Step Up Medicine Updates/Errata?

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BiologyBY said:
Just wanted to let everyone know, I got in touch with Dr. Agabegi and he is thanking everyone for putting your time into posting your corrections. Next edition will have these corrections in place
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Please ask him not to pull a "First Aid" & mess up previously correct info in the new edition in order to keep struggling med students on the hook for newer & newer editions every year. :D
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He didn't seem the type to pump a new edition every year; still awaiting a response from LWW about posting on their website, should have a response this coming week
 
Here is another one, under Crohn's disease, in section D it mentions pseudopolyps. These are seen in ulcerative colitis, not Crohn's
 
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Pg 300 Under Hormonal Control, point 2. Calcitonin, should be: "Kidney - decreased Ca++ reabsorption and decreased PO4 reabsorption.
Also, under 3. Vitamin D, should be "increased Ca++ and increased PO4 reabsorption."

Pg 463 Under B. Determine Rate. At the end of point 1, in parenthesis, (300-150-100-75-60-50)
 
TSisk23 said:
Says treatment consists of Aspirin
Then points out that NSAIDs and steroids are contraindicated...checked some sources and it points out NSAIDs/Aspirin are treatment of choice. Steroids are not first line, however, if unsuccessful with the NSAIDs steroids may be used. Anyone else agree what they wrote is misleading/wrong?

Sorry...its on page 12
Click to expand...
As you and others have already said, in general, mainstays for pericarditis are NSAIDs or aspirin. Corticosteroids should only be used if NSAIDs/aspirin don't work. So, I would change point a under number 5 on page 12 to read that "Treatment consists of aspirin or NSAIDs." For point b, cross out "NSAIDs and", and add "unless aspirin/NSAIDs fail to work" at the end of the sentence.

BiologyBY said:
Here is another one, under Crohn's disease, in section D it mentions pseudopolyps. These are seen in ulcerative colitis, not Crohn's
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This is on p. 153 in section C, number 1 if anyone is looking for it.

Actually, both Crohn's and UC can have pseudopolyps, so I'd leave that one alone. If you have big Robbins, look at table 17-10 on p. 851. Colonic Crohn's disease has "marked" pseudopolyps (as does UC), and even small intestinal Crohn's can have "slight" pseudopolyps. Maybe we should add the caveat on p. 153, section C, number 1 that pseudopolyps mainly occur in colonic Crohn's.

PenguinHead said:
Pg 300 Under Hormonal Control, point 2. Calcitonin, should be: "Kidney - decreased Ca++ reabsorption and decreased PO4 reabsorption.
Also, under 3. Vitamin D, should be "increased Ca++ and increased PO4 reabsorption."
Click to expand...
The only thing I'd add to this is to specify that Penguin's second point (for vitamin D) is also referring specifically to the kidney, not to vitamin D in general, which is already correct as written.

So, for section 2 (calcitonin) point b (kidney), both calcium and phosphate reabsorption should be decreased. For section 3 (vitamin D) point b (kidney), both calcium and phosphate reabsorption should be increased.

Ok, and I found one more. This is a minor error, but it might as well be corrected while we're at it. On p. 332, Hemophilia A section, part A (general characteristics), number 1, the part in parentheses should read "approximately 1/10,000 male patients", *not* 1/1000. (On a side note, some sources reported the incidence of hemophilia A to be 1/10,000-1/5000, but never as high as 1/1000.)

At some point, I'll update the master list once more. Thanks again to everyone for contributing. You've done a heck of a job. :thumbup:
 
you are correct about pseudopolyps, it should say predominantly UC.
 
p. 203, second quick hit says that there is no known association between essential tremor and Parkinson's disease. This does not seem to be strictly true. Several studies suggest that at least some patients can have both ET and PD, that some PD kindreds also have members with ET, that there is overlap in pathology and imaging findings of ET vs. PD, and that early-onset ET may be a risk factor for developing PD. Here is a recent review article that summarizes the data concerning an ET/PD relationship. I would change that sentence to say "there may be some" instead of "there is no known".
 
I got an e-mail saying the list was forwarded to the editor. Let's wait and see what happens
 
The editors shouldn't be in such a hurry, BiologyBY, because there are more mistakes! Page 210, the quick hit that talks about locked in syndrome says that patients still have their respiratory muscles spared. I am on my neuro rotation right now, and I got that wrong on a pimp question a few days ago when I said respiratory muscles. The only movements they can make spontaneously are vertical eye movements (not horizontal) and blinking their eyelids, nothing else.

This is sort of a tangent, but have any of you ever seen someone with locked in syndrome? I haven't, but it must be interesting!
 
CCLCMer said:
The editors shouldn't be in such a hurry, BiologyBY, because there are more mistakes! Page 210, the quick hit that talks about locked in syndrome says that patients still have their respiratory muscles spared. I am on my neuro rotation right now, and I got that wrong on a pimp question a few days ago when I said respiratory muscles. The only movements they can make spontaneously are vertical eye movements (not horizontal) and blinking their eyelids, nothing else.

This is sort of a tangent, but have any of you ever seen someone with locked in syndrome? I haven't, but it must be interesting!
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There are more mistakes almost always. Just keep finding them and we'll keep adding them and forwarding to Lippincott
 
I found another one:

p. 225-Table 5.5

The bottom entry talking about nystagmus direction is wrong for peripheral vertigo (on the right side, very bottom). It should say, "Direction of nystagmus: unilateral horizontal with torsional component; nystagmus is never vertical."

I double checked this, and it is central vertigo that can have a vertical component, not peripheral. One source went so far as to say that a vertical nystagmus was pathognomonic for central vertigo in a patient presenting with vertigo.
 
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Just wanted to thank everyone for their contributions. It's really helping me review with Step-Up. Thanks!
 
QofQuimica said:
I found another one:

p. 225-Table 5.5

The bottom entry talking about nystagmus direction is wrong for peripheral vertigo (on the right side, very bottom). It should say, "Direction of nystagmus: unilateral horizontal with torsional component; nystagmus is never vertical."

I double checked this, and it is central vertigo that can have a vertical component, not peripheral. One source went so far as to say that a vertical nystagmus was pathognomonic for central vertigo in a patient presenting with vertigo.
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you beat me to that one :) i thought i was going crazy reading that line
 
On p. 430 under D. Treatment (for IBS), both cisapride and Zelnorm are listed, but these have been taken off the market in the US.
 
CCLCMer said:
The editors shouldn't be in such a hurry, BiologyBY, because there are more mistakes! Page 210, the quick hit that talks about locked in syndrome says that patients still have their respiratory muscles spared. I am on my neuro rotation right now, and I got that wrong on a pimp question a few days ago when I said respiratory muscles. The only movements they can make spontaneously are vertical eye movements (not horizontal) and blinking their eyelids, nothing else.

This is sort of a tangent, but have any of you ever seen someone with locked in syndrome? I haven't, but it must be interesting!
Click to expand...

OT, but the diving bell and the butterfly is an EXCELLENT french film about exactly this. you should check it out.:thumbup:
 
On p. 189 under B. Hyperosmolar hyperglycemic nonketotic syndrome, 2. Clinical features, point a. should say "thirst, polyuria" not "thirst, oliguria" ~ unless he is suggesting that the pt is in prerenal failure?

On p. 283, the first quick hit says that ACEIs are contraindicated in renovascular HTN, but then in the text it says ACEIs are indicated. I think the quick hit maybe should read "ACEIs are contraindicated in bilateral renal artery stenosis."
 
This is a just a minor type-o but on p. 60 under A. "general characteristics" of septic shock, point 3 says to refer to Box 1-14 when really it should be box 1-15. The same correction should be made under B. "clinical features" for point 2 when it says to refer to Box 1-14 for the signs of SIRS.
 
p. 191
B. Causes
4. Ethanol ingestion
b. Metabolism of EtOH that INCREASES (not decreases) NADH
 
p. 210
A. General characteristics
2. Sites of herniation
a. Uncal herniation
-IPSI-(not CONTRA) lateral hemiparesis due to the ipsilateral uncus compressing the contralateral cerebral peduncle
 
Page 83 Sarcoidosis, under 3. Diagnosis, letter g: Pulmonary function tests for Sarcoidosis the FEV1/FVC ratio is increased/normal (it is a restrictive lung disease) NOT decreased. Maybe FEV1/FVC ratio can also be decreased with airway obstruction, i.e. bronchial involvement?
 
jsong812 said:
p. 210
A. General characteristics
2. Sites of herniation
a. Uncal herniation
-IPSI-(not CONTRA) lateral hemiparesis due to the ipsilateral uncus compressing the contralateral cerebral peduncle
Click to expand...
I think you are correct due to the fact that uncus compresses on the midbrain affecting the fibers in the contralateral crus which will lead to ipsilateral hemiparesis, thus false localizing sign
 
Tommy1496 said:
Page 83 Sarcoidosis, under 3. Diagnosis, letter g: Pulmonary function tests for Sarcoidosis the FEV1/FVC ratio is increased/normal (it is a restrictive lung disease) NOT decreased. Maybe FEV1/FVC ratio can also be decreased with airway obstruction, i.e. bronchial involvement?
Click to expand...
Correct, FEV1/FVC is increased in general due to restrictive pattern. When enlarged lymph nodes in the chest compress airways or when internal inflammation or nodules impede airflow, obstructive changes are seen.
 
Geeez, aside from the medical errors, these guys can't even spell words correctly.

p.449: Quick Hit in the margins - "Tympanic Mimbane Perforation".

Someone please tell me what the hell a "mimbane" is.
 
BiologyBY said:
I think you are correct due to the fact that uncus compresses on the midbrain affecting the fibers in the contralateral crus which will lead to ipsilateral hemiparesis, thus false localizing sign
Click to expand...

The localization of classical symptoms of uncal herniation is not always the same. Here's what Blumenfeld says on page 141.

"In uncal herniation, the dilated pupil is ipsilateral to the lesion in 85% of the cases."

"...often the hemiplegia is contralateral to the lesion either because of uncal herniation compressing the ipsilateral corticospinal tract in midbrain, or because of a direct effect of the lesion on the ipsilateral motor cortex, or both. However, sometimes in uncal herniation the midbrain is pushed all the way over until it is compressed by the opposite side of the tentorial notch. In these cases the contralateral corticospinal tract is compressed, producing hemiplegia that is ipsilateral to the lesion. This is called Kernohan's phenomenon."

Also, compression on the midbrain or CNIII causes ipsilateral mydriasis (not anisocoria, which just mean unequal pupil sizes, ispilateral anisocoria is meaningless).

The midbrain is never compressed against bone. See the above quote from Blumenfeld. It's sometimes compressed against the cerebellar tent (tentorial notch) contralateral to the herniated uncus.
 
On page 208 in the Delirium Versus Dementia table, it has "Sundowning" as a delirium course. I'm pretty sure it's a feature of dementia, Alzheimer's in particular.

Someone please correct me if I'm wrong.
 
Colbert said:
On page 208 in the Delirium Versus Dementia table, it has "Sundowning" as a delirium course. I'm pretty sure it's a feature of dementia, Alzheimer's in particular.

Someone please correct me if I'm wrong.
Click to expand...
You are right about patients with Alzheimer's sundowning, but sundowning is definitely a feature of delirium too. I guess it should be added to both sides of the table rather than differentiating them, although a confounding factor is that many demented patients are also delirious. (Dementia is one of the major risk factors for delirium.)
 
QofQuimica said:
You are right about patients with Alzheimer's sundowning, but sundowning is definitely a feature of delirium too. I guess it should be added to both sides of the table rather than differentiating them, although a confounding factor is that many demented patients are also delirious. (Dementia is one of the major risk factors for delirium.)
Click to expand...
100% correct, I've seen sundowning in delirious patients
 
BiologyBY said:
100% correct, I've seen sundowning in delirious patients
Click to expand...
As have I. After almost getting clocked by one of my surgery patients during a post-op check that had to be hastily aborted, I have a healthy respect for the effects of delirium at night. :laugh:
 
QofQuimica said:
Originally Posted by TSisk23
Says treatment consists of Aspirin
Then points out that NSAIDs and steroids are contraindicated...checked some sources and it points out NSAIDs/Aspirin are treatment of choice. Steroids are not first line, however, if unsuccessful with the NSAIDs steroids may be used. Anyone else agree what they wrote is misleading/wrong?

Sorry...its on page 12
Click to expand...
As you and others have already said, in general, mainstays for pericarditis are NSAIDs or aspirin. Corticosteroids should only be used if NSAIDs/aspirin don't work. So, I would change point a under number 5 on page 12 to read that "Treatment consists of aspirin or NSAIDs." For point b, cross out "NSAIDs and", and add "unless aspirin/NSAIDs fail to work" at the end of the sentence.
Click to expand...

Sorry to dwell on this point but
I just wanted to make a clarification in the errata regarding pg. 12

The treatment listed on pg. 12 I believe is in reference to treating acute pericarditis in the context of a complication of acute MI. On pg 33, however, when the text discusses Acute Pericarditis alone, it does list NSAIDs as the mainstay of therapy.

Does anyone else have any thoughts on this point?

In my research, I found this as a good summary of treatment for Acute Pericarditis (it seems to agree with other reputable sources as well) because treatment depends on the etiology:
---------------------------------------------------------------------------------------
Pericarditis, Acute: Treatment & Medication - emedicine Cardiology

"Treatment for specific causes of pericarditis is directed according to the underlying cause. For patients with idiopathic or viral pericarditis, therapy is directed at symptom relief. NSAIDs are the mainstay of therapy. These agents have a similar efficacy with relief of chest pain in about 85-90% of patients within days of treatment. Ibuprofen has the advantage of few adverse effects and increased coronary flow. Indomethacin has a poor adverse effect profile and reduces coronary flow.

Aspirin is recommended for treatment of pericarditis after STEMI.

Colchicine, in combination with an NSAID can be considered in the initial treatment to prevent recurrent pericarditis. Colchicine, alone or in combination with an NSAID, can be considered for patients with recurrent or continued symptoms beyond 14 days.

Corticosteroids should not be used for initial treatment of pericarditis unless it is indicated for the underlying disease, the patient has no response to NSAIDs or colchicine, or both are contraindicated."
---------------------------------------------------------------------------------------

I bolded some key points from the article. Also, I think point b may have some truth in that corticosteroids may interfere with myocardial healing/scar formation in the post-MI setting. Could NSAIDs possibly also interfere with this process and that is why it is specified here?


:thumbup::thumbup: And thank you QofQuimica and others for the excellent errata :thumbup::thumbup:
 
Pg 306 Section C. Treatment (top/middle) add for tx of hyperK (below diuretics):
4. Beta2 Agonist (like albuterol) which also shifts K+ into cell. [Source]
 
P. 293, Section A. Anyone notice that their math is a little funny? Under number four, part b, the first point should say that plasma is *1/4* of ECF, not 1/3. The second point should say that interstitial fluid is *3/4* of ECF, not 2/3. If you change those fractions, the math will work out for the percentages.

(Actually, different books give different numbers, but this 25/75 ratio seems to be the most common one out there.)

Ok, this list needs to be majorly collated. I'll try to do it this weekend. Thanks to all of you who keep finding and reporting mistakes. I hope the authors appreciate your hard work. :)
 
Page 411, Table 12-2: Thiazide diuretics, hyperuricemia is written twice

Page 382, Under number 2 (stage 2 of Lyme disease), letter c: Encephalitis is written twice (bullet points 2 and 4)
 
Page 74 General Characteristics of Pleural Effusion

Point 2 should say "visceral or parietal pleura" not "parenteral"
 
Another mistake:
Pg 20, Quick hit box

PVC with Trigeminy is two normal beats, followed by a PVC...

NOT as is written: a normal a sinus beat followed by 2 PVCs.
 
wedgeoli said:
Another mistake:
Pg 20, Quick hit box

PVC with Trigeminy is two normal beats, followed by a PVC...

NOT as is written: a normal a sinus beat followed by 2 PVCs.
Click to expand...
good catch. What was written is called a couplet in case anyone cares
 
Thanks everyone for the updates. Here's some more stuff I found in the cardiac section

p. 37 Part D: Treatment, 1. Medical, point b--Cross out Infective Endocarditis Prophylaxis. It is no longer recommended.

p. 39 Part E. Treatment, 4. "Endocarditis prophylaxis..." Cross out this line

p. 42 Part C: Treatment, point 3 "Patients with a history of rheumatic fever...." Can also cross out this line

Here's the link to the recommendations for endocarditis prophylaxis from the American Heart Association
http://www.americanheart.org/presenter.jhtml?identifier=11086
Basically it says you only give ATB prophylaxis before dental & GI/GU procedures if you've previously had endocarditis, have a prosthetic heart valve, or certain congenital heart diseases

p. 41: *Epstein's anomaly* should be changed to Ebstein's anomaly. Also, you may want to add a quick hit next to it: Ebstein's anomaly can be caused by Lithium use in the 1st trimester of pregancy, and in those with Wolff Parkinson White Syndrome

Hope this helps!

 
do we have any update to this list?
 
Schatzki's Ring (page 144) 4th bullet: is NOT due acid/alkali ingestion (suicide attempt). As a matter of fact it is somewhat common. Unknown why they occur, but here are 4 from e-medicine (link):

  1. The ring is a pleat of redundant mucosa that forms when the esophagus shortens transiently or permanently for unknown reasons.
  2. The ring is congenital in origin.
  3. The ring is actually a short peptic stricture occurring as a consequence of gastroesophageal reflux disease.
  4. The ring is a consequence of pill-induced esophagitis.
Also known as B rings (esophogeal rings - see pic on uptodate.com).

In case someone is wondering about acid/alkali ingestion (also from e-medicine):
Ingestion of alkaline or acidic agents can cause caustic injury to the esophagus. Severe injuries have occurred from ingestion of alkaline agents, such as lye, sodium and potassium hydroxides in oven cleaners, washing detergents, Clinitest tablets, cosmetics, soaps, and button batteries. Ingestion of caustic agents can lead to esophageal stricture. [emphasis added] ...

By definition, the Schatzki ring is a web because it is composed of only mucosa and submucosa. [whereas a stricture is formed as a result of scar formation from swallowing the caustic substance, from what I've gathered - if someone knows otherwise, plz post]
 
Typo on pg 62 - Quick Hit on bottom of page should say:

"In COPD, the FEV1/FVC ratio is <0.75-0.80." NOT how it is written as "...FEV1/FEV..."

I suppose you could also write it as FEV1/FEV6 because FEV6 supposedly gives you a value close to FVC in these patients as is indirectly noted at the bottom of the page in part B, 2, a, but FEV1/FVC is more commonly used and perhaps more accurate.
 
i have been using first edition of step up to medicine. could anyone please let me know where to find errata for it.

thank you
 
Mech Vent, p 63
A. General characteristics
2 e. PaO2 should be either 50 or 60, I don't think <70 would qualify - but I honestly don't know what the true answer is. definition is <60

Correct me if I'm wrong!
 
Glad to find this thread! Past posters - thanks so much for pointing these out! Was there ever an updated document or something similar to possibly these and more from the 2nd ed authors directly? i.e. website?

I just got the book and used the scratch-off code to access lww's "thepoint," hoping to find an errata list - but nothing there except for the online e-book version of this. :rolleyes:
 
Tommy1496 said:
Page 411, Table 12-2: Thiazide diuretics, hyperuricemia is written twice

Page 382, Under number 2 (stage 2 of Lyme disease), letter c: Encephalitis is written twice (bullet points 2 and 4)
Click to expand...

I can't believe I didn't see this thread before (tried to find an errata thread) but at any rate I noticed the hyperuricemia thing myself too and am about 99% sure that one of the hyperuricemias should be hypercalcemia since HCTZ can cause hypercalcemia.
I don't have any good ideas for what the other encephalitis is :laugh:
 
Confusion:

p. 300 - "in hypoalbuminemia the total calcium is low but ionized calcium is normal" ... how does this make sense? shouldnt total calcium be same and ionized calcium be increased?
 
Doctor4Life1769 said:
Confusion:

p. 300 - "in hypoalbuminemia the total calcium is low but ionized calcium is normal" ... how does this make sense? shouldnt total calcium be same and ionized calcium be increased?
Click to expand...

It sounds correct like is written in the book. Think of it like total thyroid and TBG being up in pregnancy but free thormone is normal. I think anyway.
 
p. 31
The Quickhit says leg raise decreases LV volume, but the text (2. Signs, c, first bullet) says it increases LV filling.

I believe the text is right and leg raise causes increase in LV filling due to increase venous return.
 
bonnielass13 said:
On p. 283, the first quick hit says that ACEIs are contraindicated in renovascular HTN, but then in the text it says ACEIs are indicated. I think the quick hit maybe should read "ACEIs are contraindicated in bilateral renal artery stenosis."
Click to expand...

ACE inhibitors are first line medical therapy for unilateral AND bilateral renovascular HTN.

See UpToDate articles "Treatment of unilateral atherosclerotic renal artery stenosis" and "Treatment of bilateral atherosclerotic renal artery stenosis":

On unilateral: "If medical therapy is chosen, the preferred antihypertensive regimen is an angiotensin inhibitor"

On bilateral: "For hypertension control, we recommend an ACE inhibitor or angiotensin II receptor blocker (ARB), often in combination with diuretic"

The reason this is works: So, yes, we know if you block AII in a patient with renovascular disease you'll get a creatinine bump. But remember, the goal of therapy is not to improve or maintain GFR, it's to keep blood pressure down. Most patients will have a large GFR reserve. Since the effect is reversible, you can always stop it if you get into trouble.

Per UpToDate on bilateral disease: "The net effect is a rise in the serum creatinine concentration in most patients with severe bilateral renovascular disease [8] and some of those with less severe disease. However, these observations do not mean that ACE inhibitors or ARBs are contraindicated in this disorder as long as the patient is carefully monitored."
 
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