Questions

The Osler Institute

Pathology Board Review Course

Self-directed Study Faculty Question Book AP

Table of Contents

SYSTEMIC PATHOLOGY......................................1
CARDIOVASCULAR PATHOLOGY................................1
Edited by Allen Burke, MD...................................1
FEMALE REPRODUCTION.........................................16
Edited by Karen Hughs, MD..............................16
MALE REPRODUCTIVE PATHOLOGY ........................24
Edited by Mahul Amin, MD................................24
HEMATOPATHOLOGY...............................................33
Edited by Harry L. Ioachim, MD........................33
DERMATOPATHOLOGY ............................................36
Edited by Rosalie Elenitsas, MD........................36
NEUROPATHOLOGY .................................................41
Edited by Eugene Hoenig, MD...........................41
RENAL AND URINARY .............................................44
Edited by Guillermo Ferrera, MD......................44
SPECIAL TECHNIQUES .......................................57
ELECTRON MICROSCOPY .........................................57
M. L. Christ, MD................................................57
GENERAL PATHOLOGY.....................................62
DEFICIENCY DISEASE ...............................................62
Edited by James L. Caruso, MD.........................62
FORENSIC PATHOLOGY ...........................................62
Edited by James L. Caruso, MD.........................62
INFECTIOUS DISEASE...............................................68
Edited by Barbara A. Sampson, MD..................68
INFLAMMATION AND REPAIR...................................75
Edited by Gregory J. Pomper, MD.....................75
GENERAL PATHOLOGY -- OTHER.............................78
Edited by Gregory J. Pomper, MD.....................78
CYTOLOGY.............................................................78
CYTOLOGY NON-GYNECOLOGICAL......................78
Edited by Tamara Handerson, MD....................78
FINE NEEDLE ASPIRATION ......................................81
Edited by George Cook, MD..............................81

Preface
These questions and answers, provided by previous participants, were edited by the faculty and typeset
but have not had the final proofreading by the faculty.

Most of the questions are single best choice. Some of the questions are K-type which have four answers
designated 1, 2, 3, 4. One or more of the K-type answers may be correct as follows:

Directions Summarized
A B C D E
1,2,3 1,3 2,4 4 all are
only only only only correct

There are a few matching questions and occasional simple true/false questions as well as some open -
ended response questions which are not in multiple choice format.
Pathology Review Course
Ap99que.doc
1
Systemic Pathology
Cardiovascular Pathology
Edited by Allen Burke, MD
Note: There is no guarantee regarding the
correctness of the answers. The questions are
approximate, as remembered by previous
residents. Even slight variations in wording
may result in different answers being correct,
due to semantic reasons, and many questions
are repeated in different ways. Developments
in medical knowledge since the questions
were recorded may change which answer is
most accurate. Errors in the answer discus-
sion (in bold type) have, we hope, been kept
to a minimum, as a fair degree of effort has
been given to researching the probable best
answer. What is important about this study
guide is to become acquainted with the topics
that have been previously used on the exami-
nation and to direct your study to these areas,
always keeping in mind that a significant
percentage of questions each year are not
repeats.
Aortic Dissection
1. [Gross photograph depicts the ascending
aorta with a linear transverse tear situated two
centimeters from the aortic valve] Which of
the following statements is correct?
a. The patient most likely had systemic
hypertension.
b. The patient most likely had tertiary lues.
c. Examination of the distal aorta reveal
marked aneurysmal dilation.
d. This condition affects men and women
equally.
e. This is a common complication follow-
ing coronary artery bypass graft surgery.

2. [Gross of a heart with an intimal tear in the
ascending aorta]. Which of the following is
associated with these findings?
a. rheumatic fever
b. lupus
c. hypertension
d. none of the above

3. [Microscopic slide of a dissecting aneurysm
of the aorta with cystic medial change] This
vascular lesion may be caused by which of
the following?
a. a gene defect located on a sex
chromosome
b. a autosomal recessive disease
c. syphilis
d. Arfans syndrome
e. Ehlers-Danlos syndrome

4. [An aorta with dissection] Which of the
following statements is false regarding this
finding?
a. This condition occurs most commonly
in the 40-60-year-old age group.
b. This finding is two to three times more
frequent in men.
c. Hypertension is almost invariably an
antecedent.
d. This finding is rare in pregnant females.

5. [Gross photo of an abdominal aorta cut off
at either end, but with the intercostal vessels
visible. The inner wall was very smooth, but
there was a dissecting aortic aneurysm.]
Which of the following is not characterized
by these findings?
a. pregnancy
b. syphilis
c. an autosomal dominant disorder
d. hypertension

6. Which of the following is the most frequent
site of tears in an aortic dissecting aneurysm?
a. at the level of the ligamentum arteriosum
b. ascending aorta
c. abdominal aorta above the level of the re-
nal arteries
d. abdominal aorta below the level of the re-
nal arteries
e. just proximal to the left subclavian artery
Aortic Trauma
7. Which of the following statements is true
regarding aortic lacerations secondary to
trauma?
a. Lacerations usually occur at aortic
isthmus at the level of the ligamentum.
b. Lacerations may cause the formation of
an aneurysm.
c. The mediastinum may become filled with
The Osler Institute
Ap99que.doc
2
blood. Later, the patient may decompen-
sate suddenly.
d. Formed aneurysms may persist for years
without rupture.
e. none of the above

8. Which of the following are true regarding
an aortic lacerations secondary to trauma?
a. usually occurs at aortic isthmus at the
level of the ligamentum
b. may cause the formation of an aneurysm
c. may fill mediastinum with blood and
patient sudden decompensates

9. Which of the following are true regarding
aortic lacerations? (K-type)
1. usually occurs at the aortic isthmus at the
level of the ligamentum arteriosus
2. may fill the mediastinum with blood,
with the patient later decompensating
suddenly
3. may cause the formation of an aneurysm
4. formed aneurysms may persist for years
without rupture

10. What is the anatomic location of an aortic
tear after blunt trauma to the chest wall?
a. ascending aorta
b. descending thoracic aorta near diaphragm
c. isthmus
d. abdominal aorta
e. none of the above
Aortitis
11. Which of the following are features of
syphilitic (luetic) cardiac valvular disease?
a. widening and incompetence of aortic valve
ring
b. widening and incompetence of pulmonary
valve ring
c. widening and incompetence of mitral valve
ring
d. widening and incompetence of tricuspid
valve ring
e. none of the above

12. Complete the following: Common features
of syphilitic heart disease includes all of the
following except...
a. mitral valvulitis
b. aortic valvular insufficiency
c. so called tree barking of aorta intimal
surface
d. involvement of the heart usually does not
become evident until 15-20 years after
contracting the infection.

13. Which of the following statements is false
regarding syphilitic aortitis?
a. It is a potentially lethal complication
from tertiary syphilis.
b. It most commonly affects the thoracic
aorta.
c. Inflammatory infiltrate characteristically
begins within the muscularis layer.
d. Progressive disease can lead to aortic valve
insufficiency.
e. Luetic aortitis can predispose to athero-
sclerosis.

14. Which of the following is associated with
syphilitic aortitis? (K-type)
1. saccular aneurysm formation
2. obstruction of coronary arteries
3. fusiform aneurysm formation
4. a negative VDRL test

15. [Syphilitic aneurysm of aorta] Which of the
following associations are false regarding
this finding?
a. cystic medial necrosis
b. aortic arch
c. protects from severe atherosclerosis
d. none of the above

16. [Microscopic slide shows syphilitic athritis]
Complete the following: The disease shown
here... (K-type)
1. results from obliteration of the lumina of
the small vessels by monocytes and lym-
phocytes
2. can cause a functionless lower leg at birth
3. can be congenital, resulting in osteochon-
drosis and periostitis
4. in the acquired form, most often involves
the shoulder

17. Which of the following is characteristic of
Takayasus disease? (K-type)
1. involves the aortic arch
Pathology Review Course
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3
2. common in men
3. involves main branches of aortic arch
4. occurs in old age

18. [A photomicrograph of Takayasus arteritis
shows irregular thickening of the arterial
wall and intimal wrinkling] Which of the
following statements are true regarding this
lesion? (K-type)
1. 90% of patients are less than 30 years of
age.
2. A predilection to females has been noted.
3. The aortic arch is primarily affected.
4. The pulmonary artery is affected in 50%
of cases.
Miscellaneous Aortic Disease
19. Discuss the histologic features which distin-
guish aortic atherosclerosis from cystic medi-
al necrosis. (This question must have been
worded differently, as essay questions are not
yet on the boards!)

20. [A cross-section of the contents of an abdom-
inal aortic aneurysm shows a large, rubbery,
yellow-tan-brown laminated mass with a
round, eccentric, small lumen] This most
likely represents which of the following?
a. dissecting aneurysm
b. mural thrombus
c. myxoma
d. none of the above

21. Ehlers-Danlos syndrome is characterized by
a. tearing of the arteries
b. skin laxity
c. joint symptoms
d. ectopia lentia

22. Matching:
1. Focal separation of the tunica media by
cleft-like or cystic spaces filled with
ground substance.
2. Composed of three components cells,
connective tissue and lipid depositions
3. Complications include calcification, ul-
ceration, thrombosis, and hemorrhage
4. There is no inflammatory response

a. cystic medial necrosis
b. aortic atherosclerosis
c. both
d. neither

23. [Aorta with intimal atherosclerotic plaque and
medial degenerative change. Ring-like calci-
fications are present within the media of small
to medium-sized muscular structures] Which
of the following is a probable diagnosis?
a. syphilitic aneurysm
b. Erdheims mucoid degeneration
c. Monckebergs arteriosclerosis
d. none of the above

24. [Section of aorta from an aneurysm] Which
of the following is the cause of aneurysm?
a. atherosclerosis
b. syphilis
c. Marfans syndrome
d. none of the above

25. [Section of thickened aorta with patchy
fibrosis and focally disrupted elastic fibers
throughout the tunica media. Myxoid change,
if present, was minimal. Intramural calcifica-
tion and lipid deposits were absent.] Which of
the following is the etiology of this change?
a. due to a congenital defect of collagen
assembly
b. autoimmune in nature
c. secondary to spirochetal infection
d. related to serum low density lipoprotein
concentrations
e. cystic medial necrosis

26. [Gross: partially opened ascending and thora-
cic aorta] What is the diagnosis?
a. coarctation
b. Marfans syndrome
c. lues
d. hypertension
e. none of the above

Congenital heart disease
27. Which of the following congenital
malformations is known to accompany
coarctation of the aorta?

Answers

The Osler Institute
Pathology Board Review Course

Self-directed Study Faculty Answer Book AP


Table of Contents
SYSTEMIC PATHOLOGY......................................1
CARDIOVASCULAR PATHOLOGY................................1
Edited by Allen Burke, MD...................................1
FEMALE REPRODUCTION.........................................30
Edited by Karen Hughs, MD..............................30
MALE REPRODUCTIVE PATHOLOGY ........................59
Mahul Amin, MD................................................66
HEMATOPATHOLOGY...............................................85
Edited by Harry L. Ioachim, MD........................88
DERMATOPATHOLOGY ............................................94
Edited by Rosalie Elenitsas, MD........................94
RENAL AND URINARY ...........................................114
Edited by Guillermo Herrera, MD...................114
SPECIAL TECHNIQUES .....................................135
ELECTRON MICROSCOPY.......................................135
M. L. Christ, MD..............................................135
GENERAL PATHOLOGY...................................139
DEFICIENCY DISEASE............................................139
Edited by James Caruso, MD...........................139
FORENSIC PATHOLOGY .........................................140
Edited by James Caruso, MD...........................140
INFECTIOUS DISEASE.............................................146
Edited by Barbara A. Sampson, MD................146
CYTOLOGY...........................................................162
CYTOLOGY NONGYNECOLOGICAL......................162
Edited by Tamara Handerson, MD..................162
CYTOLOGY FINE NEEDLE ASPIRATION...............166
Edited by George Cook, MD............................166

Preface
These questions and answers, provided by previous participants, were edited by the faculty and typeset
but have not had the final proofreading by the faculty.

Most of the questions are single best choice. Some of the questions are K-type which have four answers
designated 1, 2, 3, 4. One or more of the K-type answers may be correct as follows:

Directions Summarized
A B C D E
1,2,3 1,3 2,4 4 all are
only only only only correct

There are a few matching questions and occasional simple true/false questions as well as some open -
ended response questions which are not in multiple choice format.
Pathology Review Course
Ap99ans.doc
1
Systemic Pathology
Cardiovascular Pathology
Edited by Allen Burke, MD
General references:
Rubin and Faber, 1994:494; Robbins 1989:584;
Virmani 1996:123-4 (Saunders Atlas Series);
Heart Disease, Braunwald E (ed.), WB Saun-
ders. Philadelphia 1992. Fourth edition.

Note: There is no guarantee regarding the
correctness of the answers. The questions are
approximate, as remembered by previous
residents. Even slight variations in wording
may result in different answers being correct,
due to semantic reasons and many questions
are repeated in different ways. Developments
in medical knowledge since the questions
were recorded may change which answer is
most accurate. Errors in the answer discussion
(in bold type) have, we hope, been kept to a
minimum, as a fair degree of effort has been
given to researching the probable best answer.
What is important about this study guide is to
become acquainted with the topics that have
been previously used on the examination and
to direct your study to these areas, always
keeping in mind that a significant percentage
of questions each are not repeats.
Aortic Dissection
1. A An intimal tear of the ascending aorta led
to a fatal aortic dissecting hematoma.
Systemic hypertension is an antecedent
condition in 70-90% of cases with proximal
intimal tears (like this one) (types I, II) and
95% of cases of distal intimal tears (types III).
Other risk factors, especially for proximal
intimal tears, include bicuspid/ unicuspid
aortic valve and Marfan syndrome. About
10% of patients with type I dissection have
bicuspid aortic valves (general population 1-
2%). There is a 2-3:1 male to female ratio for
all aortic dissections combined. Syphilitic
aortitis may cause aortic rupture, but not
dissection. In aortic dissection, there is gener-
ally aortic root dilatation, especially after
dissection (these may heal), but not of the
distal aorta. Aortic dissections at anastomotic
sites of for saphenous grafts may occur, but
these are very rare. Reference: Virmani R,
Burke AP, Farb A. Atlas of Cardiovascular
Pathology. WB Saunders Co, Philadelphia.
1996:123.

2. Since most of the choices were valvular, you
immediately focused on them and there was a
suggestion of very fine nodularity. While you
were sweating this, it was easy to forget to
look at the aorta which was just at the margin
of the picture. Not only was there a huge
intimal tear, it even had a marker through it.
This is a rehash of the last question. As far as
intimal tears and valves are concerned, always
look at the aortic valve. A congen-itally
bicuspid (or unicuspid) valve imparts an
increased risk for aortic dissection.
Aortic dissection, if untreated, is fatal in 35%
of patients within 15 minutes. Current surgi-cal
therapy (and antihypertensive therapy) has
resulted in a 65-75% salvage of all dissection
for two to four years. The dissection usually
occurs between the middle and outer third of
the aortic media, often without significant
aortic dilatation (especially in type III, although
in I aortic root dilatation is the rule). The peak
incidence is in patients, age 40-60, more often
in males (In Marfan syndrome, the patients are
younger). Type I (extension beyond arch) and
type II (no extension beyond arch) have
proximal intimal tears; in these cases, the risk
factors are bicuspid aortic valve, Marfans
syndrome and hypertension. Type III (tear in
distal thoracic aorta), 94% are preceded by
hypertension, 2-3% Marfan. The other choices
involve valvular lesions. In lupus, small
vegetations may be seen on the mitral and
tricuspid valve (Libman-Sachs disease). Ma-
rantic vegetations are variable in size (1-5 mm),
usually single vegetations along the line of
closure of a valve leaflet, usually seen in
patients with debilitating disease. In rheumatic
fever, verrucous, 1-2 mm vegetations may be
seen along lines of valve closure, over eroded,
inflamed endocardial surfaces. Mitral and/or
aortic valve involvement is most common. Ref:
Robbins Pathologic Basis of Disease. p. 582.
The Osler Institute
Ap99ans.doc 2
3. D X-linked diseases are not associated with
aortic dissection. Familial aortic dissection is
usually caused by Marfans syndrome, which is
inherited in an autosomal dominant fashion. It is
a collagen disorder, causing a faulty media in
the aorta, leading to dilatation of the ascending
aorta. Dissecting aneurysm is the most common
cause of death in Marfans syndrome. Ehlers-
Danlos syndrome is a collagen disorder as well,
but causes hyperelasticity of the skin and a
bleeding diathesis and the one that involves the
aorta (type IV) is autosomal dominant and is
associated with aortic rupture, not dissection.
Syphilis may cause aortic rupture, but does not
cause dissection. The most common cause of
aortic dissection, hypertension, is not a choice.
Generally, there is less cystic medial change in
hypertension than Marfans.

4. D Dissecting aortic aneurysms most commonly
occur in the 40-60 year age group and are two
to three times more frequent in men. However,
before the age of 40, the male/female ratio is
equal owing principally to the occurrence of
dissections in women in pregnancy. Hyper-
tension is almost invariably an antecedent and
may play a role in initiating the intramural
hemorrhage. The hemorrhage characteristically
occurs between the middle and outer thirds of
the media. The intimal tear, presumably the
origin of dissection, is found in the ascending
portion of the arch in 90% of the cases, usually
within ten centimeters of the aortic valve. Ref:
Robbins and Cotran: Pathologic Basis of
Disease, pp. 582-4.
Anecdotally, the association between pregnancy
and aortic dissection has been questioned and
never rigorously demonstrated epidemiolo-
gically. Some of the more recent series of aortic
dissection include few or no cases in pregnant
women.

5. B Rehash of previous question. Pregnancy
has been associated with aortic dissections;
Marfans syndrome is autosomal dominant;
hypertension is a risk factor for all types of
aortic dissections, especially type III; but
syphilis does not predispose to dissections.

6. B 80% of the cases of dissecting aortic a-
neurysm show an intimal tear in the ascending
aorta, usually within three centimeters of the
aortic valve. The tears are transverse or
oblique. These would be classified as type I or
II (in I, the dissection itself extends beyond
the arch). The other 20% have intimal tears in
the proximal descending thoracic aorta, distal
to the left subclavian (type III). There may be
tears in the arch itself (less than 5% of total).
Tears near the ligamentum arteriosum (at
level of left subclavian) are associated with
trauma; these usually cause rupture and/or
pseudoaneurysms as opposed to dissections.
Abdominal aorta is not a site for the initiation
of aortic dissection.
Aortic Trauma
References: Virmani p 125
7. A, B, C, D are all true Traumatic tears to the
aorta are almost always at the isthmus, be-
cause thats where the ligamentum arterio-
sum is. There is not always external evidence
of trauma. The patient either dies right then
and there, or there is formation of pseudo-
aneurysm. These can persist for years and
then leak or rupture. Reference: Virmani R,
Burke AP, Farb A. Atlas of Cardiovascular
Pathology. WB Saunders Co. Philadelphia.
1996:125

8. A, B, C (See last question) The most common
site of aortic lacerations due to trauma is the
descending aorta-thoracic region just above
the aortic rout. The mediastinum fills with
blood and the patient quickly decompensates.
Formed aneurysms may persist for years
without rupture. Ref: DiMaio DJ , et al.
Forensic Pathology. 1989:114-7.

9. E (All) Traumatic laceration of the aorta occurs
immediately distal to the left subclavian artery
at the junction of the aortic arch and the
descending aorta. (The aortic isthmus is distal
to the origin of the L. subclavian artery and
extends to the ligamentum or arteriosus.) The
laceration may not extend completely through
the wall. These tears may heal, slowly erode
through the aortic wall and cause delayed ex-
sanguination, initiate a localized leak through
the aortic wall with formation of a false
Pathology Review Course
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3
aneurysm (post traumatic aneurysm). Formed
aneurysms can persist for years without
rupture. Ref: Dimaio. Forensic Pathology, pp.
116-7. A rehash of the last question.

10. C Rupture occurs in the isthmus in 90% of
cases of blunt trauma to the chest wall, be-
cause here the ligamentum arteriosum anchors
the aorta. In the other 10% it is the ascending
aorta near the root. Ref: Braunwald. Heart
Disease. 1980:1574, 1593.
Aortitis
References: Virmani, p.l 138, Robbins p. 580,
Rubin p. 494
11. A Syphilitic heart disease is characterized by
an inflammation of the adventitia and media
of the aorta developing in tertiary syphilis.
Manifestation occurs years to decades after
the initial infection and causes inflammatory
scarring of the tunica media (mesaortitis) with
weakening and dilation (aneurysm formation),
widening and incompetence of the aortic
valve ring and narrowing of the coronary
ostia. Contraction scars in the media may lead
to wrinkling of intervening segments of the
aortic intimacy producing the tree-barking
of the intimal surface. Treebarking may be
seen in any aortitis, however! When luetic
aortitis involves the aortic valve ring, it dilates
causing valvular insufficiency and over time it
worsens. A consequence is left ventricular
hypertrophy and dilatation, sometimes
producing a massively enlarged heart.
Remember the triad: syphilis causes aortitis,
aneurysm and aortic insufficiency. Ref.:
Virmani R, Burke AP, Farb A. Atlas of Car-
diovascular Pathology. W.B. Saunders Co.
Philadelphia. 1996:138.

12. A This is a rehash of the previous question.
Mitral valvulitis is not a feature. Syphilitic
heart disease is marked by thoracic aortic
aneurysms, dilatation of the aortic ring and
the aortic valve and so-called tree barking
of the aortic intima. Ref: Robbins: Pathologic
Basis of Disease, 4th Ed, p. 581.
13. C The inflammatory infiltrate in luetic aortitis
characteristically begins in the adventitia. This
leads to an obliterative endarteritis involving
the vasa vasorum which results in ischemia to
the aortic media. The rest of the statements are
true. Rehash of previous question. Ref:
Robbins and Cotran.

14. All (1, 2, 3, 4) (best answer) Coronary ostial
stenosis is a known complication of syphilis
aortitis (10-25% of patients), fusiform
aneurysms of the ascending aortic aneurysms
are typical. Non-treponemal serologic tests
(VDRL, RPR) may revert to negative in
tertiary syphilis, treated or not, in over 10% of
cases, but the treponemal tests (eg, FTA-abs
or newer Western blot or ELISA tests)
generally stay positive (but may be less
sensitive in early syphilis). Saccular aneu-
rysms are not typical of syphilis, but certainly
may occur, especially in the descending
thoracic aorta. Therefore, all of the answers
are potentially correct, 4 being somewhat
questionable.

15. C is false. Syphilitic aneurysms occur mainly
in the aortic arch. Their development is based
on the medial destruction characteristic of
tertiary luetic aortitis. The inflammatory
involvement begins in the adventitia of the
aorta, particularly involving the vasa vasorum
with the production of obliterative endarteritis
rimmed by an infiltration of lymphocytes and
plasma cells. The narrowing of the lumina of
the vasa causes ischemic injury to the aortic
media with patchy, uneven loss of the medial
elastic fibers and muscle cells followed by
inflammatory scarring and vascularization of
the damaged media. The focal areas of scarring
may appear as subintimal pearly-gray plaques
that tend to encircle the mouths of exiting small
aortic branches. Contraction of fibrous scars
may lead to wrinkling of intervening segments
of aortic intima producing tree barking.
Luetic involvement of the aorta (as might any
form of aortitis) may favor the development of
superimposed atherosclerosis, inducing
sometimes florid atheromatosis of the aortic
root. Ref: Robbins and Cotran: pp. 581-2.

16. A (1, 2, 3) Syphilis causes arthritis by oblitera-
tion of the lumina of the small vessels by
inflammatory cells. These cells permeate the
bony cortex through Volkmann and Haversian
The Osler Institute
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canals. The spirochetes are present in the
congenital form of arthritis in the epiphysis and
periosteum. The epiphysis can produce
discoloration of the affected limb and pseudo-
paralysis. The knee is most often affected.
Periostitis stimulates the periosteum to produce
new bone. Acquired syphilis most commonly
affects the tibia (saber shin deformity with
new bone formed in the anterior shaft) and
skull (thickened bone because of periosteal
stimulation). Ref: Rubin E and Farber JL.
Pathology. Philadelphia, Lippincott. 1988:456,
1335-6. [Not really a cardiovascular question]

17. C (1, 3) Takayasus disease is an
inflammatory disease of the large arteries,
especially the aorta and its larger branches. It
is characterized by luminal stenosis
(frequently) aneurysms (relatively
infrequently). The disease most frequently
affects the young. 80% of patients are
between the ages of eleven and thirty years.
Female patients account for 90% of all cases.
Four types of Takayasus disease have been
defined. Type I is characterized by active,
chronic inflammation of the ascending aorta,
arch and the great vessels and is associated
with pulseless syndrome. Type II is atypical
coarctation of the aorta. Type III, which is the
most common type, is a combination of aortic
arch involvement with involvement of its
branches and the abdominal aorta. Type IV is
a combination of one of the first three types
with involvement of pulmonary artery. Ref:
Robbins and Cotran: Pathologic Basis of
Disease, pp. 576-7; Anderson: p. 703.
18. E (All) Rehash of previous question.
Takayasus arteritis is histologically charac-
terized by irregular thickening of the arterial
wall with intimal wrinkling, a mononuclear
infiltrate of the adventitia and media with
perivascular cuffing of the vasa vasorum and
fibrosis of the media. It shares endarteritis
obliterans and tree-barking with syphilis.
These are not specific for syphilis.
Most patients are younger than 50; there is a
female predilection (8:1); the aortic arch is
almost always involved (in tropical countries,
abdominal Takayasus is common) and the
pulmonary artery may be involved (so-called
type IV). Ref: Robbins and Cotran: 576.
Miscellaneous Aortic Disease
19. Cystic medial necrosis (also called medial
degeneration) is characterized by proteogly-
can pools within the media, associated with
loss of elastic lamellae and smooth muscle
cells. Atherosclerosis you have all seen; the
initial lesion is intimal, not medial and is
composed of fibrointimal proliferation, foam
cell accumulation, pultaceous debris, calcifi-
cation, inflammation and secondary destruc-
tion of the media. The risk factors for cystic
medial necrosis are hypertension and collagen
diseases such as Marfans.

20. A, B The gross differential to be able to
discern here are dissecting and atherosclerotic
aneurysm. In a chronic dissection, there is a
false lumen with varying amounts of mural
thrombus; it is often larger than the true
lumen, which is compressed and eccentrically
located. In an atherosclerotic aneurysm, there
is a single lumen with laminated thrombus. It
is impossible to know by the description
which of the answers is correct.
21. A, C Ehlers-Danlos syndrome is actually a
heterogeneous group of genetic disorders due
to defects in collagen synthesis or structure.
Traditionally, ten variants are present
involving all three modes of inheritance.
Patients all demonstrate hypermobile joints
and fragile, hyperextensible skin. The type
that involves vessels is type IV, which is
autosomal dominant and involves mutations
in the structural gene which produce type III
collagen found in large amounts in vessels
and the bowel wall results in vessel rupture
and intestinal rupture. Ref: Robbins Patho-
logic Basis of Disease, pp. 155-7.

22. 1-A; 2-B; 3-B; 4-A Ref: Robbins and Cotran.
4th ed. pp. 565, 584.

23. It is difficult to determine the most correct
answer here. Medial degeneration is a synonym
for Erdheims mucoid degeneration and is
characterized by deposits of proteoglycans
(seen best by Alcian blue stain) and loss of
elastic lamellae and smooth muscle cells.

Questions
The Osler Institute
Pathology Board Review Course
Self-directed Study Faculty Question Book CP

ADMINISTRATION...........................................1
ADMINISTRATION...............................................1
Edited by Leo Mc Carthy, MD ......................1
BLOOD BANK....................................................3
IMMUNOHEMATOLOGY.......................................3
Edited by D.Joe Chaffin, MD........................3
COMPONENT THERAPY.......................................9
Edited by D.Joe Chaffin, MD........................9
DONOR SELECTION AND COLLECTIONS...........13
Edited by D. Joe Chaffin, MD.....................13
BLOOD BANK PRINCIPLES AND REGULATIONS.17
Edited by D.Joe Chaffin, MD......................17
HEMOLYTIC DISEASE OF THE NEWBORN AND
NEONATAL TRANSFUSION................................21
Edited by D.Joe Chaffin, MD......................21
TRANSFUSION REACTIONS ...............................22
Edited by D.Joe Chaffin, MD......................22
TRANSFUSION-TRANSMITTED DISEASES..........24
Edited by D.Joe Chaffin, MD......................24
CHEMISTRY....................................................24
VARIATION SOURCES.......................................25
Edited by D. Robert Dufour, MD................25
BLOOD GAS......................................................26
Edited by D. Robert Dufour, MD................26
ACID BASE AND LYTES....................................26
Edited by D. Robert Dufour, MD................26
LIPIDS ..............................................................27
Edited by D. Robert Dufour, MD................27
HEPATIC TESTS................................................28
Edited by D. Robert Dufour, MD................28
ENZYMES .........................................................29
Edited by D. Robert Dufour, MD................29
Edited by D. Robert Dufour, MD................32
ENDOCRINE THYROID....................................32
Edited by D. Robert Dufour, MD................32
ENDOCRINE ADRENAL...................................33
Edited by D. Robert Dufour, MD................33
ENDOCRINE PITUITARY/GONADAL ................35
Edited by D. Robert Dufour, MD................35
ENDOCRINE MINERAL AND BONE
METABOLISM...................................................36
Edited by D. Robert Dufour, MD................36
CARBOHYDRATES ............................................37
Edited by D. Robert Dufour, MD................37
TOXICOLOGY....................................................39
Edited by D. Robert Dufour, M.D............... 39
INTERMEDIATES AND IONS............................... 40
Edited by D. Robert Dufour, MD................ 40
OTHER............................................................. 42
Edited by D. Robert Dufour, M.D............... 42
QUALITY CONTROL ......................................... 43
Edited by D. Robert Dufour, M.D............... 43
HEMATOLOGY .............................................. 44
RED CELLS ...................................................... 44
Edited by Katherine Anderegg, MD............ 44
HEMATOLOGY OTHER................................... 53
Edited by Katherine Anderegg, MD............ 53
IMMUNOPATHOLOGY ................................ 55
IMMUNOPATHOLOGYAB AS REAGENT ......... 55
Edited by Katherine Anderegg, MD............ 55
AB STRUCTURE................................................ 55
Edited by Katherine Anderegg, MD............ 55
COMPLEMENT.................................................. 56
Glyn Porter, MD......................................... 56
AUTOIMMUNITY .............................................. 59
Edited by George W. Cook, MD................. 59
LYMPHOCYTES ................................................ 63
Edited by Katherine Anderegg, MD............ 63
PHAGOCYTES................................................... 65
Edited by Katherine Anderegg, MD............ 65
HLA................................................................ 66
Edited by Katherine Anderegg, MD............ 66
MONOCLONAL GAMMOPATHY......................... 67
Edited by Katherine Anderegg, MD............ 67
HYPERSENSITIVITY .......................................... 68
Vivian Luo, MD........................................... 68
IMMUNODEFICIENCY........................................ 69
Vivian Luo, MD........................................... 69
IMMUNOPATHOLOGYOTHER........................ 72
Edited by Katherine Anderegg, MD............ 72
MICROBIOLOGY........................................... 73
TECHNIQUES.................................................... 73
Edited by Derrina L. Wu, MD..................... 73
MYCOBACTERIA .............................................. 77
Edited by Derrina L. Wu, MD..................... 77
SPIROCHETES................................................... 79
Edited by Derrina L. Wu, MD..................... 79
QUALITY CONTROL ......................................... 80
Edited by Derrina L. Wu, MD..................... 80
MYCOLOGY ..................................................... 80

Edited by E.W. Koneman, MD.....................80
VIRUS, RICKETTSIA, CHLAMYDIA AND
MYCOPLASMA..................................................84
Edited by James L. Caruso, MD..................84
SEROLOGY .......................................................89
Edited by Derrina L. Wu, MD.....................89
MICROBIOLOGY OTHER.................................90
Edited by Derrina L. Wu, MD.....................90
PARASITOLOGY.............................................90
PARASITOLOGY ................................................90
Edited by E.W. Koneman, MD.....................90
Pathology Review Course
CP99que.doc 1
Administration
Administration
Edited by Leo McCarthy, MD
1. Who is ultimately responsible for the
laboratory?
a. lab director
b. hospital administrator
c. board of director and trustees
d. lab supervisor
e. lab technician

2. Which of the following are indirect costs to
the laboratory?
a. building maintenance and cost
b. hospital personnel
c. utilities
d. administration expenses
e. all

3. Which of the following are direct costs to the
lab?
a. lab supplies and reagents
b. salary of a technician
c. maintenance contract
d. equipment leasing
e. all

4. Which of the following is an effective method
for motivating employees?
a. reduction of time on job
b. removal of difficult duties
c. threats
d. removal of some controls and allow some
independence

5. Who should purchase supplies?
a. authorized staff members such as
supervisors of the lab who are familiar
with the quality of service and reliability
of suppliers
b. a pathologist
c. the lab director
d. the lab technician

6. Which of the following best defines the term
release order?
a. Release orders are annual contracts in
which the vendor agrees to deliver goods
at a predetermined price and on an
established schedule.
b. Release orders are annual contracts in
which the vendors agree to deliver goods
at a predetermined price as notified by the
lab.
c. Release orders are the same as standing
orders.
d. Release orders are used for the
maintenance of equipment.

7. Which of the following should be included in
a job description?
a. supervisory controls
b. description of duties and responsibilities
c. classifying position
d. setting employees performance standards
e. all

8. In a dying statement, a man who has been
shot uttered the name of his assassin. What
type of evidence is this?
a. not admissible
b. admissible
c. admissible only in certain states
d. admissible only if uttered to a police
officer

9. Which of the following is true regarding
medical reimbursement for inpatient lab tests
Diagnosis Related Group (DRG) payments?
(K-type)
1. 60% of costs are reimbursed.
2. The cost of each test is not considered.
3. Reimbursement is independent of DRG
disease classification.
4. Reimbursement is not related to the
number or types of tests.

10. What should the administrator of the
laboratory do when a patient is injured in a
laboratory related incident? (K-type)
1. Suppress idle chat about the incident.
2. Inform his malpractice carriers.
3. Inform the hospital administrator.
4. Write to the patient and assume
responsibility for the incident.

The Osler Institute
2 CP99que.doc
11. What are the responsibilities of the laboratory
director?
a. setting legal rules
b. setting medical rules
c. implementing new procedures
d. none of the above

12. Which of the following is a addressed by span
of control? (K-type)
A=1,2,3 B=1,3 C=2,4 D=4 only E= all
1. theory Y type organization
2. the need for centralized authority in
management
3. the number of persons or operations one
person can effectively direct
4. theory X type organization

13. Which of the following would not be included
in a medical technicians evaluation?
a. employee agenda
b. raises in salary
c. expected goals
d. performance
e. continuing education

14. Which of the following are not indirect costs
of the lab?
a. building depreciation
b. janitorial services
c. laboratory and institutional administrative
expense
d. lab supplies

15. Which of the following should be laboratory
policy and not a decision?
a. no more than two people hired for a
certain task
b. rejection of blood specimen if improperly
labeled
c. changing methodology for an isoenzyme
assay
d. none of the above

16. If the administrator is bad-mouthing you,
what should you do?
a. call a meeting with him/her
b. send him/her a letter
c. ignore the whole thing
d. none of the above

17. For which of the following is the pathologist
responsible?
a. setting legal rules
b. setting medical rules with regard to cases
c. implementing new procedures
d. none of the above

18. Who may not be the director of a pathology
lab?
a. a PhD chemist
b. a pathologist not licensed by boards
c. a nonpathologist MD
d. a pathologist who is a part of the teaching
staff but not a member of the medical
staff

19. As the director of a lab, which of the
following are responsibilities?
a. Play a legal part in the retention of
records and material.
b. Help build a new hospital wing.
c. Assume an active medical managerial role
in the lab
d. Personally perform each new lab test.

20. What is the purpose of delegating authority in
the laboratory?
a. makes individual employees feel useful
b. allows development of the full potential
of personnel
c. delegates others to perform undesirable
jobs
d. none of the above

21. Which of the following are explosive
chemicals? (K-type)
A=1,2,3 B=1,3 C=2,4 D=4 only E= all
1. picric acid
2. formaldehyde
3. xylol
4. lactic acid

22. Which of the following are considered direct
costs? (K-type)
A=1,2,3 B=1,3 C=2,4 D=4 only E= all
1. new equipment
2. laboratory supplies
3. timed depreciation of equipment
4. nonmedical personnel salaries

Pathology Review Course
CP99que.doc 3
23. What is not the best location for an electron
microscope?
a. near the elevator
b. near the laundry
c. near an electric generator
d. near a supporting pillar or steel beam
e. basement

24. A piece of lab equipment costs $70,000 and is
depreciated over five years. The equipment
performs 60 tests per minute. At the same
reagent cost, a tech can perform four tests per
minute at $6.00 per hour. How many tests per
year must be performed to justify the purchase
of the equipment?
a. $100,000 per year
b. $50,000 per year
c. $10 per week
d. $14,000 per year

25. The administration would not increase
overtime or laboratory staff. Now you are
overworked. What is your best course of
action?
a. Tell them you quit.
b. Ask the clinicians to prioritize their
specimens and run the highest priority
specimens first.
c. Request a meeting with the hospital
administrators and physicians to work out
a practical solution to your problem.
d. none of the above

Blood Bank
Immunohematology
Edited by D. Joe Chaffin, MD
1. All of the following statements regarding the
Direct Antiglobulin Test (DAT) are true
except:
a. It is often used to investigate drug-
induced hemolysis
b. It demonstrates in-vivo complement
binding to RBCs
c. An antibody known as Anti-Human
Globulin is useD.
d. It may be used to investigate Hemolytic
Disease of the Newborn
e. It demonstrates in-vitro binding of
antibody to RBCs

2. Failure to wash the red cells prior to
performing a DAT will lead to:
a. False positives due to complement binding
b. False positives due to nonspecific globulin
binding
c. False negatives due to unbound globulin
binding
d. False negatives due to failure to remove
unbound RBC antigens
e. None of the above

3. An individual has the ability to make H
antigen from type I oligosaccharide chains,
and then make soluble ABO antigens. Should
we be impressed? Approximately what
percentage of the population can do this?
a. 100%
b. 80%
c. 50%
d. 20%
e. <5%

4. Approximately what percentage of group A
individuals could be further classified as
subgroup A
1
?
a. 20%
b. 40%
c. 60%
d. 80%
e. >95%

5. All of the following statements are true
regarding the A
2
blood group except:
a. Dolichos biflorus lectin generally does
not agglutinate A
2
RBCs.
b. Ulex europaeus lectin may agglutinate
some A
2
RBCs.
c. A
2
RBCs have more A antigen than A
1

RBCs.
d. If anti-A
1
is made, it is usually clinically
insignificant.
e. Most A
2
individuals have the same anti-B
as A
1
individuals.

Answers
The Osler Institute
Pathology Board Review Course
Self-directed Study Answer Book

ADMINISTRATION..................................................1
ADMINISTRATION......................................................1
Edited by Leo McCarthy, MD...............................1
BLOOD BANKING....................................................3
IMMUNOHEMATOLOGY ..............................................3
Edited by D. Joe Chaffin, MD..............................3
COMPONENT THERAPY ............................................11
Edited by D. Joe Chaffin, MD............................11
DONOR SELECTION AND COLLECTIONS...................17
Edited by D. Joe Chaffin, MD............................17
BLOOD BANK PRINCIPLES AND REGULATIONS........23
Edited by D. Joe Chaffin, MD............................23
HEMOLYTIC DISEASE OF THE NEWBORN AND
NEONATAL TRANSFUSION.......................................29
Edited by D. Joe Chaffin, MD............................29
TRANSFUSION REACTIONS.......................................31
Edited by D. Joe Chaffin, MD............................31
TRANSFUSION-TRANSMITTED DISEASES..................34
Edited by D. Joe Chaffin, MD............................34
CHEMISTRY ...........................................................36
VARIATION SOURCES..............................................36
Edited by D. Robert Dufour, MD .......................36
BLOOD GAS.............................................................37
Edited by D. Robert Dufour, MD .......................37
ACID BASE AND LYTES ...........................................38
Edited by D. Robert Dufour, MD .......................38
LIPIDS......................................................................38
Edited by D. Robert Dufour, MD .......................38
HEPATIC TESTS .......................................................39
Edited by D. Robert Dufour, MD .......................39
ENZYMES.................................................................41
Edited by D. Robert Dufour, MD .......................41
ENDOCRINE GENERAL ..........................................45
Edited by D. Robert Dufour, MD .......................45
ENDOCRINE THYROID...........................................46
Edited by D. Robert Dufour, MD .......................46
ENDOCRINE ADRENAL ..........................................47
Edited by D. Robert Dufour, MD .......................47
ENDOCRINE PITUITARY/GONADAL .......................50
Edited by D. Robert Dufour, MD .......................50
ENDOCRINE MINERAL AND BONE METABOLISM...51
Edited by D. Robert Dufour, MD .......................51
TOXICOLOGY...........................................................56
Edited by D. Robert Dufour, MD .......................56
INTERMEDIATES AND IONS......................................58
Edited by D. Robert Dufour, MD.......................58
OTHER.....................................................................62
Edited by D. Robert Dufour, MD.......................62
QUALITY CONTROL .................................................64
Edited by D. Robert Dufour, MD.......................64
HEMATOLOGY......................................................65
RED CELLS..............................................................65
Edited by Katherine Anderegg, MD...................65
HEMATOLOGY OTHER..........................................77
Edited by Katherine Anderegg, MD...................77
IMMUNOPATHOLOGY........................................79
AB AS REAGENT......................................................79
Edited by Katherine Anderegg, MD...................79
AB STRUCTURE.......................................................79
Edited by Katherine Anderegg, MD...................79
COMPLEMENT..........................................................81
Edited by Glyn Porter, MD ................................81
AUTOIMMUNITY ......................................................85
Edited by George W. Cook, MD.........................85
LYMPHOCYTES........................................................92
Edited by Katherine Anderegg, MD...................92
PHAGOCYTES ..........................................................94
Edited by Katherine Anderegg, MD...................95
HLA........................................................................95
Edited by Katherine Anderegg, MD...................95
MONOCLONAL GAMMOPATHY ................................97
Edited by Katherine Anderegg, MD...................97
HYPERSENSITIVITY..................................................98
Edited by Vivian Luo, MD..................................98
IMMUNODEFICIENCY .............................................100
Edited by Vivian Luo, MD................................100
IMMUNOPATHOLOGY OTHER..............................106
Edited by Katherine Anderegg, MD.................106
MICROBIOLOGY.................................................108
TECHNIQUES .........................................................108
Edited by Derinna L. Wu, MD..........................108
MYCOBACTERIA....................................................112
Edited by Derinna L. Wu, MD..........................112
SPIROCHETES ........................................................114
Edited by Derinna L. Wu, MD..........................114
MYCOLOGY ...........................................................115
Edited by E.W. Koneman, MD..........................115
VIRUS, RICKETTSIA, CHLAMYDIA, AND
MYCOPLASMA.......................................................121
The Osler Institute
CP99ans.doc
Edited by James L. Caruso, MD.......................121
SEROLOGY.............................................................128
Edited by Derinna L. Wu, MD..........................128
QUALITY CONTROL ...............................................115
Edited by Derinna L. Wu, MD..........................115
MICROBIOLOGY OTHER......................................130
Edited by Derinna L. Wu, MD..........................130
PARASITOLOGY..................................................131
PARASITOLOGY .....................................................131
Edited by EW. Koneman, MD...........................131
Pathology Review Course
CP99ans.doc
1
Administration
Administration
Edited by Leo McCarthy, MD
1. A Lab Director. No reference could be found,
but the choice is obvious.

2. E (All) Other indirect costs include heater
purification, janitorial services, and building
depreciation. Ref. Henry. 17th ed. p. 1395;
Dr. Heustis notes from the May 1990 review
course.

3. E (All) Ref. Henry. 17th ed. p. 1395; Dr.
Heustis notes from the May 1990 review
course.

4. D Remove some controls to allow more
independence. Also, create a working
environment in which there is concern for
each patient served, mutual respect for each
co-worker, and enthusiasm for teaching and
advancement. Ref. Henry. 17th ed. p. 1389.

5. A Ref. Henry. 17th ed. p. 1388.

6. B A is the definition of a standing order.
Ref. Henry. 17th ed. p. 1388.

7. E (All) Other items to be included in a job
description are the determination of pay
grades and the definition of the purposes of
the job and the relationship to other jobs in
the organization. Technical details of the job
are not required in a job description. Ref.
Henry. 17th ed. p. 1390.

8. C This type of evidence is admissible in
California, Washington, Michigan and
Washington, DC Ref. King Co. MEO.

9. C (2, 4) DRG reimbursement is dependent on
the disease related group. Reimbursement is a
lump sum for that particular diagnosis. Not
considered are the costs of each test, the
number of tests, or the types of tests
performed on a patient. Ref. DRGs and the
Prospective Payment System: A Guide for
Physicians:12, AMA, 1984.

10. B (1, 3)
11. C. The responsibilities of the laboratory
director include administration of the
operations of the laboratory. This includes the
reporting of test findings, proper performance
of tests, employment of properly qualified
personnel, and training of personnel. The lab
director determines the procedures to be
performed, the nature of quality control
programs, and the format of report forms. He
also confers with physicians on matters
relating to test performance. Ref. Halper HR
and Foster HS. J uly, 1985, Laboratory
Regulation Manual, vol I, Washington, DC,
OConnor and Hannan, supplement, pp.
3.2:11-3.2:12.

12. B (1,3). The need for delegated authority and
shared responsibility is related to the concept
of span of control, for example, how many
persons or operations can one person
effecttively direct. The traditional view is that
one person can direct the activities of four to
eight other persons or groups. This concept
fits in with the theory Y organization which
includes decentralized, delegated authority,
and shared responsibility. This is in contrast
to the theory X organization which includes
centralized, little delegated authority or shared
responsibility. Ref. Henry J B, Todd, Sanford,
Davidsohn, Clinical Diagnosis and
Management by Laboratory Methods, 17th ed,
1984, Philadelphia: WB Saunders, pp. 1389-
90.

13. A. Evaluations are an important part of
employee feedback. Past performance and
future expectations may be discussed. The
format may vary, but the same form should be
used for all employees. Frequently measured
aspects of performance are attendance,
adaptability, job knowledge and skill, quality
and quantity of work, and working
relationships. Continuing education and raises
in salary were not mentioned in Todd and
Sanford. Initiative and organizational ability,
continuing technical education, participation
in quality control and preventive maintenance
programs and flexibility in work hours
including the willingness to work weekends
or more than one shift were mentioned in
Clinics in Laboratory Medicine. Ref. Henry
J B, Todd, Sanford and Davidsohn, Clinical
The Osler Institute
CP99ans.doc
2
Diagnosis and Management by Laboratory
Methods, 17th ed, Philadelphia, 1984, WB1
Saunders, pp. 1389-92; Dorsey DB. Personnel
Management, Clinics in Laboratory Medicine,
Sept, 1983, 3, pp. 453-65.

14. D Ref. Todd and Sanford, Clinical Diagnosis
and Management, 17th ed:1395.

15. B. All laboratories should have readily
available administrative policy manuals which
state the laboratory and institutional policy for
the guidance of those working in the
laboratory. Recurrent crises concerning the
same problems are symptomatic of a
laboratory that has not clearly understood and
documented policies. The policy should
reflect the philosophy and overall goals of the
larger organization as well as those of the
laboratory. Policy should be written in
consultation with the persons involved, and
reviewed by appropriate persons in the
institution such as individuals in the Personnel
Department to be certain that they are
consistent with institutional policy. Like the
laboratory procedure manuals, policies should
be dated and approved by the laboratory
director. Because of the rapidly changing
nature of most laboratory operations, they
should be reviewed and updated at least
annually, with a signature or initials and a
date to document this review. Ref. Todd,
J .W., et al.: Clinical Diagnosis and
Management by Laboratory Medicine, 1979,
16th ed Philadelphia: W.B. Saunders
Co:1989.

16. A.

17. C According to Standard IV established by
the College of American Pathologists, the
pathologist is responsible for selection and
implementation of laboratory test procedures
that will fulfill the mission of the laboratory.
Beyond this, she/he is responsible for
monitoring the quality of the results generated
by the procedure. This includes the reporting
of test findings, insuring proper performance
of tests, employing properly qualified
personnel, and training personnel. The
pathologist determines the procedures to be
performed, is in charge of quality control
programs, and formats report forms. She/he
also confers with physicians in matters
relating to test performance. Legal rules
would refer to laws involving the judicial
process which the pathologist could not solely
perform. Medical rule would require
consideration by at least the medical staff and
therefore could not be solely decided by the
pathologist. Ref. Halper HR and Foster HS.
J uly 1985, Laboratory Regulation Manual, vol
I, Washington, DC. OConnor and Hannon.
Supplement. pp. 3.2: 11-13.2:12.

18. D The answer depends on whether the lab is a
hospital lab or an independent lab. In a
hospital lab, the director should be a qualified
physician, preferably a pathologist certified in
AP and/or CP, or possess qualifications
required for that Board certification. The
individual must be a member of the hospitals
medical staff. In an independent lab, the
director must be one of the following: (1) a
physician certified by the Pathology Board (2)
a physician certified by the Board of
Microbiology or Clinical Chemistry who has
four years of experience in the laboratory (3)
a doctoral degree with Board certification plus
four years of experience who can direct only
the area of his expertise. Ref. Standard II in
the Standards for Laboratory Accreditation,
College of American Pathologists. 1982:5.

19. C. In addition to pursuing his other
professional and scientific endeavors, the
pathologist should assume an active medical
managerial role and become intimately
involved in the actual day-to-day running of
each area with the intent of streamlining the
work force and eliminating waste. Ref. Todd
and Sanford: 16th e. p. 2040.

20. B. The degree of delegation of authority and
sharing of responsibility will be a reflection of
the size of the laboratory and the management
style of the persons in charge. As the
laboratory organization becomes larger, the
need for more delegation should be apparent.
One of the most common management
failures in clinical laboratories is the
reluctance to share responsibility, thus
resulting in the under utilization of talented
persons. Ref. Todd and Sanford: Clinical
Pathology Review Course
CP99ans.doc
3
Diagnosis and Management by Laboratory
Methods. 1979, 16th ed p. 1988.

21. A (1,2,3) Formaldehyde gas is flammable with
a heat of combustion of 4.47 K cal/gram. It
forms explosive mixtures with air and 02.
Picric acid is a water soluble, poisonous acid
used chiefly as an explosive. Xylol (xylene) is
a water insoluble benzene which is flammable.
Ref. Random House Dictionary, 1971:1089;
Walker: Formaldehyde. 1964, 3rd e. p. 39.

22. A (1,2,3) Two general types of costs are
involved in operating a laboratory or in
testing any simple procedure. The first of
these costs are direct costs which includes the
costs of materials, supplies, and personal time
directly attributed to the specific measurement
or examination. Equipment depreciation may
be included as part of direct or indirect costs
depending on the accounting method in use.
Equipment leasing is a direct cost. Indirect
costs are those costs necessary to operate a
laboratory that are not directly attributable to
specific measurements or examinations. Such
costs include an allocated portion of utilities,
laboratory and institutional administrative
expenses, building depreciation, and janitorial
services. Ref. Todd and Sanford: Clinical
Diagnostic Management by Laboratory
Methods, 1984:1395.

23. B All types of electron microscopes are
sensitive detectors of mechanical vibration,
magnetic fields and electrical and thermal
disturbances. Therefore, an EM room requires
an environment in which these disturbances
have been reduced to a sufficiently low level.
Motors used for elevators, air conditioning
and other hoisting devices are commonly
located in the basement. Laundries are usually
located in the basement and certainly have
mechanical vibration.

24. D. The equipment costs $14,000 per year
($70,000/5). The cost per test performed by
the tech is $0.025 ($6.00/hr)/(4 tests/min x 60
min/hr). The tech can perform 560,000 tests
for $14,000 ($14,000/$0.025). More than
560,000 tests/year must be performed to
justify the cost of the machine. Fewer than
560,000 can be performed for less cost by a
tech.

25. C The best course of action would be
negotiation before confrontation. Present
information documenting the inability to meet
demand. Evaluate resources and possible
solutions.
Blood Banking
Immunohematology
Edited by D. Joe Chaffin, MD
1. E. The DAT (also known as the Direct
Coombs test or the antihuman globulin
test) demonstrates in vivo immunoglobulin or
complement coating of RBCs, not in vitro.
HDN and drug-induced hemolysis are just
two of the situations in which knowing the
status of the DAT will help (Others include
transfusion reaction workups and evaluation
of autoimmune hemolytic anemias). The
Indirect Antiglobulin Test (IAT), on the other
hand, is the test used to demonstrate in-vitro
coating of RBCs. It is used in antibody
screening tests and in complete crossmatches.

2. C. Antihuman globulin (AHG) is designed to
attach itself to human globulins (duh!). As a
result, it really, really, really likes to grab on
to free (unbound) globulins. Think about it:
The test is done by adding AHG to a sample
of red cells removed from the body. If we
didnt wash those red cells, then all kinds of
free-floating globulins would be hanging
around and would neutralize the AHG before
it could bind to the globulins that are actually
on the cells! Such an interaction would
potentially result in a false-negative DAT due
to binding of the AHG with these free
globulins.

3. B. The ability to make H antigen from type I
chains is better known as being a secretor,
and roughly 80% of us have this ability. Type
I oligosaccharide chains are found primarily
in secretions (and to a lesser extent in
plasma), so being a secretor enables ABO
testing to be done on saliva. By the way, the
answer to the other question is, of course, that
we should not be impressed!