new_n_lost
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We All Love the Author But Mistakes can Happen by Anyone So here is a List of His Own Updated Errata.
Page 41
Under 1. Acute inflammation (see Fig. 2-13A)
Under 2. Chronic inflammation (see Figure 2-13B)
Edited by new_n_lost on 04/18/07 - 09:14 PM
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| new_n_lost
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Page 106
Margin note
Triple marker for Down syndrome: decreased AFP, increased hCG, decreased urine estriol
Edited by new_n_lost on 04/18/07 - 09:14 PM
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Page 128
Under D. Vitamin K, 3. Function
a. g-Carboxylates glutamate residues in vitamin K-dependent procoagulants and anticoagulants (protein C and S)
(1) Procoagulants include factors II (prothrombin), VII, IX, and X (delete protein C and S, which are anticoagulants)
Edited by new_n_lost on 04/18/07 - 09:14 PM
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Page 129
Table 7-3
Thiamine (vitamin B1)
Korsakoff’s psychosis: antegrade and retrograde
Edited by new_n_lost on 04/18/07 - 09:15 PM
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NEOPLASIA
Page 138
D. Growth rate
3. Thirty doubling…
· Equivalent to 109…..
Page 142
Table 8-1
Autosomal dominant cancer syndromes Retinoblastoma
(two-hit theory)
Page 145
5. DNA repair genes (see Table 8-1 and Table 8-4)
Edited by new_n_lost on 04/18/07 - 09:16 PM
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Page 162
Table 9-1
Under Sturge-Weber syndrome
Delete (AD)
Actually, it is now considered somatic mosacism
Edited by new_n_lost on 04/18/07 - 09:16 PM
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| new_n_lost
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Heart Disorders
Page 173
Under Prinzmetal’s angina
Increase in endothelin
Page 182
Tetralogy of Fallot
(7) Tet spells
(a) Sudden increase in hypoxemia and cyanosis
Edited by new_n_lost on 04/18/07 - 09:17 PM
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RBC
Page 203
Under C. 3. (c) Microcytic and normocytic cells with increased central area of pallor (Fig. 11-6)
Edited by new_n_lost on 04/18/07 - 09:17 PM
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RESPI
Page 300
Table 16-3
Put Chlamydia, Rickettsia, Mycoplasma under Bacteria not Viruses heading
Page 323
Table 16-5
Under Bronchial hamartoma
Put- Peripheral (90%), Central (10%)
Edited by new_n_lost on 04/18/07 - 09:18 PM
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GI
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 Anderson’s textbook of Pathology and Sabiston’s 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 Anderson’s 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.
Edited by new_n_lost on 04/18/07 - 09:18 PM
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Hepato - Biliary
Page 371
Under e. Chronic HBV, (1) …converts to anti-HBc-IgG
Page 375
Margin Note
Fulminant hepatic failure: ¯ transaminases, PT and ammonia
Pages 377 and 378
Under A. Alcohol related disorders
1. Should say (Chapter 6)
3. Should say (Chapter 6)
4. Should say (Chapter 6)
Edited by new_n_lost on 04/18/07 - 09:21 PM
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| new_n_lost
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Renal
Page 396
Table 19-1
See the Attached Doc for the Table
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
Attached Files:
Table 19-1.doc (25 KB, 36 downloads)
Edited by new_n_lost on 04/18/07 - 09:45 PM
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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.
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Page 446 (not an errata; just a better term)
IX. Erectile dysfunction
Drop the definition underneath since it is self-explanatory
Page 479
Under 3. Traumatic fat necrosis
c. Painless, indurated mass
add: · Painful in acute stage
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 516 (not an errata; just an additional designation)
C. Syndrome X (metabolic syndrome)
Page 532
Under Septic arthritis, change C5-C9 to C6-C9.
Page 537
Table 23-3
Compartment syndrome
Volkmann’s ischemic contracture: supracondylar fracture of humerus….
Page 543
Under A. Staphylococcus aureus skin infections
Add d. Impetigo
Page 544
Under C. Impetigo
1. Most often caused by Staphylococcus aureus
· Streptococcus pyogenes second most common cause
3. Presence of bullae commonly occurs with Staphylococcus aureus
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 569
Under 4. Sturge-Weber syndrome
a. Somatic mosaicism or sporadic
It is not autosomal dominant
Page 578, Table 25-2
Under Rabies virus: Most often transmitted by raccoon bite (40%)
Other vectors are dog, skunk, bat, coyote
Page 579
Under Table 25-4: Treponema pallidum
Argyll-Robertson pupil (pupils accommodate but do not react)
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.
Page 586
Under F. Werdnig-Hoffman disease
· Lower motor neuron disease that occurs in children.
QUESTION 10 (Page 652 has question, page 657 has discussion)
A 9-month-old girl has an infection on her face that began as erythematous macules. She later develops pustules that rupture and cause honey-colored crusted lesions. The girl's 5-year-old brother develops similar lesions. Which of the following is the causal agent?
A. Staphylococcus aureus
B. Herpes simplex virus type 1
C. Malassezia furfur
D. Propionibacterium acnes
E. Trichophyton rubrum
A (Staphylococcus aureus) is correct. The child has impetigo, which causes honey-colored crusted lesions that cover shallow ulcerations of the skin. Staphylococcus aureus is the most common cause of this superficial skin lesion. Streptococcus pyogenes is the second most common cause of impetigo. Impetigo is highly contagious, which explains why the child's brother develops similar lesions.
B (herpes simplex virus type 1) is incorrect. Herpes simplex virus type 1 produces vesicles and pustules on the vermilion border of the lip. It does not produce honey-colored crusted lesions on the face.
C (Malassezia furfur) is incorrect. M. furfur, a superficial dermatophyte, causes tinea versicolor and seborrheic dermatitis (dandruff). It does not produce honey-colored crusted lesions on the face.
D (Propionibacterium acnes) is incorrect. P. acnes is an anaerobe involved in producing the inflammatory reaction associated with acne vulgaris. It does not produce honey-colored crusted lesions on the face.
E (Trichophyton rubrum) is incorrect. T. rubrum, a superficial dermatophyte, causes tinea corporis (body), tinea cruris (groin), and tinea pedis (foot). It does not produce honey-colored crusted lesions on the face.
Edited by new_n_lost on 04/18/07 - 09:56 PM
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| ShweHope99.9998
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Thanks 
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| new_n_lost
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Plz Chk the Table on PG 396 Table 19-1
NEPHROTIC SYN HAS SELECTIVE PROTIENURIA & LOSS OF ALBUMIN ONLY WHEREAS IN NEPHRITIC SYN WE HAVE NON SELECTIVE LOSS OF PROTEINS ALBUMIN N GLOBULINS, TOO
Attached Files:
Table 19-1.doc (25 KB, 26 downloads)
Edited by new_n_lost on 05/24/07 - 07:55 PM
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| mylife_step1
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thanks doc. great job
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| hedieh
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Thanks 1000 times, New_n_lost, great job.  I found another mistake and posted it in a separate topic to be noticed.
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| yoga
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thanx nnl
ki have suggestion ,,why dont u email the author & give ur correction? usually they $$$$$
u will recieve $$$ & acknowledgement in next edition
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| edie
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Some students contacted himabout this when the book came out last fall. Dr Goljan has a file for errata for download here: http://www.healthsciences.okstate.edu/college/bio...
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| new_n_lost
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Yup thts it i have downloaded and posted the file in under separate posts so that ppl can edit and correct mistake easily. Thanks Edie for posting the link i had forgotten that.
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| angelsmile
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Where can I get this book? I found one on Amazon but it was published in 2004. Any new edition?
Thanks!
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| new_n_lost
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angelsmile wrote:
Where can I get this book? I found one on Amazon but it was published in 2004. Any new edition?
Thanks!
U can get it from here.
http://search.barnesandnoble.com/booksearch/isbnI...
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| angelsmile
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Thanks!
How about this one: http://search.barnesandnoble.com/booksearch/isbnI...
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| somdatta.gupta
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Hi folks, Just wanted to add a new correction to the Goljan Notes of Systemic Pathology :
Respiratory System, Page 79 of my notes
Causes of an increased A-a gradient..
It's written Ventilation without perfusion produces intrapulmonary shunting eg. Atelectasis.
It should be - Perfusion without Ventilation (ventilation problem)
produces intrapulm shunts and eg is atelectasis, Giving 100% Oxygen
won't help raise the PaO2.
Pg 80 - It's written Perfusion without Ventilation produces increased
Dead Space eg. Pulmonary Embolus. Giving 100% oxygen does increase PaO2
since normally ventilated lung can make up the difference.
CORRECTION - It should be :
Ventilation without Perfusion (Perfusion problem) ... the rest is the same .
Goljan's book ( Pathology Review) doesn't contain the mistakes. You can re check it there too - Pg 133 of 2004 edition.
Hope this helps !
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