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 Mistypes in the Goljan New RR  

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Author30 Posts

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 Apr 18, 2007 - 7:14 PM


Page 106
Margin note

Triple marker for Down syndrome: decreased AFP, increased hCG, decreased urine estriol

Edited by new_n_lost on Apr 18, 2007 - 7:14 PM


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 Apr 18, 2007 - 7:14 PM


Page 129

Table 7-3

Thiamine (vitamin B1)

Korsakoff’s psychosis: antegrade and retrograde

Edited by new_n_lost on Apr 18, 2007 - 7:15 PM



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 Apr 18, 2007 - 7:16 PM


Page 162

Table 9-1

Under Sturge-Weber syndrome

Delete (AD)

Actually, it is now considered somatic mosacism

Edited by new_n_lost on Apr 18, 2007 - 7:16 PM


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 Apr 18, 2007 - 7:17 PM



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 Apr 18, 2007 - 7:17 PM



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 Apr 18, 2007 - 7:18 PM



Page 352

Table 17-7

Under Hernia


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 Apr 18, 2007 - 7:18 PM


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 Apr 18, 2007 - 7:21 PM



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

Page 412

Table 19-8



Attached Files:
Table 19-1.doc (25 KB, 51 downloads)

Edited by new_n_lost on Apr 18, 2007 - 7:45 PM


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 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 Apr 18, 2007 - 7:56 PM


Thanks nodnodnod


Plz Chk the Table on PG 396 Table 19-1


Attached Files:
Table 19-1.doc (25 KB, 36 downloads)

Edited by new_n_lost on May 24, 2007 - 5:55 PM


thanks doc. great job


Thanks 1000 times, New_n_lost, great job. smiling face I found another mistake and posted it in a separate topic to be noticed.


thanx nnl

ki have suggestion ,,why dont u email the author & give ur correction? usually they $$$$$

u will recieve $$$ & acknowledgement in next edition


Some students contacted himabout this when the book came out last fall. Dr Goljan has a file for errata for download here: www.healthsciences.okstate....dical/pathology/goljan.cfm

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