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13. Steroids impair wound healing by:
CHAPTER 9
A. Decreasing angiogenesis and macrophage migration.
B. Decreasing platelet plug integrity.
C. Increasing release of lysosomal enzymes.
D. Increasing fibrinolysis.
Wound Healing
14. Which of the following does not significantly impair
would healing?
A. Low-oxygen tension
B. Hypoperfusion
C. Arterial insufficiency
D. Mild to moderate anemia
Answer: A
The major effect of steroids is to inhibit the inflammatory
phase of wound healing (angiogenesis, neutrophil and macrophage migration, and fibroblast proliferation) and the release
of lysosomal enzymes. The stronger the anti-inflammatory
effect of the steroid compound used, the greater the inhibitory effect on wound healing. Steroids used after the first 3 to
4 days postinjury do not affect wound healing as severely as
when they are used in the immediate postoperative period.
Therefore if possible, their use should be delayed or, alternatively, forms with lesser anti-inflammatory effects should be
administered.
In addition to their effect on collagen synthesis, steroids
also inhibit epithelialization and contraction and contribute to increased rates of wound infection, regardless of the
time of administration. Steroid-delayed healing of cutaneous
wounds can be stimulated to epithelialize by topical application of vitamin A. Collagen synthesis of steroid-treated
wounds also can be stimulated by vitamin A. (See Schwartz
11th ed., p. 283.)
Answer: D
Low-oxygen tension has a profoundly deleterious effect on
all aspects of wound healing. Fibroplasia, although stimulated initially by the hypoxic wound environment, is significantly impaired by local hypoxia. Optimal collagen synthesis
requires oxygen as a cofactor, particularly for the hydroxylation steps. Increasing subcutaneous oxygen tension levels by
increasing the fraction of inspired oxygen (Fio2) of inspired
air for brief periods during and immediately following surgery results in enhanced collagen deposition and in decreased
rates of wound infection after elective surgery.
Major factors affecting local oxygen delivery include hypoperfusion either for systemic reasons (low volume or cardiac
failure) or due to local causes (arterial insufficiency, local
vasoconstriction, or excessive tension on tissues). The level of
vasoconstriction of the subcutaneous capillary bed is exquisitely responsive to fluid status, temperature, and hyperactive
sympathetic tone as is often induced by postoperative pain.
Correction of these factors can have a remarkable influence on
wound outcome, particularly on decreasing wound infection
rates. Mild to moderate normovolemic anemia does not appear
to adversely affect wound oxygen tension and collagen synthesis. However, profound anemia with 15% less hematocrit can
interfere with wound healing. (See Schwartz 11th ed., p. 283.)
15. How does diabetes mellitus impair wound healing?
A. Local hypoxemia, reduced angiogenesis, and inflam-
mation due to vascular disease
B. Glycosylation of proteoglycans and collagen in
wound bed due to hyperglycemia
C. Decreased collagen accretion noted in patients with
type II diabetes mellitus
D. Increased bacterial load due to hyperglycemia
Answer: A
Uncontrolled diabetes results in reduced inflammation,
angiogenesis, and collagen synthesis. Additionally, the large
and small vessel disease that is the hallmark of advanced diabetes contributes to local hypoxemia. Defects in granulocyte
function, capillary ingrowth, and fibroblast proliferation all
have been described in diabetes. Obesity, insulin resistance,
hyperglycemia, and diabetic renal failure contribute significantly and independently to the impaired wound healing
observed in diabetics. (See Schwartz 11th ed., p. 284.)
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16. Nutrition is important in recovery from trauma or surgical injury. Which of the following is not TRUE about
nutrition in wound healing?
A. Adequate protein and calorie intake is needed for
wound healing.
B. Brief periods of starvation, or absence of nutrient
intake has no impact on wound healing.
C. Arginine supplementation is associated with
improved outcome.
D. Brief nutritional interventions can correct collagen
deposition deficits seen in malnutrition and postoperative starvation.
Answer: B
Malnutrition correlates clinically with enhanced rates of
wound complications and increased wound failure following
diverse surgical procedures. This reflects impaired healing
response as well as reduced cell-mediated immunity, phagocytosis, and intracellular killing of bacteria by macrophages
and neutrophils during protein-calorie malnutrition.
First, the degree of nutritional impairment need not be
long-standing in humans, as opposed to the experimental
situation. Thus, patients with brief preoperative illnesses or
reduced nutrient intake in the period immediately preceding the injury or operative intervention will demonstrate
impaired fibroplasias. Second, brief and not necessarily
intensive nutritional intervention, either via the parenteral or
enteral route, can reverse or prevent the decreased collagen
deposition noted with malnutrition or with postoperative
starvation.
The possible role of single amino acids in enhanced wound
healing has been studied for the last several decades. Arginine
appears most active in terms of enhancing wound fibroplasia. Arginine deficiency results in decreased wound-breaking
strength and wound-collagen accumulation in chow-fed rats.
Rats that are given 1% arginine HCl supplementation, and
therefore are not arginine-deficient, have enhanced woundbreaking strength and collagen synthesis when compared to
chow-fed controls. Studies have been carried out in healthy
human volunteers to examine the effect of arginine supplementation on collagen accumulation. Young, healthy, human
volunteers (age 25–35 years) were found to have significantly
increased wound-collagen deposition following oral supplementation with either 30 g of arginine aspartate (17 g of free
arginine) or 30 g of arginine Hall (24.8 g of free arginine)
daily for 14 days. (See Schwartz 11th ed., p. 284.)
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Wound Healing
17. Vitamins most closely involved with wound healing are:
A. Vitamin C only.
B. Vitamin C and vitamin D.
C. Vitamin C and vitamin E.
D. Vitamin C and vitamin A.
Answer: D
The vitamins most closely involved with wound healing are
vitamin C and vitamin A. Scurvy or vitamin C deficiency
leads to a defect in wound healing, particularly via a failure
in collagen synthesis and cross-linking. Biochemically, vitamin C is required for the conversion of proline and lysine to
hydroxyproline and hydroxylysine, respectively. Vitamin C
deficiency has also been associated with an increased incidence of wound infection, and if wound infection does occur,
it tends to be more severe. These effects are believed to be
due to an associated impairment in neutrophil function,
decreased complement activity, and decreased walling-off of
bacteria secondary to insufficient collagen deposition. The
recommended dietary allowance is 60 mg daily. This provides
a considerable safety margin for most healthy nonsmokers. In
severely injured or extensively burned patients, this requirement may increase to as high as 2 g daily. There is no evidence
that excess vitamin C is toxic; however, there is no evidence
that supratherapeutic doses of vitamin C are of any benefit.
Vitamin A deficiency impairs wound healing, while supplemental vitamin A benefits wound healing in nondeficient
humans and animals. Vitamin A increases the inflammatory
response in wound healing, probably by increasing the lability
of lysosomal membranes. There is an increased influx of macrophages, with an increase in their activation and increased
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CHAPTER 9
Wound Healing
18. The most dangerous deep infection is necrotizing fasciitis: Which of the following is NOT TRUE about necrotizing fasciitis?
A. Skin demonstrated hemorrhagic bullae and/or frank
necrosis.
B. Fascial necrosis is wider and more extensive than the
skin involvement.
C. Most commonly this is due to Clostridia perfringens
and other related species.
D. Removal of all necrotic material is essential for infec-
tion control.
collagen synthesis. Vitamin A directly increases collagen
production and epidermal growth factor receptors when it is
added in vitro to cultured fibroblasts. As mentioned before,
supplemental vitamin A can reverse the inhibitory effects of
corticosteroids on wound healing. Vitamin A also can restore
wound healing that has been impaired by diabetes, tumor
formation, cyclophosphamide, and radiation. (See Schwartz
11th ed., p. 285.)
Answer: C
The most dangerous of the deep infections is necrotizing fasciitis. It results in high mortality, particularly in the elderly.
This is an invasive process that involves the fascia and leads
to secondary skin necrosis. Pathophysiologically, it is a septic thrombosis of the vessels between the skin and the deep
layers. The skin demonstrates hemorrhagic bullae and subsequent frank necrosis, with surrounding areas of inflammation and edema. The fascial necrosis is usually wider than the
skin involvement or than the surgeon estimates on clinical
grounds. The patient is toxic and has high fever, tachycardia, and marked hypovolemia, which if uncorrected, progresses to cardiovascular collapse. Bacteriologically, this is a
mixed infection, and samples should be obtained for Gram
stain smears and cultures to aid in diagnosis and treatment.
As soon as bacteriologic studies have been obtained, highdose penicillin treatment needs to be started (20–40 million
U/d intravenously) due to concern over the presence of
C. perfringens and other related species; broad-spectrum antibiotics should be added and the regimen modified based on
culture results. Cardiovascular resuscitation with electrolyte
solutions, blood, and/or plasma is carried out as expeditiously
as possible prior to induction of anesthesia. The aim of surgical treatment is thorough removal of all necrosed skin and
fascia. (See Schwartz 11th ed., p. 288.)
19. Signs of malignant transformation in a chronic wound
include:
A. Persistent granulation tissue with bleeding.
B. Overturned wound edges.
C. Nonhealing after 2 weeks of therapy.
D. Distal edema.
20. What is the difference between hypertrophic scars (HTS)
and keloids?
A. Keloids are an overabundance of fibroplasia as a
result of healing, hypertrophic scars are a failure of
collagen remodeling.
B. HTS often regress over time, whereas keloids rarely
regress.
C. HTS are more common in darker-pigmented
ethnicities.
D. HTS extend beyond the border of the original wound.
Answer: B
Malignant transformation of chronic ulcers can occur in
any long-standing wound (Marjolin’s ulcer). Any wound
that does not heal for a prolonged period of time is prone
to malignant transformation. Malignant wounds are differentiated clinically from nonmalignant wounds by the presence of overturned wound edges. In patients with suspected
malignant transformations, biopsy of the wound edges must
be performed to rule out malignancy. Cancers arising de novo
in chronic wounds include both squamous and basal cell carcinomas. (See Schwartz 11th ed., p. 289.)
Answer: B
HTS and keloids represent an overabundance of fibroplasia
in the dermal healing process. HTS rise above the skin level
but stay within the confines of the original wound and often
regress over time. Keloids rise above the skin level as well, but
extend beyond the border of the original wound and rarely
regress spontaneously (Fig. 9-2). Both HTS and keloids occur
after trauma to the skin, and may be tender, pruritic, and
cause a burning sensation. Keloids are 15 times more common in darker-pigmented ethnicities, with individuals of
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African, Spanish, and Asian ethnicities being especially susceptible. Men and women are equally affected. Genetically,
the predilection to keloid formation appears to be autosomal
dominant with incomplete penetration and variable expression. (See Schwartz 11th ed., p. 292.)
CHAPTER 9
Wound Healing
FIG. 9-2. Recurrent keloid on the neck of
a 17-year-old patient that had been revised
several times. (Reproduced with permission from
Cohen IK, Diegelmann RF, Lindblad WJ: Wound
Healing: Biochemical and Clinical Aspects.
Philadelphia, PA: WB Saunders/ Elsevier; 1992.)
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CHAPTER 10
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Oncology
1. Which of the following is not a hallmark of cancer?
A. Ability to invade and metastasize
B. Ability to evade apoptosis
C. Ability to evade autophagy
D. Ability to evade immune destruction
2. Characteristics of tumorigenic transformation of cells
include which of the following?
A. Enhanced adherence to other cells
B. Halt in proliferation after monolayer confluence
C. Acquisition of chemoresistance
D. Immortalization
3. The cell cycle includes all of the following phases
EXCEPT:
A. S phase
B. G1 phase
C. G2 phase
D. G3 phase.
Answer: C
There are six essential alterations in cell physiology that dictate malignant growth: self-sufficiency of growth signals,
insensitivity to growth-inhibitory signals, evasion of apoptosis (programmed cell death), potential for limitless replication, angiogenesis, and invasion and metastasis. Recently,
two additional hallmarks have emerged—reprogramming of
energy metabolism and evading immune destruction. (See
Schwartz 11th ed., p. 310.)
Answer: D
Abnormally proliferating transformed cells outgrow normal
cells in the culture dish (ie, in vitro) and commonly display
several abnormal characteristics. These include loss of contact
inhibition (ie, cells continue to proliferate after a confluent
monolayer is formed); an altered appearance and poor adherence to other cells or to the substratum; loss of anchorage
dependence for growth; immortalization; and gain of tumorigenicity (ie, the ability to give rise to tumors when injected
into an appropriate host). (See Schwartz 11th ed., p. 310.)
Answer: D
The cell cycle is divided into four phases. During the synthetic or S phase, the cell generates a single copy of its genetic
material, whereas in the mitotic or M phase, the cellular components are partitioned between two daughter cells. The G1
and G2 phases represent gap phases during which the cells
prepare themselves for completion of the S and M phases,
respectively. When cells cease proliferation, they exit the cell
cycle and enter the quiescent state referred to as G0. (See
Schwartz 11th ed., pp. 311–312.)
4. All of the following factors are suggestive of a hereditary
cancer EXCEPT:
A. Tumor development at a younger than typical age.
B. Presence of bilateral disease.
C. Association with paraneoplastic syndromes.
D. Presence of multiple primary malignancies.
Answer: C
The following factors may suggest the presence of a hereditary cancer: tumor development at a much younger age than
usual, presence of bilateral disease, presence of multiple
primary malignancies, presentation of a cancer in the less
affected sex (eg, male breast cancer), clustering of the same
cancer type in relatives, and occurrence of cancer in association with other conditions such as mental retardation or
pathognomonic skin lesions. (See Schwartz 11th ed., p. 320.)
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5. Anticancer chemotherapy agents include all of the
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following EXCEPT:
A. Alkylating agents.
B. Antitumor antibiotics.
C. Prometabolites.
D. Plant alkaloids.
6. Approved strategies for cancer chemoprevention include
Oncology
all of the following EXCEPT:
A. Neurontin for malignant peripheral nerve sheath
tumor.
B. Tamoxifen for breast cancer.
C. Celecoxib for FAP syndrome.
D. 13-cis-retinoic acid for oral leukoplakia.
7. Which of the following statements is TRUE of apoptosis
in cancer cells?
A. Beclin 1 is an important apoptosis regulatory gene.
B. Chloroquin is an important inhibitor of apoptosis.
C. Anti-caspases are a family of genes involved in regu-
lation of apoptosis.
D. DNA laddering is a typical characteristic observed
with apoptosis.
Answer: C
(See Schwartz 11th ed., p. 340.)
Answer: A
(See Schwartz 11th ed., p. 348.)
Answer: D
Apoptosis is a genetically regulated program to dispose of
cells. Cancer cells must avoid apoptosis if tumors are to arise.
Late in apoptosis, there are characteristic changes in nuclear
morphology, such as chromatin condensation, nuclear fragmentation, and DNA laddering. The apoptosis effectors are
a family of proteases called caspases. The Beclin 1 gene is an
important gene for autophagy. Chloroquine is an antimalarial
drug that acts as an autophagic inhibitor. (See Schwartz 11th
ed., pp. 314–315.)
8. Components of cancer invasion include which of the
following?
A. In situ cancers involve cells which have breached the
basement membrane.
B. Integrins regulate cell adhesion to the extracellular
matrix.
C. Matrix metalloproteinases (MMPs) enhance the
structural integrity of the extracellular matrix.
D. Vascular endothelial growth factor (VEGF) induces
metastases exclusively through vascular channels.
9. Which of the following statements is TRUE of metastasis?
A. If a cell can detach from a primary tumor and invade
the lymphovascular system, it has a high likelihood of
successfully implanting in a distant site.
B. Late development of metastasis as long as 20 years
after primary tumor curative treatment is a common
occurrence.
C. Tumor dormancy may be due to the host losing
immunologic control of subclinical disease.
D. The “seed and soil” conception of metastasis is
explained by organ-specific patterns of blood flow
determinants.
Answer: B
A feature of malignant cells is their ability to invade the surrounding normal tissue. Tumors in which the malignant cells
appear to lie exclusively above the basement membrane are
referred to as in situ cancer. Integrins are a family of glycoproteins that regulate cell adhesion and also relay molecular
signals regarding the cellular environment that influence
shape, survival, proliferation, gene transcription, and migration. MMPs comprise a family of metal-dependent endopeptidases. Upon activation, MMPs degrade a variety of
ECM components. VEGF has various functions, including
increasing vascular permeability, inducing endothelial cell
proliferation and tube formation, and inducing endothelial
cell synthesis of proteolytic enzymes. The proliferation of
new lymphatic vessels, lymph angiogenesis, is also thought
to be controlled by the VEGF family. (See Schwartz 11th ed.,
pp. 315–316.)
Answer: C
Metastases arise due to the spread of cancer cells from the
primary site and the formation of new tumors in distance
locations. Overall, metastasis is an inefficient process; only a
small subset of cancer cells is able to initiate micrometastases,
and an even smaller portion goes on to grow into macrometastases. Recurrences are rare after 20 years; however, cancer
recurrences have been reported decades after the original
tumor episode. This phenomenon is referred to as dormancy.
An explanation for preferential metastasis is what is referred
to as the “seed and soil” theory, the dependence of the seed
(the cancer cell) on the soil (the secondary site). According to
this theory, once cells have reached a secondary organ, their
growth efficiency in that organ is based on the compatibility
of the cancer cell’s biology with its new microenvironment.
(See Schwartz 11th ed., pp. 316–317.)
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10. Which of the following is TRUE regarding biomarkers?
A. Prognostic biomarkers predict response to specific
treatments.
B. Predictive biomarkers predict likelihood of survival
for specific tumors.
C. Results of multigene assays can be linked together to
provide optimal survival predictability.
D. Circulating free DNA is more informative as solid
tumor biomarkers than circulating free proteins.
11. Surgical resection of distant metastatic disease for tumor
control is enhanced by all of the following EXCEPT:
A. Pre-resection tumor shrinkage using chemotherapy.
B. Long interval between primary tumor treatment and
subsequent development of metastasis.
C. Tumor type.
D. Open versus minimally invasive surgical approaches.
Answer: C
Tumor markers are substances that can be detected in higher
than normal amounts in the serum, urine, or tissues of patients
with certain types of cancer. The term “prognostic marker”
generally is used to describe molecular markers that predict
disease-free survival, disease-specific survival, and overall
survival, whereas the term “predictive marker” often is used in
the context of predicting response to certain therapies. Multigene profiles to predict prognosis are in validation phase for
many solid tumor types. (See Schwartz 11th ed., pp. 334–335.)
Answer: D
The treatment of a patient with distant metastases depends
on the number and sites of metastases, the cancer type, the
rate of tumor growth, the previous treatments delivered and
the responses to these treatments, and the patient’s age, physician condition, and desires. Patient selection is the key to the
success of surgical therapy for distance metastases. The cancer
type is a major determinant in surgical decision-making. The
growth rate of the tumor also plays an important role. Patients
with longer disease-free intervals have a higher survival rate
after surgical metastasectomy than those with a short diseasefree interval. In curative surgery for distance metastases,
as with surgery for primary tumors, the goal is to resect the
metastases with negative margins, whether or not open or MIS
approaches are used. (See Schwartz 11th ed., p. 339.)
CHAPTER 10
Oncology
12. Which of the following is established as an improvement
in cancer management?
A. Use of immunotherapy as initial therapy in some
types of lung cancer
B. Replacement of biopsy with serum biomarkers
C. Elimination of radical surgery approaches
D. Use of molecular radiotherapy sensitizers
Answer: A
The current trend in surgery is toward more conservative
resections. With earlier identification of tumors, more conservative operations may be possible. The goal, however, is
always to remove the tumor en bloc with wide negative margins. With the advent of effective immune-based therapies, it
is likely that patients may be given treatments that can specifically target the alterations driving tumor growth in combination with drugs that can enhance the anticancer immune
response, as is now standard of care for several; tumors, including some types of lung carcinoma. (See Schwartz 11th ed.,
pp. 349–350.)
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CHAPTER 11
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Transplantation
1. Which of the following definitions is FALSE?
A. Transplantation is the process of transferring only
intact organs from one person to another.
B. Orthotopic transplanted organs are implanted in the
same place as the native organ.
C. Heterotopic transplanted organs in a different place,
so that the native organs do not need to be removed.
D. Allotransplant means transplant of cells or organs
from one person to another.
Answer: A
Transplantation is the process of transferring an organ, tissue, or cell from one place to another. An organ transplant is
a surgical procedure in which a failing organ is replaced by a
functioning one. The organ is transplanted either orthotopically (implanted in the same anatomic location in the recipient as it was in the donor) or heterotopically (implanted in
another anatomic location). Orthotopic transplants require
the removal of the diseased organ (heart, lungs, liver, or intestine); in heterotopic transplants, the diseased organ is kept in
place (kidney, pancreas).
According to the degree of immunologic similarity between
the donor and recipient, transplants are divided into three
main categories: (a) an autotransplant is the transfer of cells,
tissue, or an organ from one part of the body to another part
in the same person, so no immunosuppression is required;
this type of transplant includes skin, artery or vein, bone, cartilage, nerve, and islet cell transplants; (b) an allotransplant
is the transfer of cells, tissue, or an organ from one person
to another of the same species; with the exception of identical twins, the immune system of the recipient recognizes the
donated organ as a foreign body, so immunosuppression is
required in order to avoid rejection; and (c) a xenotransplant
is the transfer of cells, tissue, or an organ from one organism to
another of a different species. (See Schwartz 11th ed., p. 356.)
2. In humans:
A. Antigen encoding genes are located on chromosome 8.
B. Major histocompatibility complex (MHC) system in
humans is called the human histocompatibility complex (HHC).
C. Class I antigens (HLA-A, HLA-B, HLA-C) are expressed
on all nucleated cells.
D. Class II antigens are expressed on all nucleated cells.
Answer: C
The main antigens responsible for this process are part of the
MHC. In humans, these antigens make up the human leukocyte antigen (HLA) system. The antigen-encoding genes are
located on chromosome 6. Two major classes of HLA antigens are recognized. They differ in their structure, function,
and tissue distribution. Class I antigens (HLA-A, HLA-B,
and HLA-C) are expressed by all nucleated cells. Class II antigens (HLA-DR, HLA-DP, and HLA-DQ) are expressed by
antigen-presenting cells (APCs) such as B lymphocytes, dendritic cells, macrophages, and other phagocytic cells. (See
Schwartz 11th ed., p. 358.)
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