Dr. RAJENDRAN’S INSTITUTE OF MEDICAL EDUCATION

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Dr. RAJENDRAN’S INSTITUTE OF MEDICAL EDUCATION
AIIMS NOVERMBER 2013 – QUESTIONS & ANSWERS
SURGERY
1) A 35-year-old lactating mother presented with a painful breast lump. Most appropriate
initial investigation should be:
a. Mammography
b. USG
c. MRI
d. X-ray
Ans: (b)
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BREAST MASSES
Breast masses can be benign or malignant. Common causes of a benign breast mass include
fibrocystic disease, fibroadenoma, intraductal papilloma, and abscess. The main concern of
women presenting with a breast mass is the likelihood of cancer; however, most breast
masses are benign.
Breast lump (mass)

Fibrocystic disease or cyst

Fibroadenoma

Breast cancer

Intraductal papilloma

Lipoma

Breast abscess (mastitis)

Fat necrosis

Phyllodes tumor
Common causes of breast pain are engorgement during the luteal phase of the menstrual
cycle, pregnancy, hematoma, cysts, mastitis and abscess, galactocele and nipple disorders
including fissures, inflammation, and epithelioma.
Triple test
It is not possible to distinguish benign from malignant or cystic from solid breast masses by
clinical examination. Findings from clinical examination, interpreted in conjunction with
imaging and pathology (the triple test), contribute significantly to management decision. The
combination of clinical examination, imaging, and needle biopsy is called the triple test.
When all three assessments suggest a benign lesion or all three suggest a breast cancer, the
triple test is said to be concordant. A concordant benign triple test is >99% accurate. Breast
lumps in this category can be followed by clinical examination alone at 6-month intervals. If
any of the three assessments suggests malignancy, the lump should be excised regardless of
results from the other two. It is always appropriate to offer excision of a fully evaluated breast
lump, even after a benign concordant triple test, as breast lumps can be a source of
significant anxiety.
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Ultrasound is the initial test of choice for women under the age of 30; diagnostic
mammography with or without ultrasonography is performed initially in women over the age
of 30. For women under the age of 30, ultrasonography is the initial diagnostic test of choice
because the dense breast tissue found in younger women limits the sensitivity of
mammography. Ultrasonography may be coupled with diagnostic mammography if the mass
is mammographically occult or has concerning mammographic features.
The breast ultrasound is the most sensitive test for distinguishing a cystic from a solid lesion,
and also provides detailed information regarding the shape, borders, and acoustic properties
of an identified mass.
Ultrasonography is the most sensitive test for distinguishing a cystic from a solid lesion. In
addition, ultrasonography can be used to guide the biopsy of suspicious lesions. Certain
features of solid masses, such as irregular margins, internal echoes, or a width-to-height ratio
<1.7, may suggest malignancy. Not all solid masses are detected by ultrasound; thus, a
palpable mass that is not visualized on ultrasound must be presumed to be solid.
Mammography is done to further characterize the suspected breast mass. Diagnostic
mammography is different from screening mammography. Diagnostic mammography consists
of the standard views that are used in screening mammography, plus additional views, such
as spot-compression and magnification, to better delineate the area of concern. The
sensitivity of mammography ranges from 74-95%, and specificity ranges from 89-99%. In the
presence of a breast lump a negative mammogram does not rule out cancer. If a nonpalpable
mammographic lesion has a low index of suspicion, mammographic follow-up in 3–6 months
is reasonable. When a lesion is more probably malignant, open biopsy should be performed
Biopsy
Definitive diagnosis of the etiology can only be made by pathologic examination. Evaluation of
a solid breast mass is completed by needle biopsy.
BREAST MASSES IN THE PREGNANT OR LACTATING WOMAN
The development of a dominant mass during pregnancy or lactation should never be
attributed to hormonal changes. A dominant mass must be treated with the same concern in a
pregnant woman as any other. Stage for stage, breast cancer in pregnant patients is no
different from premenopausal breast cancer in nonpregnant patients. However, pregnant
women often have more advanced disease because the significance of a breast mass was not
fully considered and/or because of endogenous hormone stimulation. Persistent lumps in the
breast of pregnant or lactating women cannot be attributed to benign changes based on
physical findings; such patients should be promptly referred for diagnostic evaluation.
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Click here for more on breast masses
Evaluation of a Breast Lump. Williams Gynecology, 2e > Chapter 12. Breast Disease
Evaluation of Breast Masses in Men and Women. Harrison's Online > Chapter 90. Breast
Cance
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2) In a patient with burns, the doctor was looking for curling ulcer. Which part should be
examined?
st
a. 1 part of duodenum
nd
b. 2
part of duodenum
rd
c. 3 part of duodenum
d. Junction between 2
nd
rd
and 3
part of duodenum
Ans: (a)
STRESS ULCER (CURLING ULCERS)
Pathophysiology
Acute ulcers following major surgery, mechanical ventilation, shock, sepsis, and burns
(Curling ulcers) evolve by a similar pathogenetic mechanism. Mucosal ischemia and
breakdown of the normal protective barriers of the stomach play an important role in the
pathogenesis.
Acid is secreted by the parietal cells of the gastric mucosa under the influence of several
biological agents or activities (eg, histamine, gastrin, vagal nerve stimulation). The mucosa is
protected by the mucous gel layer, which is under the influence of prostaglandins, nitric oxide,
trefoil proteins, and vagal nerve stimulation. This mucous layer forms a barrier between the
acidic pH of the stomach and the gastric epithelium. In the presence of noxious agents or
conditions, this protective barrier is destroyed. When this occurs, the acid is able to diffuse
backward to the epithelium and cause mucosal damage.
With stress gastritis, gastric acid secretion is either normal or decreased. Thus, acid
hypersecretion is not a significant etiological factor; instead, the breakdown of the mucosal
defense mechanism is the primary cause. The mucous secretion tends to have a decrease in
bicarbonate concentration and, therefore, is unable to buffer the proton in the stomach. Stress
causes decreased blood flow to the mucosa, leading to ischemia with subsequent destruction
of the mucosal lining.
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About 70% of stress ulcers develop in the parietal cell mucosa. In about 30% of patients the
duodenum is affected, and sometimes both stomach and duodenum are involved.
Histologically, stress injury does not contain inflammation or H. pylori.
Gastroduodenal endoscopy performed early in traumatized or burned patients has shown
acute gastric erosions in the majority of patients within 72 hours after the injury.
Click here for more on stress ulcer
Chapter 23. Stomach & Duodenum > Stress Ulcer
o
CURRENT Diagnosis & Treatment: Surgery, 13e
Chapter 293. Peptic Ulcer Disease and Related Disorders > Stress-Related Mucosal
Injury
o
Harrison's Online
3) A patient with spine, chest and abdominal injury in a road traffic accident developed
hypotension and bradycardia. Most likely reason is:
a. Hypovolemic shock
b. Hypovolemic + neurogenic shock
c. Hypovolemic + septicemic shock
d. Neurogenic shock
Ans: (d)
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4 classes of shock
Hypovolemic
Vasogenic (septic)
Cardiogenic
Neurogenic
Hypovolemic shock
Hypovolemic shock is the most common type. It results from a loss of circulating blood
volume from causes such trauma, gastrointestinal bleeding, and obstetrical
bleeding. Compensatory mechanisms, such as increased heart rate, increased cardiac
contractility, and vasoconstriction can prevent hypotension to an extent.
Neurogenic Shock
Acute spinal cord injury may result in bradycardia, hypotension, cardiac dysrhythmias,
reduced cardiac output, and decreased peripheral vascular resistance.
Neurogenic shock is usually secondary to spinal cord injuries from vertebral body fractures of
the cervical or high thoracic region that disrupt sympathetic regulation of peripheral vascular
tone. Loss of vascular tone due to paralysis from a cervical cord spinal lesion can cause
hypotension and shock. Loss of vasoconstrictor impulses results in increased vascular
capacitance, decreased venous return, and decreased cardiac output.
Neurogenic shock is due to the pooling of blood in autonomically denervated venules and
small veins. This results in loss of sympathetic tone with a reduction in systemic vascular
resistance and hypotension without a compensatory tachycardia. Sympathetic input to the
heart, which normally increases heart rate and cardiac contractility, and input to the adrenal
medulla, which increases catecholamine release, may also be disrupted, preventing the
typical reflex tachycardia that occurs with hypovolemia.
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The features of neurogenic shock consists of decreased blood pressure associated with
bradycardia (absence of reflexive tachycardia due to disrupted sympathetic discharge), warm
extremities (loss of peripheral vasoconstriction), motor and sensory deficits indicative of a
spinal cord injury, and radiographic evidence of a vertebral column fracture. Hypotension is
often marked if the patient is tilted in reverse Trendelenburg).
In trauma, any patient, even with paralysis, should be assumed to have an alternate source of
hemorrhage before assigning the hypotension to neurogenic shock. The key point is to not
assume that the cause is only neurogenic shock until all other sources of traumatic shock
have been excluded. In the multiply injured patient, other causes of hypotension including
hemorrhage, tension pneumothorax, and cardiogenic shock, must be sought and excluded.
Once hemorrhage has been ruled out, norepinephrine or a pure α-adrenergic agent
(phenylephrine) may be necessary to augment vascular resistance and maintain an
adequate mean arterial pressure.
Septic Shock
The reduction in systemic vascular resistance results in inadequate cardiac output and tissue
hypoperfusion despite normal circulatory volume. Sepsis is typically secondary to bacteremia
caused by such gram-negative organisms as Escherichia coli, Klebsiella,
Proteus, and Pseudomonas and less often due to gram-negative anaerobes (eg, Bacteroides).
The incidence of sepsis from gram-positive bacteria (eg, S aureus) and fungal organisms is
increasing.
Chapter 13. Management of the Injured Patient > Neurogenic Shock
o
CURRENT Diagnosis & Treatment: Surgery, 13e
Chapter 11. Shock > Neurogenic Shock
o
CURRENT Diagnosis & Treatment Emergency Medicine, 7e
Chapter 5. Shock > Neurogenic Shock
o
Schwartz's Principles of Surgery, 9e
Chapter 12. Blood Vessel & Lymphatic Disorders > Neurogenic Shock
o
CURRENT Medical Diagnosis & Treatment 2014
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4) FAST stands for:
a. Focused assessment with sonography for trauma
b. Focused abdominal sonography for trauma
c. Fast assessment with sonography for trauma
d. Fast assignment with sonography and tomography (computed)
Ans: (a)
FOCUSED ASSESSMENT WITH SONOGRAPHY FOR TRAUMA
Focused assessment with sonography for trauma (FAST) is a rapid bedside ultrasound
examination performed by emergency physicians and certain paramedics as a screening test
for hemoperitoneum or pericardial effusion. The underlying premise behind the use of the
FAST examination is that clinically significant injuries will be associated with the presence of
free fluid accumulating in dependent areas. The four areas that are examined for free fluid are
the perihepatic space (also called Morison's pouch or the hepatorenal recess), perisplenic
space, pericardium, and the pelvis.
The extended FAST (E-FAST) examination includes views of bilateral hemithoraces to assess
for hemothorax and views of bilateral upper anterior chest walls to assess for pneumothorax.
Pneumothorax is detected by the absence of normal ‘lung-sliding’ and ‘comet-tail’ artifact.
Compared with supine chest radiography or with CT, bedside sonography has superior
sensitivity (49–99 versus 27–75%), similar specificity (95–100%), and can be performed in
under a minute.
FAST examination is an accurate screening tool for abdominal trauma. FAST is most useful in
trauma patients who are hemodynamically unstable.
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Indications
Blunt thoracoabdominal trauma.
Penetrating thoracoabdominal trauma.
Suspected pericardial tamponade.
Undetermined origin of hypotension in trauma patient.
Chapter e299.4. Emergency Ultrasonography > Trauma
o
Tintinalli's Emergency Medicine
Chapter 7. Emergency Procedures > Focused Assessment with Sonography for
Trauma
o
CURRENT Diagnosis & Treatment Emergency Medicine, 7e
5) A couple has been on treatment of infertility for the last four years. The female partner is
normal. Male partner has 0.8 ml semen volume per ejaculate on two repeated samples and
absent fructose, with no sperms on examination under microscope. What is the next line
of management?
a. A per-rectal examination to check ejaculatory duct obstruction
b. Give antioxidants
c. Testicular biopsy
d. Transrectal ultrasound to detect duct obstruction
Ans: (d)
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MALE INFERTILITY
4 main causes of male infertility
Seminiferous tubule dysfunction - 60 to 80 percent including microdeletions of the Y chromosome
Post-testicular defects (disorders of sperm transport) - 10 to 20 percent
Primary hypogonadism — 10 to 15 percent
Hypothalamic pituitary disease (secondary hypogonadism) - 1 to 2 percent
Post-testicular defects
The epididymis is an important site for sperm maturation and an essential part of the sperm
transport system. The vas deferens then transports sperm from the epididymis to the urethra,
where they are diluted by secretions from the seminal vesicles and prostate. Abnormalities at
any of these sites, particularly the epididymis and vas deferens, can cause infertility.
Abnormalities of the vas deferens
Male infertility can result from acquired or congenital abnormalities of the vas deferens.
Bilateral obstruction, ligation, or altered peristalsis of the vas deferens results in infertility.
Obstruction may result from infection (e.g., gonorrhea, chlamydia, tuberculosis). Ligation of
the vas deferens (vasectomy) is an intentional, medically-induced cause of infertility.
One to 2 percent of infertile men have congenital absence of the vas deferens. Most have
mutations of the cystic fibrosis transmembrane conductance regulator, CFTR, gene.
A primary ciliary dyskinesia affects cilia function and structure. The clinical presentations
include recurrent sinopulmonary infections, bronchiectasis, situs inversus and male infertility
(with asthenozoospermia or oligozoospermia. Genetic mutations of dynein proteins or
thioredoxin-nucleoside diphosphate kinase cause primary ciliary dyskinesia.
Standard semen analysis
The semen analysis is the cornerstone of the assessment of the male partner of an infertile
couple. The standard semen analysis consists of the following:

Measurement of semen volume and pH

Microscopy for debris and agglutination

Assessment of sperm concentration, motility, and morphology

Sperm leukocyte count

Search for immature germ cells
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The WHO has published revised lower reference limits for semen analyses.

Volume 1.5 to 5 mL

Sperm concentration > 15 million spermatozoa/mL

Motility > 50%

Sperm morphology (>60% of sperm should be normal, and fewer than 2-3% should be
immature)
Semen volume - The mean semen volume is 3.5 mL. The lower reference limit is 1.5 mL. A
small ejaculate volume may be observed in patients with retrograde ejaculation, absence of
the vas deferens or seminal vesicles, ductal obstruction, hypogonadotropism, or poor
sympathetic response. An increased volume is often caused by a contaminant, such as urine.
A low volume in the presence of azoospermia (no sperm) or severe oligozoospermia (severely
subnormal sperm concentration) suggests genital tract obstruction (eg, congenital absence of
the vas deferens and seminal vesicles or ejaculatory duct obstruction). Congenital absence of
vas deferens is diagnosed by physical examination and low semen pH. Ejaculatory duct
obstruction is diagnosed by the finding of dilated seminal vesicles on transrectal
ultrasonography.
Low semen volume with normal sperm concentration is most likely due to semen collection
problems (loss of a portion of the ejaculate) and partial retrograde ejaculation. Androgen
deficiency is also associated with low semen volume and low sperm concentration. Postejaculation urine can be collected to assess whether there is retrograde ejaculation.
If serum concentrations of FSH, LH, and testosterone are normal and the man has
azoospermia, a post-ejaculatory urine sample to examine for spermatozoa will provide
evidence about retrograde ejaculation if sperm are seen in the urine. If spermatozoa are not
present in the postejaculatory urine, the man has obstructive azoospermia or impaired
spermatogenesis.
Seminal fructose concentration
The seminal vesicles provide 40-80% of the semen volume, which includes fructose for sperm
nutrition, prostaglandins and other coagulating substances, and bicarbonate to buffer the
acidic vaginal vault. Normal seminal fructose concentration is 120-450 mg/dL, with lower
levels suggesting ejaculatory duct obstruction or absence of the seminal vesicles.
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Absence of fructose indicates obstruction of the ejaculatory duct. If semen fructose is present
in a man with azoospermia, normal-sized testes, and normal serum LH, FSH, and testosterone
concentrations, epididymal obstruction is likely. In this situation, fine needle aspiration or
open biopsy of the testis should be considered to demonstrate the presence of normal
testicular histology.
Sperm density
The WHO 2010 lower reference limit is 15 million sperm per mL, or greater than 50-60 million
total sperm. Oligospermia is defined as fewer than 20 million sperm/mL, severe oligospermia
is less than 5 million/mL, and azoospermia is defined as no sperm present.
Azoospermia
Total absence of sperm in semen may result from obstruction in the male reproductive tract or
from nonobstructive causes.
Obstructive azoospermia may be due to ejaculatory duct obstruction or prior vasectomy.
Congenital absence of the vas deferens is a common cause of azoospermia and unfortunately,
is not treatable surgically. Congenital absence of the vas deferens is associated with cystic
fibrosis.
Nonobstructive azoospermia may be caused by Klinefelter syndrome (47,XXY) or balanced
translocation, by deletion of a small portion of the Y chromosome, by testicular failure, or by
unexplained causes.
Testicular Biopsy
Testicular biopsies are indicated in azoospermic patients to distinguish obstructive versus
parenchymal disease. If the serum FSH is more than two times normal, one may presume the
presence of severe and irreversible testicular damage without confirmatory test is biopsy.
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Transrectal ultrasound (TRUS)
TRUS is indicated in patients with azoospermia or severe oligospermia to evaluate for
ejaculatory duct obstruction. TRUS is also useful to evaluate for the presence or absence of
the seminal vesicles. Obstruction is suggested by enlarged seminal vesicles (>1.5 cm width).
Absence of the seminal vesicles can be identified. This study should be preceded by
measurement of fructose in the ejaculate (lack of fructose suggests obstruction of the
ejaculatory duct) and examination of postejaculate urine (to determine the presence of sperm,
suggesting retrograde ejaculation).
Chapter 38. Urology > Male Infertility
o
CURRENT Diagnosis & Treatment: Surgery, 13e
Chapter 19. Evaluation of the Infertile Couple > Etiology of Infertility in the Male
o
Williams Gynecology, 2e
Chapter 12. Testes > Male Infertility
o
Greenspan’s Basic & Clinical Endocrinology, 9
6) A patient after road traffic accident presented with tension pneumothorax. What is the first
line of management?
a. Insert wide bore needle in 2
b. Immediate chest X-ray
c. CT scan
d. Emergency thoracotomy
Ans: (a)
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nd
intercostals space
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TENSION PNEUMOTHORAX
Pneumothorax is the presence of air or gas in the pleural cavity (ie, the potential space
between the visceral and parietal pleura of the lung). Tension pneumothorax is produced if air
continues to enter the pleural space with a valve preventing its exit. This is most common in
patients with traumatic pneumothorax.
Pathophysiology
Tension pneumothorax develops when injured tissue forms a 1-way valve, allowing air inflow
with inhalation into the pleural space and prohibiting air outflow. The volume of this
intrapleural air increases with each inspiration because of the 1-way valve effect. As a result,
pressure rises within the affected hemithorax. As the pressure increases, the ipsilateral lung
collapses and causes hypoxia. Further pressure increases cause the mediastinum to shift
toward the contralateral side and impinge on and compress both the contralateral lung and
impair the venous return to the right atrium. Hypoxia results as the collapsed lung on the
affected side and the compressed lung on the contralateral side compromise effective gas
exchange. This hypoxia and decreased venous return caused by compression of the relatively
thin walls of the atria impair cardiac function. Kinking of the inferior vena cava is thought to be
the initial event restricting blood to the heart. It is most evident in trauma patients who are
hypovolemic with reduced venous blood return to the heart.
Tension pneumothorax rapidly progresses to respiratory insufficiency, cardiovascular
collapse, and, ultimately, death if not recognized and treated. Therefore, if the clinical picture
fits a tension pneumothorax, it must be emergently treated before it results in hemodynamic
instability and death. Prompt recognition of this condition is life saving.
Immediate decompression of the thorax is mandatory when tension pneumothorax is
suspected. This should not be delayed for radiographic confirmation.
Tension pneumothorax occurs commonly in the ICU setting in patients, who are ventilated
with positive pressure. Infants requiring ventilatory assistance and those with meconium
aspiration have a particularly high risk for tension pneumothorax. Aspirated meconium may
serve as a 1-way valve and produce a tension pneumothorax.
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Treatment
Treatment of tension pneumothorax is emergent and should be performed before confirmatory
radiologic studies. If a tension pneumothorax is suspected, immediate needle decompression
is indicated. Needle decompression is performed before definitive treatment with tube
thoracostomy. A large-bore IV needle should be inserted into the pleural space through the
second anterior intercostal space. If large amounts of gas escape from the needle after
insertion, the diagnosis is confirmed. This procedure converts the tension pneumothorax into
an open pneumothorax. The needle should be left in place until a thoracostomy tube can be
inserted.
Once the tension pneumothorax is decompressed the patient’s perfusion often improves
immediately. A needle decompression is a temporary measure only and should be followed
promptly by the insertion of a large-bore chest tube (tube thoracostomy) on the side of the
tension pneumothorax. Place tube thoracostomy decompression tube in the second rib
interspace in the midclavicular line. A midclavicular approach is very important because the
internal mammary vessels are located approximately 3 cm away from the sternal border. Place
the catheter just above the cephalad border of the rib, because the intercostal vessels are
largest on the lower edge of the rib.
Click here for more on tension pneumothorax
Chapter 33. Pulmonary Emergencies > Tension Pneumothorax
o
CURRENT Diagnosis & Treatment Emergency Medicine, 7e
Chapter 258. Pulmonary Trauma > Tension Pneumothorax
o
Tintinalli's Emergency Medicine
Chapter 263. Disorders of the Pleura and Mediastinum > Tension Pneumothorax
o
Harrison's Online
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7) A 60-year-old male presents with fever, chills and dysuria. PSA level is 7.4 ng/dL. What is
the next best step in this patient?
a. Repeat PSA
b. TURP
c. TRUS guided biopsy
d. Antibiotics and admit
Ans: (d)
Prostate-Specific Antigen (PSA)
Prostate-specific antigen (PSA) is the best serum marker now available for cancer of the
prostate. PSA is an androgen-regulated serine protease produced by the prostate epithelium.
PSA is normally present in low concentrations in the blood of all adult males. Normal total
PSA level is < 4 ng/dL. PSA levels may be elevated in the blood of men with benign prostate
conditions such as prostatitis and benign prostatic hyperplasia, as well as in men with
prostate cancer.
Causes of increased PSA level
Prostate cancer (levels > 10/dL increase likelihood of spread)
Acute prostatitis
BPH
Prostatic infarction
Prostate surgery (after biopsy, resection levels are elevated for 4–6 wk)
Vigorous prostatic massage (routine rectal exam does not elevate levels)
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PSA levels have been shown to be useful in evaluating the effectiveness of prostate cancer
treatment and monitoring for recurrence after therapy. In monitoring for recurrence, a trend of
increasing levels is considered more significant than a single absolute elevated value.
PSA level is approved for screening for prostate cancer. A total serum PSA level of 2.6 ng/mL
should be used as a threshold for performing a prostate biopsy.
After radical prostatectomy, PSA should be “undetectable” or < 0.2 ng/dL after about six
weeks. PSA levels decrease in response to therapy for prostatic carcinoma (radiation or
hormonal therapy). PSA levels also decrease in response to antibiotics in acute bacterial
prostatitis.
PSA Velocity/PSA Doubling Time
A rate of rise in PSA of > 0.75 ng/dL/year (velocity) is suggestive of prostate cancer on the
basis of at least three separate assays 6 months apart.
Chapter 4. Laboratory Diagnosis: Chemistry, Immunology, Serology > PSA
Velocity/PSA Doubling Time
o
Clinician's Pocket Reference: The Scut Monkey, 11e
Chapter 95. Benign and Malignant Diseases of the Prostate > Rising PSA
o
Harrison's Online
Chapter 10. Oncology > Prostate-Specific Antigen
o
Schwartz's Principles of Surgery, 9e
Chapter 34. Prostate Cancer > Significance of Prostate-Specific Antigen Following
Radiation Therapy
o
The MD Anderson Manual of Medical Oncology, 2e
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8) Best management of wound contaminated with necrotic material:
a. Debridement
b. Tetanus toxoid
c. Gas gangrene serum
d. Broad spectrum antibiotics
Ans: (a)
DEBRIDEMENT
After completion of the history, examination, and administration of tetanus prophylaxis, the
wound should be meticulously anesthetized. Surgical debridement consists of excising
devitalized or severely contaminated tissues and irregular areas that interfere with wound
closure. Remove retained debris and devitalized tissue by surgical excision and mechanical
cleansing.
It is best to mechanically cleanse the wound and then perform selective debridement of all
grossly nonviable tissue. Devitalized tissue may increase the risk of infection and delay
healing by acting as a culture medium and inhibiting leukocyte phagocytosis. Signs of tissue
necrosis include gray or black color and lack of bleeding when the tissue is incised. Remove
all nonviable portions. Mangled, irregular wound edges imply severe local tissue injury and
should be sharply debrided. Debridement not only removes foreign matter, bacteria, and
devitalized tissue, but it also creates a clean wound edge that is easier to repair. After
debridement is completed, wounds should be re-irrigated.
Having ensured hemostasis and adequate debridement of nonviable tissues and removal of
any remaining foreign bodies, irregular, macerated, or beveled wound edges should be
débrided in order to provide a fresh edge for reapproximation.
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Antibiotics should be used only when there is an obvious wound infection. There is no clear
evidence that antibiotic prophylaxis prevents wound infections in most patients. Most wounds
are contaminated or colonized with bacteria. The presence of a host response constitutes an
infection and justifies the use of antibiotics. Signs of infection to look for include erythema,
cellulitis, swelling, and purulent discharge. Indiscriminate use of antibiotics should be avoided
to prevent emergence of multidrug-resistant bacteria.
Chapter 9. Wound Healing > Treatment of Wounds
o
Schwartz's Principles of Surgery, 9
Chapter 30. Wound Care > Debridement
o
CURRENT Diagnosis & Treatment Emergency Medicine, 7e
Chapter 44. Wound Preparation > Debridement
o
Tintinalli's Emergency Medicine
9) A young male patient presented with abdominal pain and altered bowel habits of 6 months
duration. CT showed dilated distal ileum, thickened ileocecal junction and thickened
cecum with sacculations on the antimesenteric border. The vascularity of adjoining
mesentery is increased. Which is not a differential diagnosis?
a. Ulcerative colitis
b. Crohn disease
c. Tuberculosis
d. Ischemic bowel disease
Ans: (d)
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INFLAMMATORY BOWEL DISEASE
Inflammatory bowel disease (IBD) is an immune-mediated chronic intestinal condition.
Ulcerative colitis (UC) and Crohn's disease (CD) are the two major types of IBD.
Ulcerative colitis is a chronic, recurrent disease characterized by diffuse mucosal inflammation
involving only the colon. Ulcerative colitis invariably involves the rectum and may extend
proximally in a continuous fashion to involve part or all of the colon. Crohn disease is a
chronic, recurrent disease characterized by patchy transmural inflammation involving any
segment of the gastrointestinal tract from the mouth to the anus.
One-third of cases of Crohn disease involve the small bowel only, most commonly the terminal
ileum (ileitis). Half of all cases involve the small bowel and colon, most often the terminal
ileum and adjacent proximal ascending colon (ileocolitis). In 20% of cases, the colon alone is
affected. One-third of patients have associated perianal disease (fistulas, fissures,
abscesses). Less than 5% patients have symptomatic involvement of the upper intestinal tract.
Unlike ulcerative colitis, Crohn disease is a transmural process that can result in mucosal
inflammation and ulceration, stricturing, fistula development, and abscess formation.
The earliest CT finding of Crohn disease is bowel wall thickening, which usually involves the
distal small bowel and colon, although any segment of the GI tract can be affected. There is
considerable overlap between CT findings of ulcerative colitis and Crohn
disease. Submucosal fat is a prominent finding in chronic ulcerative colitis and is one of the
defining features of the mural stratification seen in ulcerative colitis. In comparison, Crohn
disease has transmural involvement that over time leads to replacement of submucosal fat
with fibrosis and loss of mural stratification. In distinction to ulcerative colitis, Crohn disease
also has several extraluminal CT findings, including mesenteric fibrofatty proliferation and
abscess.
INTESTINAL TUBERCULOSIS
The most frequent site of involvement is the ileocecal region; however, any region of the
gastrointestinal tract may be involved. Abdominal CT may show thickening of the cecum and
ileocecal valve and massive lymphadenopathy. CT scans show mesenteric lymphadenopathy
with a hypoattenuating center suggestive of necrosis.
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BOWEL ISCHEMIA
Bowel ischemia is mainly a disease of old age caused by atheroma of mesenteric vessels. CT
is the single best test because it can exclude many other causes of abdominal pain and can
also establish the diagnosis of intestinal ischemia.
CT findings may include the following:

Thromboembolism in the mesenteric vessels

Intramural or portal venous gas

Segmental thickening of the bowel wall

Absence of bowel wall enhancement with contrast-enhanced CT

Irregular narrowing of the bowel lumen as a result of mucosal edema (thumbprinting)

Possible bowel dilatation proximal to the ischemic segment of the bowel

Nonspecific signs of bowel ischemia, including bowel obstruction, mesenteric edema,
mesenteric vascular engagement, and ascites
Chapter 15. Gastrointestinal Disorders > Crohn Disease
o
CURRENT Medical Diagnosis & Treatment 2014
Chapter 28. Small Intestine > Crohn’s Disease
o
Schwartz's Principles of Surgery, 9e
Chapter 295. Inflammatory Bowel Disease
o
Harrison's Online
10) Which color of triage is given the highest priority?
a. Red
b. Green
c. Yellow
d. Black
Ans: (a)
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Triage is the process of determining the priority of patients' treatments based on the severity
of their condition. This rations patient treatment efficiently when resources are insufficient for
all to be treated immediately.
Triage system involves a color-coding scheme using red, yellow, green, white, and black tags:

Red tags - (immediate) are used to label those who cannot survive without immediate
treatment but who have a chance of survival.

Yellow tags - (observation) for those who require observation. Their condition is stable
for the moment and, they are not in immediate danger of death. These victims will still
need hospital care and would be treated immediately under normal circumstances.

Green tags - (wait) are reserved for the "walking wounded" who will need medical care
at some point, after more critical injuries have been treated.

White tags - (dismiss) are given to those with minor injuries for whom a doctor's care
is not required.

Black tags - (expectant) are used for the deceased and for those whose injuries are so
extensive that they will not be able to survive given the care that is available.
Chapter 4. Disaster Medicine > Triage Categories
o
CURRENT Diagnosis & Treatment Emergency Medicine, 7e
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11) Mortality associated with emergency abdominal aortic surgery is:
a. 0.1%
b. 0.2%
c. 0.4%
d. >50%
Ans: (d)
ABDOMINAL AORTIC ANEURYSMS (AAAS)
Abdominal aortic aneurysms (AAAs) are relatively common and are potentially life
threatening. Patients at greatest risk for AAA are men who are older than 65 years and have
peripheral atherosclerotic vascular disease.
AAAs are usually asymptomatic until they expand or rupture. An expanding AAA causes
sudden, severe, and constant low back, flank, abdominal, or groin pain. Syncope may be the
chief complaint, however, with pain less prominent.
Rupture is a fatal complication of abdominal aortic aneurysm. An aneurysm is defined as
ruptured when bleeding is present outside of the wall of the aneurysm.
Ruptured AAAs require emergent repair. The primary methods of AAA repair are as follows:
Open: Requires direct access to the aorta through an abdominal or retroperitoneal
approach
Endovascular: Involves gaining access to the lumen of the abdominal aorta, usually
via small incisions over the femoral vessels; an endograft, typically a cloth graft with a
stent exoskeleton, is placed within the lumen of the AAA, extending distally into the
iliac arteries
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Elective aneurysm repair is associated with low rates of morbidity and mortality in properly
selected individuals, but in spite of advances in intensive care unit management and
techniques for repair, mortality following repair of ruptured abdominal aortic aneurysm
remains high.
Surgical outcomes may be improved using endovascular aneurysm repair (EVAR), but aortic
endografting under emergency circumstances presents many challenges. Not all institutions
are equipped to treat all ruptured AAAs using minimally-invasive technology.
Postoperative mortality following repair of ruptured AAA remains about 40 to 50 percent.
Long-term (five-year) survival following repair of ruptured AAA is 53 to 64 percent. Survival
rates following elective repair range from 69 to 74 percent.
Chapter 23. Arterial Disease > Surgical Repair of Abdominal Aortic Aneurysm
o
Schwartz's Principles of Surgery, 9e
Chapter 106. Diseases of the Aorta > Aneurysms
o
Hurst's The Heart, 13e
Chapter 248. Diseases of the Aorta > Aortic Aneurysm
o
Harrison's Online
12) Neo-adjuvant chemotherapy is not used in:
a. Osteosarcoma
b. Chest wall PNET
c. Breast cancer stage 2
d. Ovarian cancer stage 3
Ans: (c)
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NEOADJUVANT CHEMOTHERAPY
Neoadjuvant chemotherapy is usually given to facilitate surgical resection by shrinking the
primary tumor or it may convert an unresectable tumor into a resectable tumor. In some cases,
this treatment has been shown to prolong survival. Another advantage to neoadjuvant
chemotherapy is that it allows determining if the primary tumor is sensitive to a particular
chemotherapeutic regimen. The patient’s response to neoadjuvant chemotherapy can be an
important predictor of outcome.
Chapter 44. Oncology > Neoadjuvant Treatment
o
CURRENT Diagnosis & Treatment: Surgery, 13e
BREAST CANCER
Neoadjuvant chemotherapy is considered for the initial management of breast cancers judged too
large for initial lumpectomy. Preoperative chemotherapy in breast cancer is especially clinically
warranted for those with tumors greater than 3 cm and for axillary node disease.
Current recommendations for treatment of operable advanced local-regional breast cancer are
neoadjuvant chemotherapy with a doxorubicin-containing or taxane-containing regimen, followed
by mastectomy or lumpectomy with axillary lymph node dissection if necessary, and followed by
adjuvant radiation therapy. For inoperable stage IIIA and for stage IIIB breast cancer, neoadjuvant
chemotherapy is used to decrease the local-regional cancer burden. This may then permit
subsequent modified radical or radical mastectomy, which is followed by adjuvant radiation
therapy.
Chapter 17. The Breast > Neoadjuvant (Preoperative) Chemotherapy
o
Schwartz's Principles of Surgery, 9e
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13) In Glasgow coma scale for head injury, withdrawal to pain stimulus comes under:
a. M2
b. M3
c. M4
d. M5
Ans: (c)
THE GLASGOW COMA SCALE
The Glasgow Coma Scale is a 3-component scoring system. It is the main tool of the primary
neurological survey. To apply the scale, patients are asked to give their name or description of
what happened and to follow a simple command. Patients who are unresponsive to verbal
requests should receive a brief, firm, noxious stimuli. An effective approach is to apply digital
pressure to the sternum and observe for the response. Patients can localize when their
actions are purposeful and they attend specifically to a noxious stimuli in an attempt to
remove it. Patients are withdrawing when they do not attend to stimuli but do act to move
away from noxious stimuli (e.g., decorticate and decerebrate posturing).
This grading scheme is quick and accurate in terms of long-term prognosis, assuming the
examination is not clouded by sedatives or other confounding factors. The possible scores
range from 3 to 15. A score between 3 and 8 indicates severe traumatic brain injury, 9 to 12
indicates moderate brain injury, and 13 to 15 indicates mild closed head injury.
GLASGOW COMA SCALE FOR HEAD INJURY
Eye opening
Spontaneous
4
To loud voice
3
To pain
2
Nil
1
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Best motor response (m)
Obeys
6
Localizes
5
Withdraws (flexion)
4
Abnormal flexion posturing
3
Extension posturing
2
Nil
1
Verbal response (v)
Oriented
5
Confused, disoriented
4
Inappropriate words
3
Incomprehensible sounds
2
Nil
1
Chapter 36. Neurosurgery > The Glasgow Coma Scale
o
CURRENT Diagnosis & Treatment: Surgery, 13e
Chapter 42. Neurosurgery > Glasgow Coma Scale Score
o
Schwartz's Principles of Surgery, 9e
14) Tumor marker for seminoma:
a. PLAP
b. LDH
c. AFP
d. HCG
Ans: (a)
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SEMINOMAS
Testicular neoplasms are the most frequent type of cancer in men between 15 and 35 years of
age. Ninety-five percent of testicular tumors are of germ cell origin; 5% are composed of
stromal or Leydig cell neoplasms. Seminomas account for 33% to 50% of all germ cell tumors.
Although not specific, seminomas stain positive for placental alkaline phosphatase (PLAP)
and are routinely negative for AFP and hCG.
Placenta-like alkaline phosphatase levels can be elevated in patients with seminoma, especially
as the tumor burden increases; it may also increase with smoking.
Lactate dehydrogenase (LDH) is a less-specific marker for GCTs. LDH measurements have an
independent prognostic significance and reflect tumor growth rate and cellular proliferation. It
is increased in about 80% of patients with advanced seminomas and 60% of advanced
nonseminomatous tumors.
Beta–human chorionic gonadotropin (bhCG) levels are elevated in only 5-10% of patients with
seminomas; elevation may correlate with metastatic disease but not with overall survival. HCG
is found in over half of patients with teratocarcinoma or embryonal cell carcinoma and all
patients with choriocarcinoma.
An elevated AFP level rules out pure seminoma. Elevated serum alpha-fetoprotein
concentrations are found in almost 70% of patients with nonseminomatous forms of germ cell
neoplasms. The presence of an increased AFP level in a patient whose tumor shows only
seminoma indicates that an occult nonseminomatous component exists, and the patient
should be treated for nonseminomatous GCT.
Although hCG concentrations may be increased in patients with either nonseminoma or
seminoma histology, the AFP concentration is increased only in patients with nonseminoma.
Chapter 36. Germ Cell Tumors > Testicular Seminoma
o
The MD Anderson Manual of Medical Oncology, 2e
Chapter 12. Testes > Germ Cell Tumors
o
Greenspan’s Basic & Clinical Endocrinology, 9e
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Page 30 of 35
Chapter 96. Testicular Cancer > Stages I and II Seminoma
o
Harrison's Online
15) A 60-year-old man presents to the emergency department with a history of RTA in an
unconscious stat. He gains consciousness in between but again becomes unconscious.
The time when he becomes conscious is called as:
a. Lucid interval
b. Status interval
c. Revival interval
Ans: (a)
Lucid interval
A lucid interval is a temporary improvement in a patient's condition after a traumatic brain
injury, after which the condition deteriorates. A lucid interval is typical of an epidural
hematoma. An estimated 20 to 50% of patients with epidural hematoma experience a lucid
interval. After the injury, the patient is momentarily dazed or knocked out, and then becomes
relatively lucid for a period of time that can last minutes or hours. Thereafter, there is rapid
decline as the blood collects within the skull, causing a rise in intracranial pressure and coma.
Chapter 35. Craniocerebral Trauma > Concussion Followed by a Lucid Interval and
Serious Cerebral Damage
o
Adams and Victor's Principles of Neurology, 9e
Chapter 22. Head Injuries > Essentials of Diagnosis
o
CURRENT Diagnosis & Treatment Emergency Medicine, 7e
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EPIDURAL HEMATOMA
Epidural hematoma is the accumulation of blood between the skull and the dura. See figure
below. Normally the dura is fused with the periosteum on the internal surface of the skull.
Dural arteries, most importantly the middle meningeal artery, are vulnerable to injury,
particularly with temporal skull fractures in which the fracture lines cross the course of the
vessel. In children, in whom the skull is deformable, a temporary displacement of the skull
bones leading to laceration of a vessel can occur in the absence of a skull fracture.
Bleeding from a torn meningeal vessel (usually middle meningeal artery) may lead to an
extradural (outside the dura) accumulation of blood that can rapidly compress the brain,
progressing to herniation or death if not surgically evacuated. The dura is adherent to bone,
and some pressure is required to dissect between the two.
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CLINICAL PRESENTATION
Epidural hematoma has a classic three-stage clinical presentation that is probably seen in
only 20% of cases. The patient is initially unconscious from the concussive aspect of the head
trauma. The patient then awakens and has a lucid interval while the hematoma expands. As
the volume of the hematoma grows, intracranial pressure increases. Uncal herniation from an
epidural hematoma classically causes ipsilateral third nerve palsy and contralateral
hemiparesis.
Epidural Hematoma. Schwartz's Principles of Surgery > Chapter 42. Neurosurgery >
Trauma > Head Trauma > Traumatic Intracranial Hematomas
Epidural Hematoma. From: Kumar: Robbins and Cotran Pathologic Basis of Disease,
Professional Edition, 8th ed.; Chapter 28 - The Central Nervous System > ... > TRAUMATIC
VASCULAR INJURY
16) Not a criteria for admission in upper GI bleed:
a. Shock index >1.5
b. Hematocrit > 40%
c. Frank blood in nasogastric aspirate
d. BP < 100mm Hg
Ans: (b)
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UPPER GASTROINTESTINAL BLEEDING
Upper gastrointestinal bleeding (UGIB) is defined as bleeding derived from a source proximal to
the ligament of Treitz. Peptic ulcers are the most common cause of UGIB. Duodenal ulcers are
more common than gastric ulcers, but the incidence of bleeding is identical for both. In most
cases, the bleeding is caused by the erosion of an artery in the base of the ulcer. In approximately
80% of patients, bleeding from a peptic ulcer stops spontaneously. Other causes of upper GI
bleed are varices, NSAIDs, and Mallory-Weiss tears.
Measurement of the heart rate and blood pressure is the best way to initially assess a patient with
GIB. Clinically significant bleeding leads to postural changes in heart rate or blood pressure,
tachycardia, and, finally, recumbent hypotension.
Insert Nasogastric or Orogastric Tube
If hematemesis has not been documented, place a nasogastric tube, and lavage with room
temperature normal saline (cold fluids may impede normal coagulation) until aspirate is clear.
Persistent bleeding during lavage indicates potential life-threatening upper GI bleeding. Lavage
prior to endoscopy may improve visualization during endoscopic procedure, especially in the
fundus.
The role of nasogastric tube aspiration is controversial. The nasogastric tube aspirate can provide
useful information depending on its contents. Nasogastric tube aspirates, however, can be falsely
negative; false negatives may occur in patients with bleeding from duodenal ulcers due to spasm
of the pylorus and can occur in other conditions, including gastric ulcers and, rarely, esophageal
varices (if the tube is positioned in a nondependent area of the stomach).
Upper endoscopy
Upper endoscopy should be performed urgently in patients who present with hemodynamic
instability (hypotension, tachycardia, or postural changes in heart rate or blood pressure).
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Risk factors for rebleeding
Risk factors for rebleeding include age older than 60 years, the presence of shock upon admission,
coagulopathy, active pulsatile bleeding, and the presence of cardiovascular disease. The appearance of
the ulcer at the time of endoscopy provides important information regarding the risk of rebleeding.
Patients with clean-based ulcers do not have recurrent bleeding. If there is no other reason for
hospitalization, such patients may be discharged on the first hospital day, following stabilization. Patients
without clean-based ulcers should usually remain in the hospital for three days because most episodes of
recurrent bleeding occur within three days.
The ulcers at highest risk for rebleeding are those that involve active arterial bleeding or those
with a visible, protuberant, nonbleeding vessel in the base of the ulcer.
Risk Factors for Poor Outcome in Upper Gastrointestinal Bleeding
Age >60 y
Shock (systolic blood pressure <100 mm Hg); pulse >100 beats/min
Malignancy or varices as bleeding source
Onset in hospital
Comorbid illness
Active bleeding (hematemesis, bright red blood in nasogastric tube, or hematochezia)
Recurrent bleeding
Severe coagulopathy
Hemoglobin and Hematocrit
Frequent checking of hemoglobin and hematocrit (every 4 hours) is essential in patients with
active bleeding after they are hemodynamically stabilized. Often the initial hematocrit is normal.
After fluid resuscitation and equilibration of intravascular volume, the hemoglobin and hematocrit
should be rechecked.
The hemoglobin (or hematocrit) does not fall immediately with acute bleed, due to proportionate
reductions in plasma and red cell volumes. Thus, hemoglobin may be normal or only minimally
decreased at the initial presentation of a severe bleeding episode. As extravascular fluid enters
the vascular space to restore volume, the hemoglobin falls, but this process may take up to 72 h.
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Shock index
Shock index (SI) is defined as heart rate / systolic blood pressure. Isolated vital signs (for
example, heart rate or systolic blood pressure) have been shown unreliable in the assessment of
hypovolemic shock. In contrast, the Shock Index (SI), defined by the ratio of heart rate to systolic
blood pressure, has been advocated to better risk-stratify patients for increased transfusion
requirements and early mortality. When the systolic blood pressure and the pulse become equal
(for instance HR = 100BPM, BP = 100/60) shock index reaches an uncomfortable 1.0 (normally
approximately 0.6).
Chapter 30. Acute Upper Gastrointestinal Bleeding
o
CURRENT Diagnosis & Treatment: Gastroenterology, Hepatology, &
Endoscopy, 2e
Chapter 16. Gastrointestinal Bleeding
o
CURRENT Diagnosis & Treatment Emergency Medicine, 7e
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