I have been instructed by Dr. Goljan to post the following errata on this site. This is directly from him with no interpretation from me, and addresses many of the aforementioned items you have brought to his attention:
If you want me to catalogue and bring more to him for review, you can always PM me. I will try to bring up new stuff I see.
ERRATAS AND CLARIFICATION
Page 106
Margin note
Triple marker for Down syndrome: decreased AFP, increased hCG, decreased urine estriol
Page 129
Table 7-3
Thiamine (vitamin B1)
Korsakoffs psychosis: antegrade and retrograde
Page 138
D. Growth rate
3. Thirty doubling
Equivalent to 109 (superscript)
..
Page 142
Table 8-1
Autosomal dominant cancer syndromes
(two-hit theory)
Page 145
5. DNA repair genes (see Table 8-1 and Table 8-4)
Page 154
4. Apolipoprotein B deficiency (abetalipoproteinemia)
a. Autosomal recessive
Page 182
Tetralogy of Fallot
(7) Tet spells
(a) Sudden increase in hypoxemia and cyanosis
Page 352
Table 17-7
Under Hernia
Direct
Medial border of triangle is rectus abdominis muscle, lateral border is inferior epigastric artery, inferior border is inguinal ligament
Page 358
c. Peutz-Jeghers polyposis
(1) Autosomal dominant
(2) Polyps predominate in the small bowel; less common in stomach and colon
MN: Peutz-Jeghers polyposis: predominance of small intestine polyps
In Andersons textbook of Pathology and Sabistons Surgery, Peutz-Jeghers polyps are listed as hamartomas, because they are a non-neoplastic overgrowth of normal tissue. In all the major texts, the small intestine is listed as the most common site for the polyps. They are less common in stomach and colon. Key point is that it is the only hereditary polyposis syndrome with polyps more common in the small intestine than the colon.
Juvenile polyps are listed as hamartomatous polyps in Andersons Pathology and Morson Gastrointestinal Pathology. They are sometimes called retention polyps.
Hyperplastic polyps are non-neoplastic polyps that some purists consider hamartomas and others a type of metaplasia, with mucosa resembling small bowel. The key point is that they are non-neoplastic and do not transform into cancer.
Page 396
Table 19-1
Glomerular
Nephritic syndrome: protein > 150 mg/ Damage of GBM: non-selective proteinuria with loss of albumin and
24 hours but < 3.5 g/24 hours globulins; example is post-streptococcal glomerulonephritis
Nephrotic syndrome: protein > 3.5 g/ Loss of negative charge on GBM: selective proteinuria with loss of
24 hours albumin and not globulins; example is minimal change disease
I moved the causes of glomerular proteinuria to line-up with nephritic and nephrotic.
The original table was not intended to match up the cause of glomerular proteinuria with an example of a nephritic syndrome and nephrotic syndrome. Because this has caused confusion, I changed diffuse membranous glomerulopathy, the most common cause of nephrotic syndrome in adults, to post-streptococcal glomerulonephritis and lined this up with nephritic syndrome and minimal change disease, the most common cause of nephrotic syndrome in children, with nephrotic syndrome. In the original table, it looked like I was implying that minimal change disease was an example of glomerular injury in the nephritic syndrome, which is of course, incorrect.
Page 395
B. Serum creatinine
2. Creatinine is filtered in the kidneys and not reabsorbed or secreted
This sentence is a generality and is true at the normal concentration of creatinine. It was not part of a discussion of renal failure or of variations of creatinine in emaciated individuals versus muscular people or the effect of drugs on the measurement of serum creatinine. It is true that at high serum levels of creatinine, some is secreted into the urine, so it overestimates the creatinine clearance in renal failure; however, many other tests help corroborate the severity of the renal failure like serum calcium, phosphorus, BUN, and electrolytes showing hyperkalemia and metabolic acidosis. However, irrespective of this, the creatinine clearance is a more practical and cost effective test even though it is not a perfect clearance substance like inulin.
Page 409
Table 19-7
Change IgA glomerulonephritis to IgA glomerulopathy
Page 412
Table 19-8
Type I MPGN
Subendothelial ICs
Page 443
3. Prolactin
a. Prolactin enhances testosterone function and spermatogenesis.
A number of articles discuss the important role that prolactin normally has in promoting the function of the testis and accessory structures. Prolactin receptors are present in the Leydig cells, differentiating germ cells in the seminiferous tubules, and all of the accessory structures. Specifically, in the Leydig cells, prolactin is important in inducing and maintaining LH receptors; which enhances testosterone function. It also directly has an effect on enhancing spermatogenesis. When prolactin is increased, it shuts off GnRH; which, in turn, decreases testosterone production (LH effect) and spermatogenesis (FSH) effect.
Page 504 Table 22-3
Pseudohypoparathyroidism: autosomal dominant
Page 505 Clarification
Hypertension in hypercalcemia:
Hypertension is seen with increased frequency in patients with hypercalcemia (e.g., primary hyperparathyroidism). It may be caused by renal insufficiency and/or calcium-mediated vasoconstriction of arterioles.
Page 537
Table 23-3
Compartment syndrome
Volkmanns ischemic contracture: supracondylar fracture of humerus
.
Page 551-552
2. Pemphigus vulgaris (page 551)
c. Intraepithelial vesicles are located above the basal layer (suprabasal).
(3) Positive Nikolsky sign
Outer epidermis separates from basal layer with minimal pressure
3. Bullous pemphigoid (page 552)
b. Vesicles are subepidermal.
(3) Negative Nikolsky sign
The oral mucosa is involved in one-third of cases, which is not rare as one medical student suggested on an Internet site. This was a really bad mistake in editing, because I had in correct in the notes I used to teach students with before the book came out.
Page 583
2. Role of beta-amyloid (Abeta) protein
b. Defects in degradation of APP by secretases cause an increase in Abeta
(1) Alpha-secretases cleave APP into fragments that cannot produce Abeta
(2) Beta and gamma-secretases cleave APP into fragments that are converted to Abeta.
Beta secretases first must cleave (clip) the APP and then subsequent cleavage by gamma secretases produces Abeta, which forms amyloid that is neurotoxic.
Page 585
Figure 25-17
Coronal section (B) shows (leave out dilated lateral ventricle and) atrophy of the caudate, putamen, and globus pallidus when compared with a normal coronal section (A).
A different picture was placed in there during publication, but the original discussion was not changed. The above is a correct discussion of the new picture.
. Don't get me wrong, I went straight to my book and wrote it in.
