercept as normal. Higher concentrations of B6 caused activity to become normal, and so Vmax will not be changing and we can cancel A and D. A has a lower Vmax and D has a much higher Vmax. The difference between B and C is in their Km. Moving to the left on the X axis makes the Km lower and tells you that affinity is higher so you would not need more B6. But in our case affinity of the enzyme for B6 is really low, which is why we need a ton more B6.

In summary, we want the same Vmax and a higher Km. We want the "normal" activity (same vmax as normal) and we need higher amounts of B6 for success so affinity of the enzyme for B6 is probably very low.

Choice B has a (-1/Km) value closer to 0 which means Km is lower and affinity of the enzyme for its substrate is super low. This makes sense as giving higher amounts of the "competitive" substrate B6 is helping.


 +0  (nbme20#37)

Very easy question. Nonbilious vomit. 1 month age. Most likely scenario is pyloric stenosis.

The vomiting causes loss of HCl so we have the hypochloremia, and renal compensation for this H loss is by preserving protons at the expense of K so that gives hypokalemia. As the disease is named, the red arrow in the image of the stomach is smooth muscle hypertrophy of the pyloric muscularis mucosae, forming the olive-shaped mass felt on palpation. This is a metabolic alkalosis because without Cl-, the basolateral HCO3/Cl exchanger will not work, so you retain HCO3.


 +1  (nbme23#41)

ECG Tracings. The distance between QRS complexes is continuously about 6 boxes, so rate is unaffected. This is a 3rd degree block where teh atria and ventricles are beating independently of eachother and the RR is equivalent all along. The 2nd QRS complex is SUPER narrow, and others are also narrow, which means theyre depolarizing thanks to bundle of His.





Subcomments ...

submitted by hungrybox(232),

Hydrochlorothiazide is a thiazide diuretic => thiazide diuretics are associated with hypokalemia.

What other diuretics are associated with hypokalemia? Loop diuretics.

Why?

Inhibition of Na+ reabsorption occurs in both loop diuretics (inhibit NKCC cotransporter) and thiazide diuretics (inhibit NaCl cortransporter). All of this increased Na+ increases Aldosterone activity.

Relevant to this problem, Aldosterone upregulates expression of the Na+/K+ ATP antiporter (reabsorb Na+ into body, expel K+ into lumen). This results in hypokalemia in the body.

Hang on, there's more high yield info!

Aldosterone does one other important thing - activation of a H+ channel that expels H+ into the lumen.

So, given that this patient has hypokalemia, you know there is upregulation of Aldosterone. Do you think her pH would be high, or low? Exactly, it would be high because inc. Aldosterone => inc. H+ expelled into the lumen => metabolic akalosis.

Now you understand why both loop diuretics and thiazide diuretics can cause what's called "hypokalemic metabolic alkalosis."

hungrybox  jesus this answer was probably too long i'm sorry +1  
meningitis  I disagree. It's the complete thought process needed for many Thiazide/Loop question that can be thrown. Thanks. +5  
amirmullick3  This is what NBME should be providing with each question's correct answer! Thanks hungrybox! +  
amirmullick3  @hungrybox did you mean "All of this DECREASED Na increases aldosterone activity."? +  


submitted by hungrybox(232),

Hydrochlorothiazide is a thiazide diuretic => thiazide diuretics are associated with hypokalemia.

What other diuretics are associated with hypokalemia? Loop diuretics.

Why?

Inhibition of Na+ reabsorption occurs in both loop diuretics (inhibit NKCC cotransporter) and thiazide diuretics (inhibit NaCl cortransporter). All of this increased Na+ increases Aldosterone activity.

Relevant to this problem, Aldosterone upregulates expression of the Na+/K+ ATP antiporter (reabsorb Na+ into body, expel K+ into lumen). This results in hypokalemia in the body.

Hang on, there's more high yield info!

Aldosterone does one other important thing - activation of a H+ channel that expels H+ into the lumen.

So, given that this patient has hypokalemia, you know there is upregulation of Aldosterone. Do you think her pH would be high, or low? Exactly, it would be high because inc. Aldosterone => inc. H+ expelled into the lumen => metabolic akalosis.

Now you understand why both loop diuretics and thiazide diuretics can cause what's called "hypokalemic metabolic alkalosis."

hungrybox  jesus this answer was probably too long i'm sorry +1  
meningitis  I disagree. It's the complete thought process needed for many Thiazide/Loop question that can be thrown. Thanks. +5  
amirmullick3  This is what NBME should be providing with each question's correct answer! Thanks hungrybox! +  
amirmullick3  @hungrybox did you mean "All of this DECREASED Na increases aldosterone activity."? +  


submitted by strugglebus(69),

So you know that 65% of the data will fall within 1SD of the mean. So if you subtract 100-65 you will get 35. Which means that about 16% will fall above and 16% will fall below 1 SD. They are asking for how many will fall above 1 SD. I'm sure there is a better way of doing this, but thats how I got it lol.

sympathetikey  Same! +  
sympathetikey  Except according to FA, it's 68% within 1 SD, so 34%, which split in half is 17%. +2  
amirmullick3  Sympathetikey check your math :D 100-68 is 32 not 34, and half of 32 is 16 :) +1  


submitted by lfsuarez(66),

20 of the 100 men without prostate cancer have abnormal test results.

Specificity = FP/FP+TN = 20/100 = 0.8 = 80%

seagull  almost. 100/120 = 83% roughly 80% +  
amirmullick3  Not sure what lfsuarez and seagull above mean. Here is my explanation. Specificity = TN/(TN+FP). This test gave 20 false positives out of 100 people, and only 15 true negatives out of 50 men. Specificity also equals 1-FPrate, and here the FP rate seems 20% so 100%-20%=80%. +3  
yb_26  abnormal test result means pt has cancer => TP = 35, FN = 15 (50-35), FP=20, TN =80 (100-20) => specificity = TN/(TN+FP) = 80/100 = 0.8 (in % will be 80%) true negatives are 80 out of 100, not 15 out of 50 +2  
bulgaine  If you replace the values from the question in the table of page 257 of FA 2019, yb_26 explanation is correct. Abnormal test = patient has cancer = test + Question says 35/50 men with prostate cancer (so all 50 have cancer) only 35 have abnormal test results, meaning that TP=35 (disease + test +) and FN= 15 (disease + test - because they do have cancer but the test was not abnormal for them ). 20/100 men without prostate cancer have abnormal test results meaning all 100 DONT have cancer but 20 show that they have cancer when its not true so FP=20 (disease - test +) and TN =80 (disease - test -) +  


submitted by yotsubato(264),

Arent we NOT supposed to use ipratropium in old people?

amirmullick3  Who said not to use it in old people? Remember "I pray that tio can breathe soon" and tio is an old uncle in spanish but its also the other drug, tiotrropium. +  
drdoom  discussion of anticholinergics & elderly also discussed at some length (but different context) here: https://www.nbmeanswers.com/exam/nbme22/1288 +  
guillo12  Ipratropium does not penetrate the blood-brain barrier, so I think this is why it can be given to old people. https://www.rxlist.com/duoneb-drug.htm#clinpharm +