A young patient is transported from the scene of an automobile accident to the ER.

The patient complains of pelvic pain. Radiography of the pelvis is ordered and reveals
the image shown (see fgure). Which of the following is the most liely diagnosis!
"#f$%&f$
A. 'racture of pubic symphysis
(. )ntra*articular fracture of the left acetabulum
+. Rupture bladder
,. Ruptured urethra
E. Transverse fracture of left femoral head
-),. /0&%%
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9ption , (Ruptured urethra) is correct. The fgure shows abnormal widening of the
pubic symphysis with an associated ruptured urethra and a high*riding bladder.
9ption A ('racture of pubic symphysis) is incorrect. There is widening of the pubic
symphysis: but no fracture is seen. The fgure shows a ruptured urethra and a high*
riding bladder.
9ption ( ()ntra*articular fracture of the left acetabulum) is incorrect. This cannot be
evaluated with this fgure. There is no abnormality of the acetabular and femoral head
regions. Abnormal widening of the pubic symphysis with an associated ruptured
urethra and a high*riding bladder are seen in this fgure.
9ption + (Rupture bladder) is incorrect. The bladder is high riding: but there is no
evidence of a rupture. Rupture of the urethra is present.
9ption E (Transverse fracture of left femoral head) is incorrect. The left femoral head
has no evidence of fracture. Abnormal widening of the pubic symphysis with an
associated ruptured urethra and a high*riding bladder are seen in this fgure.
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;rethral )n<uries
;rethral in<uries are associated with %= to $%= of all pelvic fractures$0:$> and are
more common in cases of bilateral pelvic in<uries.$?:/@ ,iagnosis of urethral in<uries is
made by a high inde# of suspicion in the presence of blood at the urethral meatus:
inability to urinate: andAor a palpable full bladder on abdominal e#amination. When
blood is present at the meatus: retrograde urethrography aids in diagnosis of any
urethral in<ury. )n the presence of minor urethral in<ury: a catheter can be placed by an
e#perienced urologist with or without the aid of a cystoscope./$
;rethral in<uries are classifed as those confned to the posterior urethra (above the
urogenital diaphragm) and to the anterior urethra (below the urogenital diaphragm).
Bosterior urethral in<uries are further subclassifed as type ) (urethral stretch): type ))
(urethral disruption pro#imal to the urogenital diaphragm): and type ))) (pro#imal and
distal disruption of the urogenital diaphragm).
'or treatment of posterior urethral in<uries: early endoscopic realignment has become
more accepted as an e#cellent initial treatment option.// Realignment of the damaged
urethra with a stented 'oley catheter can lead to complete healing of the urethral
in<ury or need for future endoscopic treatment of developed urethral strictures. )f
realignment of the damaged urethra cannot be achieved: then suprapubic
catheteriCation: followed by delayed combined antegrade and retrograde endoscopic
repair or open surgical repair are the potential treatment options.
page //?D
@
page //?0

'igure 0D*$0 E#traperitoneal bladder in<ury. +ontrast agent is e#travasated
to the space of RetCius (asteris) after retrograde flling of the bladder through the
indwelling 'oley catheter.
)n contrast to posterior urethral in<uries that are often associated with many other
pelvic in<uries: anterior urethral in<uries are often isolated and often associated with
straddle in<uries. The bulbar urethra is often the site of in<ury. The best initial
treatment modality for anterior urethral in<uries is not well defnedE however: most
would agree that primary realignment with 'oley catheter: if possible: is the best initial
treatment. )n cases of severe anterior urethral in<ury: a suprapubic catheter may be
reFuired: followed by delayed open surgical repair./&
A D&*year*old man presents to the physician: because he has been e#periencing
diGculty obtaining and sustaining an erection while being se#ually intimate with his
wife. He was diagnosed with type )) diabetes I years ago and has been poorly
compliant with therapy. He also has a history of benign prostatic hypertrophy and
stable angina. His current medications include metformin: do#aCosin: and isosorbide
dinitrate. 9n e#amination: he has reduced pinpric sensation bilaterally in the lower
e#tremities. At the end of the consultation: the patient reFuests therapy with sildenafl
for his erectile dysfunction. What is the most appropriate advice for this patient with
regard to his current therapeutic regimen!
A. ;se of sildenafl and do#aCosin is contraindicated
(. ;se of sildenafl and metformin is contraindicated
+. ;se of sildenafl is not recommended within $/ hours of
administration of isosorbide dinitrate
,. ;se of sildenafl is not recommended within % hours of
administration of metformin
E. ;se of sildenafl is not recommended within % hours of
administration of do#aCosin
-),. &&/&?
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9ption E (;se of sildenafl is not recommended within % hours of administration of
do#aCosin) is correct. Jildenafl is a Ic*cyclic guanosine monophosphate (cKLB)*
specifc phosphodiesterase type I inhibitor. This causes results in the enhancement of
nitric o#ide in the corpus cavernosum. )n patients with concurrent benign prostatic
hypertrophy: there was a signifcant decrease in blood pressure when the two drugs
were taen within % hours of each other. Therefore: it is important to avoid the use of
alpha blocers and sildenafl within % hours of use.
9ption A (;se of sildenafl and do#aCosin is contraindicated) is incorrect. ;se of these
sildenafl and do#aCosin is not contraindicated: but rather: must be separated in time
because of the potential for hypotension.
9ption ( (;se of sildenafl and metformin is contraindicated) is incorrect. ;se of these
sildenafl and metformin is not contraindicated: because clinical trials have not
demonstrated any adverse events.
9ption + (;se of sildenafl is not recommended within $/ hours of administration of
isosorbide dinitrate) is incorrect. Jildenafl potentiates nitric o#ide. Therefore: sildenafl
potentiates the hypotensive eMects of nitrates and is therefore completely
contraindicated in patients.
9ption , (;se of sildenafl is not recommended within % hours of administration of
metformin) is incorrect. Erectile dysfunction typically develops in patients with
diabetes mellitus (,L): often secondary to diabetic neuropathy. Letformin and
sildenafl are not contraindicated and should not be separated in time.
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BH9JBH9,)EJTERAJE TNBE O )PH)()T9RJ
Jildenafl: the frst selective phosphodiesterase type O inhibitor (see also +hs $%: $>):
was being developed for another possible indication and was found incidentally to
inQuence erectile function. )n contrast to intracavernosal vasodilators: it is not
suGcient of itself to cause erection independent of se#ual desire: but it enhances the
erectile response to se#ual stimulation. )t has transformed the treatment of erectile
dysfunction.
Lechanism of action
Bhosphodiesterase O is the isoform that inactivates cKLB. Pitrergic nerves release
nitric o#ide (or a related nitrosothiol): which diMuses into smooth muscle cells where it
activates guanylate cyclase. The resulting increase in cytoplasmic cKLB mediates
vasodilation via activation of protein inase K (+h. $%). +onseFuently: inhibition of
phosphodiesterase O potentiates the eMect on penile vascular smooth muscle of
endothelium*derived nitric o#ide and of nitrergic nerves that are activated by se#ual
stimulation. 9ther vascular beds are also aMected: suggesting other possible uses.RR
'rom Bharmacology IE by Rang et al
Bharmacoinetic aspects and drug interactions
Bea plasma concentrations occur appro#imately &@*$/@ minutes after an oral dose
and are delayed by eating: so it is taen an hour or more before se#ual activity. )t is
given as a single dose as needed. ('or possible long*term indications reFuiring /% hour
enCyme inhibition: it needs to be given three times daily.) )t is metabolised by the &A%
isoenCyme of cytochrome B%I@: which is induced by carbamaCepine: rifampicin and
barbiturates and inhibited by cimetidine: macrolide antibiotics: antifungal
imidaColines: some antiviral drugs (such as ritonavir) and also by grapefruit <uice (+h.
>). These drugs can potentially interact with sildenafl in conseFuence. A dramatic
pharmacodynamic interaction occurs with organic nitrates: which wor through
increasing cKLB (+h. $0) and are: therefore: maredly potentiated by sildenafl.
+onseFuenty: concurrent nitrate use contraindicates sildenafl.
A D$*year*old man presents to the emergency room following the acute onset of
crushing retrosternal chest pain $ hour ago following vigorous activity. The pain
radiates into the <aw and down both arms. )t has not been relieved by rest. His current
medications are simvastatin: metoprolol: and sildenafl: all taen within the last /%
hours. 9n e#amination: an J% gallop is heard over the precordium.
Electrocardiography (E+K) demonstrates $.%*mm elevation of the JT segment in three
anatomically contiguous leads. Troponin ) is elevated. What medication in the initial
management of this patient is contraindicated!
A. Alteplase
(. Aspirin
+. Heparin
,. Lorphine
E. Pitroglycerin
-),. &&$??
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9ption E (Pitroglycerin) is correct. This patient has taen sildenafl: a
phosphodiesterase type I enCyme inhibitor that increases smooth muscle rela#ation.
He is currently suMering an acute myocardial infarction (L)): and all the listed options
are commonly used in the management of L). +oncurrent use of sildenafl with
nitroglycerin can result in a severe hypotensive reaction causing death.
9ption A (Alteplase) is incorrect. Alteplase is a thrombolytic agent and is
contraindicated in patients with intracranial hemorrhage: an ischemic stroe within &
months: suspected aortic dissection: and malignant intracranial neoplasm.
9ption ( (Aspirin) is incorrect. Aspirin is contraindicated in children with viral illnesses:
individuals with asthma: and bleeding disorders.
9ption + (Heparin) is incorrect. Heparin is contraindicated in patients who have severe
thrombocytopenia: a suspected intracranial hemorrhage: or uncontrolled active
bleeding.
9ption , (Lorphine) is incorrect. There is no contraindication to morphine in this case.
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The I*B,E inhibitors should not be used by men who tae nitroglycerin or another
organic nitrate because the nitrates also increase cyclic KLB formation (see +hapter
$$). +oncurrent administration of I*B,E inhibitors and nitroglycerin can cause
profound hypotension: reQe# tachycardia: and worsening of angina pectoris. A number
of deaths occurred in men who too sildenafl and nitroglycerin. The I*B,E inhibitors
can also augment the hypotensive eMects of other vasodilators including adrenergic
alpha receptor antagonists (e.g.: do#aCosin) that are used to treat urinary retention in
men with benign prostatic hyperplasia (see +hapter ?).
A &/*year*old gravida ): para @ female presents to the labor and delivery ward
following a large discharge of clear Quid from her vagina $ hour ago. Her pregnancy
thus far as been unremarable e#cept for positive third*trimester vaginal group (
Jtreptococcus cultures. 9n route to the hospital: she begins to have regular
contractions and progresses to full cervical dilation after $@ hours. )ntrapartum
penicillin is administered. A compound foot presentation is discovered and immediate
cesarean section is undertaen. A &.@*g (D.D lb) male neonate is delivered with $ and
I minute ABKAR scores of ? and ?: respectively. At $ hour of age: the infant is heard
grunting on e#piration. He is tachypneic and has mild nasal Qaring. He is tachycardic:
but J$ and J/ heart sounds are auscultated and there is no murmur. The abdomen is
soft: without organomegaly and there are no masses palpated. There are no petechiae
or purpura and the sin appears pale pin. A chest S*ray (+SR) reveals prominent
perihilar streaing and Quid within the horiContal fssure. ,uring the physical
e#amination: he appears to become cyanosed and supplemental o#ygen is
commenced: resulting in a dramatic improvement in his symptoms. What is the most
liely diagnosis!
A. Peonatal sepsis
(. Bersistent pulmonary hypertension of the newborn
+. Bneumothora#
,. Respiratory distress syndrome (R,J)
E. Transient tachypnea of the newborn
-),. &&@?/
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9ption E (Transient tachypnea of the newborn) is correct. Transient tachypnea of the
newborn is the most common cause of respiratory distress in term infants. )t is caused
by a delay in the resorption of lung Quid and is more common following delivery by
cesarean section. As a result: the chest S*ray (+SR) is the most characteristic fnding
in the Fuestion. perihilar streaing and Quid noted within the horiContal fssure.
9ption A (Peonatal sepsis) is incorrect. The rapid improvement on administration of
supplemental o#ygen argues against neonatal sepsis as a cause of respiratory distress
in this infant.
9ption ( (Bersistent pulmonary hypertension of the newborn) is incorrect. Bersistent
pulmonary hypertension results when there is a failure of the pulmonary vascular
resistance to decrease at birth. This results in persistence of the fetal circulation and
bypass of the lungs causing hypo#emia. This diagnosis is usually suggested when
there is a history of perinatal asphy#iation. )n the present case: the classic radiograph
fndings and rapid improvement on supplemental o#ygen are more in eeping with
transient tachypnea of the newborn.
9ption + (Bneumothora#) is incorrect. Appro#imately /= of newborns e#perience
spontaneous: asymptomatic pneumothora#. There is no radiographic evidence of
pneumothora# in this case.
9ption , (Respiratory distress syndrome TR,JU) is incorrect. The classic fnding of
respiratory distress syndrome (R,J) is a uniform reticulonodular or Vground*glassW
appearance with prominent air bronchograms. This syndrome occurs more freFuently
in premature infants.
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0. )n addition to R,J: what are other neonatal diMuse lung diseases! How might they
be diMerentiated clinically!
9ther neonatal diMuse lung diseases include transient tachypnea of the newborn
(TTP): congestive heart failure (+H'): neonatal pneumonia: and meconium aspiration.
Peonatal pneumonia may occur in the preterm or term infant. Leconium aspiration
and TTP are generally diseases of term infants: and +H' and pneumonia may occur in
either.

'igure I0*$ 'rontal chest radiograph of a premature infant with diMuse ground*glass
lung disease and low lung volumes: which is indicative of R,J. (+ourtesy Richard
LarowitC: +hildrenXs Hospital of Bhiladelphia.)
YEN B9)PTJ. +A;JEJ 9' PE9PATAZ ,)'';JE Z;PK ,)JEAJE
Respiratory distress syndrome
Transient tachypnea of the newborn
+ongestive heart failure
Bneumonia
Leconium aspiration
A %I*year*old man presents to the physician because he has been feeling tired and
lethargic for the last D months. He states that he has e#perienced diGculty
concentrating and has become increasingly indecisive during this time. He reports that
his wife has told him on numerous occasions that he snores loudly. He does not tae
any regular medications and is allergic to acetylsalicylic acid. He typically drins I@ to
0@ g of ethanol weely and smoes a half a pac of tobacco daily. His vital signs are as
follows. blood pressure ((B): $%@A$@@ mm HgE pulse: I? beatsAminuteE temperature:
&0.I[+ (??.I[')E respirations: $/ breathsAminuteE and body mass inde# ((L)): &I
gAm/ (&I lbAin/). Bhysical e#amination is within normal limits. What is the most
appropriate ne#t step in the management of this patient!
A. Amitriptyline
(. Electroencephalography (EEK)
+. ZoraCepam
,. Bolysomnography
E. Jertraline
-),. &&I/D
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9ption , (Bolysomnography) is correct. This patient has daytime sleepiness: fatigue:
diGculty concentrating: and signifcant diastolic hypertension. He is obese and reports
loud snoring when he sleeps. This is suggestive of sleep apnea: obstructive type and
should be ruled out prior to instituting treatment. The diagnosis can be made using
polysomnography.
9ption A (Amitriptyline) is incorrect. Amitriptyline is an antidepressant with sedating
properties. Appropriate diagnosis should be made prior to any therapy.
9ption ( (Electroencephalography TEEKU) is incorrect. EEK is used in
polysomnography. The ey is obtaining an EEK while the patient is sleeping.
9ption + (ZoraCepam) is incorrect. A benCodiaCepine would be contraindicated if this
individual had untreated sleep apnea.
9ption E (Jertraline) is incorrect. Antidepressant medication would be warranted if
there were a diagnosis of ma<or depressive episode. 9ften: individuals with sleep
apnea will present with depressive symptoms.
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9bstructive Jleep Apnea
)ntermittent upper airway obstruction that causes snoring and apneic episodes
throughout the night
Batients e#perience decreased rapid eye movement (REL) sleep and wae up tired
Evaluation. 9vernight sleep study using polysomnography
Treatment. +ontinuous positive airway pressure mas: weight reduction in obese
persons: surgery
A previously healthy: $>*month*old boy is brought to the emergency room with a
cough and severe shortness of breath with hypo#emia. He is admitted to the B)+;:
where he is diagnosed with necrotiCing pneumonitis. He had no nown e#posure to
fumes or smoe. His 0*year*old brother had recently suMered from a milder respiratory
tract infection and con<unctivitis. Which of the following conditions is the patient at
higher ris for in the future!
A. Adenocarcinoma of the lung
(. (lindness from vasoproliferative retinal disease
+. +hronic bronchitis from enlargement of the airspaces distal to the
terminal bronchioles
,. )mmotile sperm and infertility
E. 9bstruction of bronchioles and smaller bronchi by fbrotic masses
of tissue
-),. /0D@I
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9ption E (9bstruction of bronchioles and smaller bronchi by fbrotic masses of tissue)
is correct. This is descriptive of the later stages of bronchiolitis fbrosa obliterans:
which follows cases of adenovirus pneumonitis in &@= to D@= of cases: depending on
the population surveyed. The condition follows the destruction of the bronchiolar
epithelium: which flls with cellular debris: followed by granulation tissue: which later
becomes fbrotic. The condition may follow infection with adenovirus and other causes
of viral pneumonitis as well as inhalation of fumes or foreign bodies or aspiration of
amniotic Quid: lipids: or stomach acid.
9ption A (Adenocarcinoma of the lung) is incorrect. There is no association between
viral pneumonitis and lung cancer. )nhalation of to#ic fumes may be associated with a
higher future ris of some inds of cancer.
9ption ( ((lindness from vasoproliferative retinal disease) is incorrect. This describes
the condition nown as retinopathy of prematurity: which is a type of retinal blindness
that a\icts premature infants and is associated with artifcial o#ygenation by a
ventilator.
9ption + (+hronic bronchitis from enlargement of the airspaces distal to the terminal
bronchioles) is incorrect. This is a description of emphysema: such as that that would
occur in a child with alpha$*antitrypsin defciency.
9ption , ()mmotile sperm and infertility) is incorrect. Respiratory disorders that are
associated with decreased fertility include cystic fbrosis (+'): due to failure of the
normal formation of mesonephric duct structures: and Yartagener]s syndrome: due to
immotile sperm.
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/%@ Adenoviruses
Yenneth Lc)ntosh
Adenoviruses cause I*>= of acute respiratory disease in infants: plus a wide array of
other syndromes: including pharyngocon<unctival fever: follicular con<unctivitis:
epidemic eratocon<unctivitis: myocarditis: hemorrhagic cystitis: acute diarrhea:
intussusception: and encephalomyelitis. Adenoviral pneumonia may have serious long*
term seFuelae: including bronchiolitis obliterans. 9nly one third of the %? serotypes
have been associated with disease.
Etiology.
The Adenoviridae are ,PA viruses of intermediate siCe: which are classifed into
subgenera A to '. The virion has an icosahedral coat (capsid) made up of /I/ subunits
(capsomers) of which /%@ are ^he#ons^ and $/ are ^pentons.^ The he#ons have a cross
reacting antigen common to all mammalian adenoviruses. The penton confers type
specifcity: and antibody to it is protective. Adenoviruses can also be classifed by their
characteristic ,PA ^fngerprints^ on gels after being digested with restriction
endonucleases: and this classifcation generally conforms to their antigenic types.
All adenovirus types: e#cept types %@ and %$: grow in primary human embryonic
idney cells: and most grow in HEp*/ or HeZa cells: producing a typical destructive
cytopathic eMect. Types %@ and %$ (and other serotypes as well) grow in /?& cells: a
line of human embryonic idney cells into which certain ^early^ adenovirus genes have
been introduced.
Lany adenovirus types: but particularly the common childhood types ($: /: and I): are
shed for prolonged periods from both the respiratory and gastrointestinal tracts. These
types also establish low*level and chronic infection of the tonsils and adenoids.
Epidemiology.
Adenoviral infections are distributed worldwide. They occur year*round but are most
prevalent in spring or early summer and again in midwinter in temperate climates.
+ertain types tend to occur in epidemics: notably types % and 0 in outbreas of febrile
respiratory disease: types &: 0: and /$ in severe pneumoniaE type & in
pharyngocon<unctival feverE type $$ in hemorrhagic cystitisE and types >: $?: and &0 in
epidemic eratocon<unctivitis. 'or une#plained reasons: adenovirus types & and 0
cause severe epidemics of pneumonia in the children of northern +hina and Yorea:
with mortality rates in hospitaliCed cases of I*$I=.
A &%*year*old gravida )O para ))) female at &0 wees of gestation is brought to the
emergency room following the sudden onset of abdominal pain and vaginal bleeding /
hours ago. The pain has been constant from onset. Jhe has also e#perienced freFuent:
strong contractions. Jhe has been otherwise well: abstinent from intercourse for the
past / months: and her previous medical and obstetric history are unremarable. Her
vital signs are blood pressure ((B): $@@ADI mm HgE pulse: $$@ beatsAminuteE
temperature: &0.0[+ (??.>[')E and respirations: $% breathsAminute. The uterus is
painful and rigid. Jpeculum e#amination demonstrates mild vaginal bleeding. 'etal
heart rate tracing is not reassuring. What is the most liely diagnosis!
A. Abruptio placenta
(. Blacenta previa
+. Jpontaneous abortion
,. ;terine rupture
E. Oasa previa
-),. &&@0@
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9ption A (Abruptio placenta) is correct. This patient is demonstrating the classic signs
of placental abruption. painful: abrupt vaginal bleeding associated with uterine
contractions and nonreassuring fetal heart tracing. The pain is constant: and the
uterus is frm because of tetanic contractions. Oaginal bleeding can be highly variable
and does not correlate well with the severity of abruption.
9ption ( (Blacenta previa) is incorrect. Blacenta previa is classically bright red painless
bleeding that is not as rapid in onset as abruption. The uterus is usually soft.
9ption + (Jpontaneous abortion) is incorrect. Jpontaneous abortion is defned as a
pregnancy that has ended spontaneously before /@ to // wees. At &0 wees: this
fetus is viable.
9ption , (;terine rupture) is incorrect. ;terine rupture is painful third trimester
bleeding: but is very rare. ;nlie abruptio placenta: it is associated with constant
heavy vaginal bleeding. A classic presentation on the e#amination is a fetus that is at
a _/ station that suddenly retracts into the *$ position.
9ption E (Oasa previa) is incorrect. Oasa previa has a classic triad of membrane
rupture followed by vaginal bleeding and then fetal bradycardia. Oasa previa is
bleeding from fetal vessels and is diagnosed using the Apt test.
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A(R;BT)9 BZA+EPTAE
Abruptio placentae: or premature separation of the normally implanted placenta:
complicates @.I= to $.I= of all pregnancies ($ in $/@ births). Abruption severe
enough to result in fetal death occurs in $ per I@@ deliveries.
A I/*year*old woman visits her primary care physician for a regularly scheduled chec*
up. Jhe has no current complaints or history of serious illness. There are no abnormal
fndings on physical e#am or any signifcant change from her last visit $ year ago. A
routine +(+ is ordered and shows a W(+ of %I:@@@ cellsAmm&. The peripheral blood
smear shows leuoerythroblastosis with many myeloblasts: myelocytes:
metamyelocytes: and nucleated red blood cells present. A bone marrow aspirate is
obtained and shows a similar microscopic appearance. +ytogenetic studies of the
immature cells are undertaen and show a ?E// chromosomal translocation. Which of
the following is appropriate treatment at this time!
A. All*trans*retinoic acid
(. (one marrow transplantation
+. )matinib
,. Lito#antrone: vincristine: prednisone: and methotre#ate
E. Jplenectomy
-),. /0/%$
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9ption + ()matinib) is correct. The cellular appearance of the peripheral smear and
bone marrow aspirate is characteristic of chronic myelogenous leuemia. The presence
of the Bhiladelphia chromosome (t?E//) mae this diagnosis virtually certain. Brotein*
tyrosine inase inhibitors such as JT)I0$ or imatinib mesylate that inhibit the bcr*abl
tyrosine inase have revolutioniCed the treatment of chronic myelogenous leuemia.
Recent studies show imatinib is superior to interferon alpha plus low*dose cytarabine
as frst*line therapy in newly diagnosed: chronic*phase +LZ.
9ption A (All*trans*retinoic acid) is incorrect. Transretinoic acid can eMectively induce
most newly diagnosed acute promyelocytic leuemia patients into remission: without
the myelosuppressive eMects of chemotherapy. The cellular appearance of the
peripheral smear and bone marrow aspire are characteristic for chronic myelogenous
leuemia. The presence of the Bhiladelphia chromosome (t?E//) mae this diagnosis
virtually certain. This is not the treatment for +LZ.
9ption ( ((one marrow transplantation) is incorrect. (one marrow transplantation
after $ year of treatment without complete or signifcant cytogenetic remission is
recommended in patients II years of age or younger with +LZ and with a sibling
donor matched for HZA*A: HZA*(: and HZA*,R.
9ption , (Lito#antrone: vincristine: prednisone: and methotre#ate) is incorrect. This
was an e#perimental induction combination for acute lymphoblastic leuemia and a
poor one at that. A cancer and leuemia Kroup ( (+AZK() study of this regimen closed
early because the median remission duration was shorter than in previous studies.
9ption E (Jplenectomy) is incorrect. Jplenectomy oMers no intrinsic beneft in the
treatment of +LZ and is not indicated in patients whose disease is well controlled.
Evidence e#ists suggesting splenectomy may accelerate the onset of myeloid
metaplasia in the liver. Jplenectomy is associated with high perioperative rates of
bleeding or thrombotic complications.
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)matinib
)matinib is a /*phenylaminopyrimidine agent selectively inhibiting the c*abl tyrosine
inase. The development of imatinib over $% years is liely to become a paradigm for
cancer therapeutic development in the future.
+hronic myelogenous leuemia (+LZ) has a characteristic chromosomal translocation:
?.//. This places the cellular homologue of the feline Abelson leuemia virus tyrosine
inase downstream from the brea point cluster region: bcr: and results in the
unregulated e#pression of the fusion p/$@(cr*Abl oncogene: which functions as a
cytoplasmic protein inase. (cr*Abl is necessary and suGcient to produce +LZ:
although additional chromosomal aberrations develop in the later stages of the
disease. )matinib interferes with the binding of ATB to the tyrosine inase site on abl.
)matinib produces hematologic remission in virtually $@@= of interferon*refractory
patients with the accelerated phase of +LZ. Pearly &@= of patients have
disappearance of the Bhiladelphia chromosomeA?.// translocation. )matinib has
activity against two tyrosine receptor inases: c*it and BK,' (platelet derived growth
factor). +*it mutations occur in 0@= of patients with gastrointestinal stromal tumors
(K)JT: a sarcoma arising from the myenteric neurons of +a<al). )matinib produces
signifcant responses in this otherwise refractory sarcoma.
Taen from )ntegrated Bharmacology /E by Bage et al
TREATLEPT
)matinib mesylate (Kleevec): an oral tyrosine inase inhibitor: is eMective and
indicated as frst*line treatment for +LZ myeloid blast crisis: accelerated phase: or
+LZ in its chronic phase. Lore than D@= of patients have ma<or cytogenetic response
(`&I= Bhiladelphia chromosome*positive cells in the marrow) and more than >@=
have progression*free survival after /% months. +omplete hematologic response
usually occurs in less than $ month.
Jymptomatic hyperleuocytosis (e.g.: +PJ symptoms) can be treated with
leuapheresis and hydro#yureaE allopurinol should also be started to prevent urate
nephropathy following rapid lysis of the leuemic cells.
+ytoto#ic therapy with hydro#yurea has largely replaced busulfan as the standard
cytoto#ic treatment.
Allogeneic stem*cell transplantation (following intense chemotherapy with busulfan
and cyclophosphamide or combined chemotherapy with cyclophosphamide and
fractionated total body irradiation to destroy residual leuemic cells) is a potentially
curative treatment for +LZ in chronic phase unresponsive to imatinib. Kenerally only
/@= of patients are candidates for stem*cell transplantation: given the limitations of
age and lac of HZA*matched donors.
)t should be considered in ^young^ patients (increased survival in patients younger
than II years) with compatible siblings.
Early transplantation is also very important for patient survival.
Transplantation of marrow from an HZA*matched: unrelated donor is also now
recogniCed as safe and eMective therapy for selected patients
.
A $@*year*old boy is brought to the emergency department by his parents following
the appearance of a rash D hours earlier. The parents report that the boy has been sic
with a sore throat and non*productive cough for the last three days: but did not see
treatment as he was eating well and otherwise active. However this morning the boy
began to complain of malaise: general muscle aches: and a headache: and his parents
measured an oral temperature of &?[+ ($@/./['). Jeveral hours later the boy suddenly
developed a rash: which is described as red spots. The lesions appeared at the same
time all over his body and are progressively worsening. There is no history of sic
contacts or recent travel. The boy has no other medical problems and no nown
allergies. Oital signs are signifcant for hypotension: tachycardia: and a temperature of
%@[+ ($@%['). The patient appears an#ious and restless but is alert. Bhysical
e#amination is signifcant for a diMuse: erythematous papular rash: shown. The rash is
present on the trun and e#tremities: but not the face: palms: and soles. There is no
blanching of the lesions when pressure is applied with a glass slide. Po nuchal rigidity
is appreciated: and Yernig]s and (rudCinsi]s signs are negative. (lood tests shown.
What is the most appropriate treatment at this time!
P#i@@?f$
W(+ (white blood cell count) Hb (hemoglobin) Hct (hematocrit) Blatelets
$% $I %I $@@
Pa Y +l H+9& (;P (blood urea nitrogen) +reatinine
Klucose
$%/ %.I $@% // $% @.D $@@
BT (prothrombin time) aBTT (activated partial thromboplastin time)
$0 %@
,*dimer 'ibrin degradation products
$I &@@
A. ,o#ycycline
(. Benicillin K
+. Blasma e#change
,. Brednisone
E. Jupportive therapy
-),. %0?D0
123456728
9ption ( (Benicillin K) is correct. This is the $st line treatment for meningococcemia:
which is a systemic infection by the bacteria Peisseria meningitides. )t is contracted by
inhalation of airborne droplets of infected nasopharyngeal secretions: which then
spread hematogenously and can result in meningitis and fulminant meningococcemia.
Batients usually present with an antecedent upper respiratory infection: which is
followed by high fever: chills: myalgias: and other constitutional symptoms. +hanges
in mental status may also occur. The hallmar rash reQects systemic endothelial
damage and diMuse intravascular coagulation (,)+): and is characteriCed by the
sudden appearance of widespread purpuric lesions with necrotic centers that do not
blanche under pressure. This patient]s history: appearance of the rash: and lab values
are strongly consistent with this diagnosis and empirical antibiotic treatment should be
immediately initiated.
9ption A (,o#ycycline) is incorrect. This is the treatment of choice for Rocy Lountain
spotted fever: which is a tic*borne disease caused by the organism Ricettsia
ricettsii. Batients classically present with a history of tic e#posure: fever: and a
petechial rash that begins on the palms and soles and spreads centripetally. This is an
unliely diagnosis in this patient given the lac of history of tic e#posure and absence
of lesions on the palms and soles. 'urthermore: the lesions illustrated are purpuric:
which coupled with an antecedent upper respiratory infection and evidence of
consumptive coagulopathy is strongly suggestive of fulminant meningococcemia.
9ption + (Blasma e#change) is incorrect. This is the treatment for thrombotic
thrombocytopenic purpura: which is a hematological disorder resulting from the
deposition of abnormal von Willebrand factor multimers in the vasculature: with
concomitant platelet consumption and microangiopathic hemolytic anemia. )t is most
often idiopathic. The classic diagnostic pentad includes mental status changes:
thrombocytopenia: microangiopathic hemolytic anemia: neurological symptoms such
as change in mental status: and evidence of nephritis or overt renal failure. This
patient]s history: appearance of the rash: leuocytosis: and normal hematocrit and
creatinine are more consistent with fulminant meningococcemia.
9ption , (Brednisone) is incorrect. This is the primary treatment for idiopathic
thrombocytopenic purpura: which is an acute: self*limiting hematological disorder
caused by antibody*mediated clearance of platelets. )t is often preceded by a viral
infection or recent immuniCation: and is a diagnosis of e#clusion. This patient]s history:
symptom comple#: leuocytosis: and evidence of ,)+ are not compatible with this
diagnosis and are strongly suggestive of an infectious process.
9ption E (Jupportive therapy) is incorrect. This is the initial treatment of Henoch*
Jchanlein purpura: which is a systemic immunoglobulin A ()gA)*mediated vasculitis
common in children. )t is idiopathic: but often follows an upper respiratory infection. )t
typically presents as Vpalpable purpuraW aMecting the buttocs and lower e#tremities:
and is accompanied by fever: arthralgias: abdominal colic: and nephritis. Burpura is a
manifestation of endothelial damage secondary to immune comple# deposition and
not abnormal platelet number or function. This patient]s distribution of the rash:
symptoms: leuocytosis: thrombocytopenia: normal creatinine: and evidence of a
consumptive coagulopathy are strongly suggestive of meningococcemia and reFuires
defnitive intervention.
123456728
Peisseria meningitidis
+lassifcation
Jerogroups based on the polysaccharide capsuleE most common b A: (: +: N: and
W$&I
Jerotypes based on the outer membrane protein
)mmunotypes based on ZBJ
Bathogenesis
Peisseria meningitidis enters the respiratory tract: invades mucous membranes: and
spreads via the bloodstream.
Antiphagocytic capsule is important for virulence.
Released endoto#in induces fever and increases vascular permeability: potentially
leading to shoc and petechiae (capillary leaage in sin).
Leningococcal diseases
Leningococcal infection is most common in children younger than I years of age and
those with defciency of terminal complement components (+I*+?).
Leningitis. acute onset of fever: headache: and stiM nec
Acute meningococcemia. septicemia with or without meningitis
+haracteriCed by fever: shoc: and generaliCed hemorrhage ranging from petechiae to
purpura
+an be rapidly fatal (mortality rate of /I= or higher) if not treated promptly
Waterhouse*'riderichsen syndrome. complication of meningococcemia
Lared by overwhelming disseminated intravascular coagulation and bilateral
hemorrhagic adrenal necrosis with septic shoc: acute hypotension: tachycardia: and
petechiae
+hronic meningococcemia. milder disease characteriCed by persistent (for wees)
bacteremia
Zow*grade fever: arthritis: and petechial sin lesions
Lild febrile disease with pharyngitis: pneumonia: arthritis: or urethritis
Transmission of P. meningitidis
)nhalation of aerosol droplets (often from asymptomatic nasopharyngeal carriers)
Berson*to*person spread from infected persons
Brevention
(reast*feeding infants for the frst D months of life
Active immuniCation of children older than / years of age with a polyvalent con<ugate:
anticapsular vaccine (not eMective against serogroup ()
Boste#posure prophyla#is with rifampin: Fuinolones: or sulfonamides (only if the
organism is proven susceptible)
Treatment
Benicillin is the drug of choice. Alternatives include broad*spectrum cephalosporins
(ceftria#one): chloramphenicol: and sulfonamides (if susceptible).
Antibiotics must be secreted from mucosa to eliminate carrier state.
A 0/*year*old man with a history of smoing D@ pacs per year comes to the
emergency room with increased shortness of breath. He usually can increase his
o#ygen and tae more freFuent puMs on his metered*dose inhalers: but this has not
helped him on this occasion. His o#ygen saturation is ?@= on & Z. He has decreased
breath sounds: which are more obvious on the left side. The remainder of his
e#amination is only notable for tachycardia. A radiograph of the chest is shown (see
fgure). Which of the following is the most appropriate ne#t step in management!
Lmf@@0f$.<pg
A. $@@= 9/ via face mas
(. +T scan of the thora#
+. )O Lethylprednisolone: AlbuterolAAtrovent inhalers: and 9/
,. Jputum cultures
-),. /0%&I
123456728
9ption A ($@@= 9/ via face mas) is correct. The frst treatment of pneumothora# is
$@@= o#ygen via face mas.
9ption ( (+T scan of the thora#) is incorrect. A +T scan of the thora# may be useful to
determine the degree of lung collapse: but the frst treatment strategy would be
administration of o#ygen.
9ption + ()O Lethylprednisolone: AlbuterolAAtrovent inhalers: and 9/) is incorrect. This
would be the correct management of solely a +9B, e#acerbationE the pneumothora#
demands o#ygen via face mas.
9ption , (Jputum cultures) is incorrect. Jputum cultures are not indicated in this caseE
the initial treatment of pneumothora# is administration of o#ygen.
123456728
Jupplemental o#ygen increases the rate of pneumothora# absorption.
+autious observation in the asymptomatic patient with `$I= pneumothora# can be
done but reFuires close daily outpatient monitoring.
A $?*year*old woman is brought to the physician by her parents because they have
noticed that she is increasingly losing weight. Jhe states that there is nothing wrong
with her behavior and that she is purposefully trying to lose weight simply because
she is overweight. Her parents state that her sole hobby is to photograph food and
that she has forsaen all other activities to devote herself to food photography. 'urther
Fuestioning reveals that she is intensely fearful of being overweight. A review of
systems fnds that she has not had menses in the last % months despite no se#ual
activity. Bhysical e#amination reveals a body mass inde# ((L)) of $I gAm/ ($I lbAin/):
lanugo: and dry sin. What is the most liely diagnosis!
A. Anore#ia nervosa
(. (inge*eating disorder
+. (ody dysmorphic disorder
,. (ulimia nervosa
E. JchiCophrenia
-),. &&I$/
123456728
9ption A (Anore#ia nervosa) is correct. The diagnosis of anore#ia reFuires four
elements. a refusal to maintain appropriate body weight: an intense fear of gaining
weight: undue inQuence of body shapeAweight on self*image: and amenorrhea (in
postmenarchal females). Jome anore#ics can purge: but the behavior is not primary
and not as freFuent as in bulimia. Also: note for the diagnosis that the patient must be
below >I= of minimally recommended weight. )n this case: all four criteria are met.
9ption ( ((inge*eating disorder) is incorrect. (inge*eating disorder occurs in
overweight individuals where there is binge eating and no compensatory behavior.
9ption + ((ody dysmorphic disorder) is incorrect. (inge*eating disorder describes
binge eating without compensatory behavior. +onseFuently: these individuals are
usually obese.
9ption , ((ulimia nervosa) is incorrect. The diagnosis of bulimia reFuires that there be
episodes of binge eating followed by inappropriate compensatory behavior. The
patient must be unduly inQuenced by body siCeAweight: and the behavior must e#ist
twice a wee for & months. Pote that the compensatory behavior does not need to be
purging in nature. E#cessive e#ercise: abuse of la#atives: enemas: and diuretics are
also considered inappropriate compensatory behaviors.
9ption E (JchiCophrenia) is incorrect. )n schiCophrenia: there must be hallucinations:
delusions: or signifcant negative symptoms for a period longer than D months.
Although this person feels that they are overweight when they have a (L) of $I gAm/
($I lbAin/): this is not considered a delusion.
123456728
Table $0*$. +omparison of Anore#ia Pervosa and (ulimia Pervosa
,isorder 'eatures +omorbid +onditions +omplicationsR
Anore#ia nervosa Laintenance of weight `>I= normal for age and height
,istorted perceptions of own body siCe
)ntense fear of gaining weight or becoming fatE self*esteem largely determined by
weight
Amenorrhea. absence of at least three consecutive menstrual cycles
,enial of serious health eMects of very low body weight
Restricting type. obsessive*compulsive behavior: social withdrawal: restrained
emotional e#pression: strong need for control ,epressive disorders
9bsessive*compulsive disorder
Bersonality disorders Hypotension
(radycardia
Hypothermia
Zeuopenia: anemia
9steoporosis
,ry sin: lanugo (fne: downy hair)
+ardiac arrhythmias
(ulimia nervosa Repeated binge eating
;se of inappropriate methods to prevent weight gain
Jense of lac of control during binge*eating episodes
Typically normal weight
Jelf*esteem largely determined by weight
Restricted intae between binges
Hiding binge eating and purging from others
)mpulsive behaviors (e.g.: stealing: promiscuity: overspending) ,epressive
disorders
An#iety disorders
Jubstance use disorders
Bersonality disorders (freFuently borderline personality disorder) Zoss of dental
enamel
'luid and electrolyte disturbances
+ardiac arrhythmias
Jwollen parotid glands
+alluses on bac of hand from self*induced vomiting
Esophageal tears or ruptures
,ehydration
A I$*year*old man is brought into the emergency room after three episodes of
vomiting bright red blood. He has a nown history of cirrhosis secondary to alcoholic
liver disease. 9n arrival: his vital signs are as follows. blood pressure: ?@AD@ mm HgE
pulse: $$I beatsAminuteE temperature &0.D[+ (??.D[')E and respirations: $>
breathsAminute. His abdomen is dull to percussion throughout. A nasogastric tube is
inserted: and bright red blood is found when stomach contents are aspirated. What is
the most appropriate ne#t step in the management of this patient!
A. (alloon tamponade
(. Endoscopic band ligation
+. )ntravenous normal saline
,. 9ctreotide
E. Bropranolol
-),. &&/0I
123456728
9ption + ()ntravenous T)OU normal saline) is correct. This patient has an upper
gastrointestinal bleed: most liely the result of bleeding esophageal varices. However:
the e#act cause is unimportant in this case: because the patient is hemodynamically
unstable. He is hypotensive and tachycardic and thus reFuires hemodynamic
resuscitation. The option of )O normal saline meets this reFuirement.
9ption A ((alloon tamponade) is incorrect. (alloon tamponade is reserved for patients
who continue to have bleeding esophageal varices despite endoscopic band ligation.
9ption ( (Endoscopic band ligation) is incorrect. )f medical therapy with octreotide
fails: endoscopic band ligation is the ne#t step in the management of bleeding
esophageal varices.
9ption , (9ctreotide) is incorrect. Were this patient hemodynamically stable: the use
of octreotide is considered the frst step in the management of bleeding esophageal
varices.
9ption E (Bropranolol) is incorrect. Bropranolol and other nonselective beta blocers
are used as prophyla#is against bleeding esophageal varices. There is no role acutely:
especially not in hypotensive patients.
123456728
ABBR9A+H T9 THE BAT)EPT W)TH A+;TE KAJTR9)PTEJT)PAZ (ZEE,)PK ('ig. &/*/)
Assessment of Oital JignsAResuscitation
The frst step in the evaluation and therapy for the patient with acute K) hemorrhage
is to determine the severity of blood loss. Oital signs should be recorded immediately.
)f the systolic blood pressure drops more than $@ mm Hg andAor the pulse increases
more than $@ beats per minute as the patient changes positions from supine to
standing: it is liely the patient has lost at least >@@ mZ ($I=) of circulating blood
volume. Hypotension: tachycardia: tachypnea: and mental status changes in the
setting of acute K) hemorrhage suggest at least a $I@@*mZ (&@=) loss of circulating
blood volume.
The goal of resuscitation is to restore the normal circulatory volume. )nitially: at least
two large*bore intravenous catheters are used to administer isotonic solutions (e.g.:
lactated RingerXs solution or @.?= Pa+l): and blood products if indicated. )f the patient
is in shoc: a central venous access should be established. The amount of blood
products to be transfused must be individualiCed. Transfusions of paced red blood
cells are provided to prevent complications (e.g.: angina: congestive heart failure:
stroe) of acute blood loss. Therefore: the need for blood transfusion depends on
multiple factors: including the patientXs age: overall health: and response of vital signs
to initial resuscitation. )n view of the riss of blood transfusion: it is not appropriate
simply to transfuse until an arbitrary hematocrit is achieved. )f coagulation studies are
abnormal: as commonly observed in cirrhotic patients: fresh*froCen plasma andAor
platelets may be reFuired to control ongoing hemorrhage. 9pinions diMer regarding
the use of nasogastric lavage in preparation for endoscopic e#amination: although
aspiration of gastric blood may be particularly important in patients with liver cirrhosis:
because blood in the K) tract may precipitate hepatic encephalopathy.
'rom +ecil Essentials of Ledicine DE by Andreoli et al
Table &/*&. +ommon Jources of Acute Kastrointestinal Hemorrhage
Jource Associated +linical 'eatures Treatments
;pper Kastrointestinal Tract
Esophagitis Heartburn: dysphagia: odynophagia LedicationR
AntireQu# surgery or procedures
Esophageal cancer Brogressive dysphagia: weight loss +hemoradiotherapy:
surgery
Balliative endoscopy procedures
KastritisAgastric ulcer AspirinAPJA), use Withdraw PJA),s
,uodenitisAduodenal ulcer Abdominal painAdyspepsia Ledicationc
Helicobacter pylori infection Endoscopic therapy for acute bleeding
Kastric cancer Early satiety: weight loss: abdominal pain Jurgery:
chemotherapy
Esophagogastric varices History of +Z, Oariceal banding: sclerotherapy
Jtigmata of +Z, on e#amination Oasopressin: octreotide
T)BJ or decompressive surgery
Lallory*Weiss tear History of retching before hematemesis Jupportive (usually self*
limited)
Endoscopic therapy
Zower Kastrointestinal Tract
)nfection History of e#posure: diarrhea: fever JupportiveAantibiotics
)nQammatory bowel diseases History of colitis: diarrhea: abdominal pain: fever
JteroidsAI*AJAAimmunotherapy
Jurgery if no response to medication
,iverticula Bainless hematocheCia Jupportive
Jurgery for recurrent disease
Angiodysplasia Bainless hematocheCia Endoscopic therapy
9ften in ascending colon Jupportive
+ommonly involves stomach and small bowel as well Jurgery for localiCed
disease
+olon cancer +hange in bowel habit: anemia: weight loss Jurgery
+olon polyp ;sually asymptomatic Endoscopic or surgical removal
)schemic colitis Typically elderly patients
History of vascular disease
Lay present with abdominal pain Jupportive (self*limited)
LecelXs diverticulum Bainless hematocheCia in young patient
Zocated at distal ileum Jurgery
Hemorrhoids Rectal bleeding associated with bowel movement Jupportive
'rom +ecil Essentials of Ledicine DE by Andreoli et al

'igure &/*/ Approach to the patient with acute gastrointestinal bleeding. EK, b
esophagogastroduodenoscopy.
'rom +ecil Essentials of Ledicine DE by Andreoli et al
The medical intern on call is summoned to the bedside of a 0@*year*old woman who is
complaining of chest pain. Jhe is postoperative day / after a hysterectomy for
endometrial cancer. A $/*lead electrocardiogram (E+K) is ordered: and the tracing is
shown (see fgure). (ased only on the evidence presented: which of the following is
the most liely diagnosis!
"#f@0$f$
A. Acute pericarditis
(. Acute pulmonary embolism
+. )nferior myocardial infarction
,. Zeft bundle branch bloc
E. Pond-*wave myocardial infarction
-),. /0/0/
123456728
9ption ( (Acute pulmonary embolism) is correct. This is a classic $/*lead E+K
indicating an acute pulmonary embolism. There is an J wave in lead ): a - wave in
lead ))): and an inverted T wave in lead ))) (J$: -&: T& pattern). There is sinus
tachycardia ($D@ bpm) and an incomplete right bundle branch bloc pattern (an R
wave in aOR and O$ and an J wave in OD).
9ption A (Acute pericarditis) is incorrect. The E+K in acute pericarditis generally shows
diMuse JT*segment elevation. This is the classic E+K for an acute pulmonary
embolism: showing an J wave in lead ): a - wave in lead ))): and an inverted T wave in
lead ))) (J$: -&: T& pattern).
9ption + ()nferior myocardial infarction) is incorrect. The E+K of an inferior myocardial
infarction would show raised JT segment and - waves in the inferior leads ()): ))): and
aO'). This is the classic E+K for an acute pulmonary embolism: showing an J wave in
lead ): a - wave in lead ))): and an inverted T wave in lead ))) (J$: -&: T& pattern).
9ption , (Zeft bundle branch bloc) is incorrect. There is an incomplete right bundle
branch bloc pattern (an R wave in aOR and O$ and an J wave in OD). The E+K
showing left bundle branch bloc would typically show -RJ duration greater than @.$/
sE broad notched R waves with JT depression in leads ): aOZ: and ODE and broad -J
waves in O$ to O&. This is the classic E+K for an acute pulmonary embolism: showing
an J wave in lead ): a - wave in lead ))) and an inverted T wave in lead ))) (J$: -&: T&
pattern).
9ption E (Pond-*wave myocardial infarction) is incorrect. The E+K leads
corresponding to the infarct region usually show JT depression and deeply inverted
symmetrical T waves in nond-*wave: or subendocardial: infarcts. This is the classic
E+K for an acute pulmonary embolism: showing an J wave in lead ): a - wave in lead
))): and an inverted T wave in lead ))) (J$: -&: T& pattern).
123456728
EZE+TR9+AR,)9KRABHN.
page ID/
@
page ID&
Table ?%*&. ,ETERL)P)PK THE BRETEJT BR9(A()Z)TN 9' A+;TE B;ZL9PARN
EL(9Z)JL (AJE, 9P B9)PT JNJTEL AP, ,*,)LER REJ;ZT
OAR)A(ZE B9)PTJ
,OT symptomsAsignsR &.@
BE as or more lielyc &.@
HR e$@@ beatsAmin $.I
)mmobiliCationAsurgeryf $.I
Brevious ,OT or BE $.I
Hemoptysis $.@
Lalignancy $.@
T9TAZ J+9RE BRETEJT BR9(A()Z)TNg
`/.@ Zow
/.@ to D.@ Loderate
eD.@ High

R)ncluding ob<ectively measured leg swelling and pain with palpation in the deep vein
region.
cBE as liely or more liely than an alternative diagnosis. Bhysicians were told to use
clinical information: along with chest radiography: electrocardiography: and laboratory
tests.
f)f in previous % wees.
g9f the %&0 patients with a negative ,*dimer result (by the JimpliRE, assay) and low
clinical probability: only one developed BE during follow*upE thus: the negative
predictive value for the combined strategy of using the clinical model with ,*dimer
testing in these patients was ??.I=.
,OT bdeep venous thrombosis: BE bpulmonary embolism: HR bheart rate.
'rom Wells BJ: Anderson ,R: Rodger L: et al. E#cluding pulmonary embolism at the
bedside without diagnostic imaging. Lanagement of patients with suspected
pulmonary embolism presenting to the emergency department by using a simple
clinical model and ,*dimer. Ann )ntern Led /@@$E$&I.?>.
Electrocardiographic fndings: which are present in the ma<ority of patients with acute
BE: include JT*segment abnormalities: T*wave changes: and left or right a#is deviation.
9nly one third of patients with massive or submassive emboli have manifestations of
acute cor pulmonale such as the J$*-&*T& pattern: right bundle branch bloc: B*wave
pulmonale: or right a#is deviation. All of these fndings are also nonspecifc. The utility
of electrocardiography in suspected acute BE is derived more from its ability to
establish or e#clude alternative diagnoses: such as acute myocardial infarction: rather
than diagnosing or e#cluding BE.
+HEJT RA,)9KRABHN.

'igure ?%*/ High probability ventilation*perfusion scan.
The chest radiograph is often abnormal in patients with acute BE: but it is nearly
always nonspecifc. +ommon radiographic fndings include pleural eMusion:
atelectasis: pulmonary infltrates: and mild elevation of a hemidiaphragm. +lassic
fndings of pulmonary infarction: such as HamptonXs hump or decreased vascularity
(WestermarXs sign): are suggestive of the diagnosis: but they are infreFuent. A normal
chest radiograph in the setting of dyspnea and hypo#emia without evidence of
bronchospasm or anatomic cardiac shunt is strongly suggestive of BE. ;nder most
circumstances: however: the chest radiograph cannot be used for conclusive diagnosis
or e#clusion. Although the radiograph may e#clude other processes: such as
pneumonia: pneumothora#: or rib fracture: which may cause symptoms similar to
acute BE: BE may freFuently coe#ist with other underlying heart or lung diseases.
Jymptoms: signs: radiographic fndings: electrocardiography: and the plasma ,*dimer
measurement cannot be considered diagnostic of BE or ,OT. When these entities are
suspected: further evaluation with noninvasive or invasive testing is necessary.
A DD*year*old man visits the emergency department with a high fever. The fever has
persisted for over a wee. The patient also has been very tired: has lost weight: and
has bac pain. He has a history of an enlarged prostate: which was treated by
transurethral resection of the prostate $ month ago. The patient loos ill and has a
temperature of &?[+ ($@/.&['). There are petechia on the palpebral con<unctiva and
small: tender: red nodules on the palms of his hands. What is the ne#t step in
diagnosis!
A. +hest radiography (BA and lateral)E blood cultures h/: $ hour
apart from two diMerent sitesE sputum and urine cultures
(. +omputed tomography (+T) scan of chest to rule out embolic
phenomenon
+. Erythrocyte sedimentation rate: plasma fbrinogen: ,*dimer and
+*reactive protein levels
,. Transthoracic echocardiogram and three sets of blood cultures
with at least $ hour between the frst and last cultures
E. Transthoracic echocardiogram only
-),. /0@&D
123456728
9ption , (Transthoracic echocardiogram and three sets of blood cultures with at least
$ hour between the frst and last cultures) is correct. )n $??%: clinical criteria for
diagnosing infective endocarditis were published by ,urac and colleagues. Batients
must fulfll a certain combination of ma<or criteria (positive blood cultures and
echocardiographic evidence or new murmur) and minor criteria (fever: "aneway
lesions: or 9sler nodes).
9ption A (+hest radiography Tposteroanterior (BA) and lateralUE blood cultures h/: $
hour apart from two diMerent sitesE sputum and urine cultures) is incorrect. )nfectious
endocarditis must be ruled in or out. This would not be sensitive enough because
another set of blood cultures at least $/ hours later would need to be drawn. A
transthoracic echocardiogram is also needed.
9ption ( (+omputed tomography T+TU scan of chest to rule out embolic phenomenon)
is incorrect. This by itself will not rule endocarditis in or out.
9ption + (Erythrocyte sedimentation rate: plasma fbrinogen: ,*dimer and +*reactive
protein levels) is incorrect. These studies will not rule bacterial endocarditis in or out.
The patient]s clinical picture is not presently consistent with a coagulopathy or
disseminated intravascular coagulopathy. This complication is liely to ensue if the
patient has infectious endocarditis and diagnosis is delayed.
9ption E (Transthoracic echocardiogram only) is incorrect. Transthoracic
echocardiogram has a sensitivity of only about I@=dD@= for detecting endocarditis
lesions. 9ne problem is that it does not view some structures well: such as the mitral
valve: and it is also not good with prosthetic valves. A transesophageal
echocardiogram is much better in this regard: but even then should not serve as the
sole test.
123456728
Table >*$@. Lodifed ,ue +riteria for the ,iagnosis of )nfective EndocarditisR
+R)TER)A +9LLEPTJ
LA"9R +R)TER)A
Licrobiologic
Typical microorganism isolated from two separate blood cultures. viridans
streptococci: Jtreptococcus bovis: HA+EY group: Jtaphylococcus aureus: or
community*acFuired enterococcal bacteremia without a primary focus )n patients
with possible infective endocarditis: at least two sets of cultures of blood collected by
separate venipunctures should be obtained within the frst $ to / hours of
presentation. Batients with cardiovascular collapse should have three cultures of blood
obtained at I*to*$@*minute intervals and thereafter receive empirical antibiotic
therapy.
or
Licroorganism consistent with infective endocarditis isolated from persistently
positive blood cultures
or
Jingle positive blood culture for +o#iella burnetii or phase ) )gK antibody titer to +.
burnetii e$ . >@@ +. burnetii is not readily cultivated in most clinical microbiology
laboratories.
Evidence of endocardial involvement
Pew valvular regurgitation (increase or change in pree#isting murmur not suGcient)

or
Bositive echocardiogram (transesophageal echocardiogram recommended in patients
who have a prosthetic valve: who are rated as having at least possible infective
endocarditis by clinical criteria: or who have complicated infective endocarditis)
Three echocardiographic fndings Fualify as ma<or criteria. a discrete:
echogenic: oscillating intracardiac mass located at a site of endocardial in<uryE a
periannular abscessE and a new dehiscence of a prosthetic valve.
L)P9R +R)TER)A
Bredisposition to infective endocarditis that includes certain cardiac conditions and
in<ection*drug use +ardiac abnormalities that are associated with infective
endocarditis are classifed into three groups.
High*ris conditions. previous infective endocarditis: aortic*valve disease:
rheumatic heart disease: prosthetic heart valve: coarctation of the aorta: and comple#
cyanotic congenital heart diseases
Loderate*ris conditions. mitral*valve prolapse with valvular regurgitation
or leaQet thicening: isolated mitral stenosis: tricuspid*valve disease: pulmonary
stenosis: and hypertrophic cardiomyopathy
Zow* or no*ris conditions. secundum atrial septal defect: ischemic heart
disease: previous coronary*artery bypass graft surgery: and mitral*valve prolapse with
thin leaQets in the absence of regurgitation
'ever Temperature e&>[+ ($@@.%[')
Oascular phenomena Betechiae and splinter hemorrhages are e#cluded.
Pone of the peripheral lesions are pathognomonic for infective endocarditis.
)mmunologic phenomena Bresence of rheumatoid factor: glomerulonephritis:
9slerXs nodes: or Roth spots
Licrobiologic fndings Bositive blood cultures that do not meet the ma<or
criteria
Jerologic evidence of active infectionE single isolates of coagulase*negative
staphylococci and organisms that very rarely cause infective endocarditis are e#cluded
from this category.
Taen from Bractical Kuide to the +are of the Ledical Batient DE by 'erri
A patient with infective endocarditis almost always has a fever and a heart murmur
The signs and symptoms of infective endocarditis are very varied: but relate
essentially to four ongoing processes.
the infectious process on the valve and local intracardiac complicationsE
septic emboliCation to virtually any organE
bacteremia: often with metastatic foci of infectionE
circulating immune comple#es and other factors.
The patient almost always has a fever and a heart murmur and may also complain of
non*specifc symptoms such as anore#ia: weight loss: malaise: chills: nausea: vomiting
and night sweats: symptoms that are common to many of the causes of ';9 listed in
'igure /?.%. Beripheral manifestations may also be evident in the form of splinter
hemorrhages and 9slerXs nodes ('ig. /?.$$). Licroscopic hematuria resulting from
immune comple# deposition in the idney is characteristic (see +hapter $0).
(lood culture is the most important test for diagnosing infective endocarditis
Licrobiologic and cardiologic investigations are of critical importance. The blood
culture is the single most important laboratory test. )deally three separate samples of
blood should be collected within a /%*hour period and before antimicrobial therapy is
administered. Lethods for processing blood cultures are described in the Appendi#.
)solation of the causative organism is essential so that antibiotic susceptibility tests
can be performed and optimum therapy prescribed. Putritionally variant strains of oral
streptococci are nown to cause infective endocarditis. These may fail to grow in blood
culture media unless pyrido#al is added to the broth. Alternatively they grow as
satellite colonies around Jtaph. aureus colonies on blood agar.
Taen from Ledical Licrobiology &E by Lims et a
A biotechnology company is seeing to develop a new test for the detection of
diabetes using an optical fnger probe similar to a pulse o#imeter. They screen $@@@
random individuals using the current diagnostic criteria of having two fasting blood
glucose readings more than$/D mgAdZ. They compare the results obtained with their
new test to those of a standard blood test. Their results are as follows.
Healthy ,iabetes
Bositive optical test
I@
?@
Pegative optical test
>I@
$@
What is the accuracy of the new optical test!
A. $@=
(. D%=
+. ?@=
,. ?%=
E. ??=
-),. &&%$0
123456728
9ption , (?%=) is correct. Accuracy is defned as the proportion of individuals who are
correctly diagnosed by the screening test. ;sing the eFuation (true positive TTBU _ true
negative TTPU)A$@@@: we get (>I@ _ ?@)A$@@@ b ?%=.
9ption A ($@=) is incorrect. The prevalence of diabetes found in this random
population of individuals can be calculated as the TBs plus the false negatives ('Ps)
divided by $@@@ individuals. This calculation yields a $@= prevalence of diabetes.
9ption ( (D%=) is incorrect. Bositive predictive value is the proportion of people with a
positive test who actually have the condition. ;sing the formula TBA(TB_ false positive
T'BU): we get ?@A(?@ _ I@) b D%=.
9ption + (?@=) is incorrect. Jensitivity is defned as the proportion of individuals who
have the condition that are correctly identifed by the screening test. ;sing the
formula TBA(TB_ 'P): we get ?@A(?@_$@) b ?@=.
9ption E (??=) is incorrect. The negative predictive value is how liely a negative test
is truly negative. ;sing the formula TPA(TP_ 'P): we get >I@A(>I@ _ $@) b ??=.
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Oalidity of Jcreening Tests
The validity of a test is defned as its ability to distinguish between who has a disease
and who does not. Oalidity has two components. sensitivity and specifcity. The
sensitivity of the test is defned as the ability of the test to identify correctly those who
have the disease. The specifcity of the test is defned as the ability of the test to
identify correctly those who do not have the disease.
Tests with ,ichotomous Results (Bositive or Pegative)
Juppose we have a hypothetical population of $:@@@ people: of whom $@@ have a
certain disease and ?@@ do not. A test is available that can yield either positive or
negative results. We want to use this test to try to distinguish persons who have the
disease from those who do not. The results obtained by applying the test to this
population of $:@@@ people are shown in Table I*$.
'rom Epidemiology &E by Kordis
Table I*$. +oncept of the Jensitivity and Jpecifcity of Jcreening E#aminations
E#ample. Assume a population of $:@@@ people: of whom $@@ have a disease and ?@@
do not have the disease
Jcreening Test to )dentify the $@@ Beople with the ,isease
True +haracteristics in the Bopulation
Results of Jcreening,isease Po ,isease Total
Bositive >@ $@@ $>@
Pegative /@ >@@ >/@
Total $@@ ?@@ $:@@@
'rom Epidemiology &E by Kordis
How good was the test! 'irst: how good was the test in correctly identifying those who
had the disease! Table I*$ indicates that of the $@@ people with the disease: >@ were
correctly identifed as ^positive^ by the test: and a positive identifcation was missed in
/@. Thus: the sensitivity of the test: which is defned as the proportion of diseased
people who were correctly identifed as ^positive^ by the test: is >@A$@@ or >@=.
Jecond: how good was the test in correctly identifying those who did not have the
disease! Zooing again at Table I*$: of the ?@@ people who did not have the disease:
the test correctly identifed >@@ as ^negative.^ The specifcity of the test: which is
defned as the proportion of nondiseased people who are correctly identifed as
negative by the test: is therefore >@@A?@@ or >?=.
Pote that to calculate the sensitivity and specifcity of a test: we must now who
^really^ has the disease and who does not from another source than the test we are
using. We are in fact comparing our test results with some ^gold standard^*an e#ternal
source of ^truth^ regarding the disease status of each individual in the population.
Jometimes this truth may be the result of another test that has been in use: and
sometimes it is the result of a more defnitive: and often more invasive: test (e.g.:
cardiac catheteriCation or tissue biopsy). However: in real life: when we use a test to
identify diseased and nondiseased persons in a population: we clearly do not now
who has the disease and who does not. ()f this were already established: testing would
be pointless.) (ut to Fuantitatively assess the sensitivity and specifcity of a test: we
must have another source of truth with which to compare the test results.
'rom Epidemiology &E by Kordis
A %D*year*old man has left lower abdominal pain: and a +T scan demonstrates sigmoid
colon thicening and mesenteric Vstranding.W After three days of )O antibiotics and
inpatient hospitaliCation for this episode of presumed acute diverticulitis: he is sent
home on oral antibiotics. He develops profuse watery diarrhea and crampy abdominal
pain over the subseFuent two to three days. Which of the following is the most liely
diagnosis!
A. Antibiotic*associated colitis
(. )schemic colitis
+. Lissed appendicitis
,. Bartial colonic obstruction
E. Recurrent diverticulitis
-),. /00@$
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9ption A (Antibiotic*associated colitis) is correct. +lostridium diGcile colitis is common
after antibiotic therapy. )t can be treated by oral antibiotics in most cases.
9ption ( ()schemic colitis) is incorrect. )schemic colitis is related to low*Qowdinduced
colonic ischemia. The history and presentation are not consistent with this diagnosis.
9ption + (Lissed appendicitis) is incorrect. The initial +T fndings and location of the
pain are consistent with the diagnosis of acute diverticulitis. The watery diarrhea and
abdominal symptoms do not call the original diagnosis into doubt but rather suggest
evolution of antibiotic*associated enterocolitis.
9ption , (Bartial colonic obstruction) is incorrect. Zarge bowel obstruction may occur
chronically if a stricture develops as a result of repeated attacs of inQammation or in
the setting of untreated acute inQammation. However: in this case: the resolution of
the to#ic symptoms and the evolution of the watery diarrhea during antibiotic therapy
mae antibiotic*associated enterocolitis more liely.
9ption E (Recurrent diverticulitis) is incorrect. This is not liely if fevers and focal
tenderness have not recurred.
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+. diGcile is part of the normal intestinal Qora in a small number of healthy people and
hospitaliCed patients. The disease develops in people taing antibiotics: because the
drugs alter the normal enteric Qora: either permitting the overgrowth of these
relatively resistant organisms or maing the patient more susceptible to the
e#ogenous acFuisition of +. diGcile. The disease occurs if the organisms proliferate in
the colon and produce their to#ins.
The diagnosis of +. diGcile infection is confrmed by demonstration of the enteroto#in
or cytoto#in in a stool specimen from a patient with compatible clinical symptoms.
)solation of the organism in stool culture documents coloniCation but not disease. The
enteroto#in and cytoto#in can be detected with a number of commercial
immunoassays. These assays vary tremendously in sensitivity and specifcity: so care
must be used in selecting the appropriate test: and a negative test result does not
e#clude the diagnosis. The cytoto#in can also be detected by an in vivo cytoto#icity
assay using tissue culture cells and specifc neutraliCing antibodies for the cytoto#inE
however: this assay is technically cumbersome and reFuires $ to / days before results
are available. Lost laboratories have replaced the cytoto#icity assay with
immunoassay methods.
,iscontinuation of the implicated antibiotic (e.g.: ampicillin: clindamycin) is generally
suGcient to alleviate mild disease. However: specifc therapy with metronidaCole or
vancomycin is necessary for the management of severe diarrhea or colitis. Relapses
may occur in as many as /@= to &@= of patients after the completion of therapy:
because only the vegetative forms of +. diGcile are illed by the antibioticsE the spores
are resistant. A second course of treatment with the same antibiotic is freFuently
successful. )t is diGcult to prevent the disease: because the organism commonly e#ists
in hospitals: particularly in areas ad<acent to infected patients (e.g.: beds: bathrooms).
The spores of +. diGcile are diGcult to eliminate unless thorough houseeeping
measures are used. Thus the organism can contaminate an environment for many
months and can be a ma<or source of nosocomial outbreas of +. diGcile disease.
Taen from Ledical Licrobiology IE by Lurray et al
(9S %@*D. Jummary of +lostridium diGcile
Bhysiology and Jtructure
Kram*positive: spore*forming rod
Jtrict anaerobe (vegetative cells are e#tremely o#ygen sensitive)
Oirulence
Refer to Table %@*%
Epidemiology
The organism is ubiFuitous
+oloniCes the intestines of a small proportion of healthy individuals (`I=)
E#posure to antibiotics is associated with overgrowth of +. diGcile and subseFuent
disease (endogenous infection)
Jpores can be detected in hospital rooms of infected patients (particularly around
beds and in the bathrooms)E these can be an e#ogenous source of infection
,iseases
Refer to (o# %@*&
,iagnosis
+. diGcile disease is confrmed by detecting the cytoto#in or enteroto#in in the
patientXs feces
Treatment: Brevention: and +ontrol
The implicated antibiotic should be discontinued
Treatment with metronidaCole or vancomycin should be used in severe disease
Relapse is common because antibiotics do not ill sporesE a second course of therapy
with the same antibiotic is usually successful
The hospital room should be carefully cleaned after the infected patient is discharged
Taen from Ledical Licrobiology IE by Lurray et al
+. diGcile produces two to#ins (Table %@*I): an enteroto#in (to#in A) and a cytoto#in
(to#in (). The enteroto#in is chemotactic for neutrophils: stimulating the infltration of
polymorphonuclear neutrophils into the ileum with release of cytoines. To#in A also
produces a cytopathic eMect: resulting in disruption of the tight cell*cell <unction:
increased permeability of the intestinal wall: and subseFuent diarrhea. The cytoto#in
causes actin to depolymeriCe: with the resultant destruction of the cellular
cytoseleton both in vivo and in vitro. Although both to#ins appear to interact
synergistically in the pathogenesis of disease: enteroto#in A*negative isolates can still
produce disease. Additionally: production of one or both to#ins does not appear to be
suGcient alone for disease (e.g.: carriage of +. diGcile and high levels of to#ins are
common in young children while disease is rare). (acterial ^surface layer proteins^
(JZBs) are important for the binding of +. diGcile to the intestinal epithelium: leading
to localiCed production of to#ins and subseFuent tissue damage. 9ther +. diGcile
virulence factors are summariCed in Table %@*I.
A I%*year*old woman is being evaluated for a routine periodic checup. Jhe has a
history of type / diabetes mellitus: which is being treated with oral hypoglycemic
agents. Although she says that she is taing her medications regularly: a random
fnger*stic evaluation for blood sugar shows a reading of //@ mgAdZ. Bast e#perience
indicates that she can be noncompliant with diet and medications. Which of the
following tests is best for evaluation of the patient]s recent diabetic control!
A. 'asting blood sugar test
(. Klycosylated hemoglobin level
+. 9ral glucose tolerance test
,. Bostprandial blood sugar level
-),. /0DI/
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9ption ( (Klycosylated hemoglobin level) is correct. The best test to evaluate diabetic
control over several wees is to estimate the percentage of hemoglobin that is
glycosylated. The test commonly used for this is hemoglobin A$+ e#pressed as a
percent. When diabetic control is optimal: it should be less than D.I=.
9ption A ('asting blood sugar test) is incorrect. A fasting blood sugar test indicates the
degree of glucose control at that point in time.
9ption + (9ral glucose tolerance test) is incorrect. The oral glucose tolerance test
indicates the rate of glucose transport at a given point in time. )n some sense: it is a
combination of 9ption A and 9ption ,.
9ption , (Bostprandial blood sugar level) is incorrect. A postprandial blood sugar level
indicates the degree of insulin lacAresistance at a given point in time.
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Although the oral glucose tolerance test (9KTT) remains the standard for diagnostic
purposes: measurement of 'BK: which is simpler: cheaper: eFually accurate: faster to
perform: more reproducible: and convenient: is used for routine diagnosis.
Leasurement of glycosylated hemoglobin (HbA$c) is a useful tool for monitoring
glycemic control and for maing therapeutic decisions: but is not recommended for
diagnostic purposes. The 9KTT is still used for diagnosing gestational diabetes (Table
D>*&).
Taen from +ecil Essentials of Ledicine DE b
A II*year*old female is brought to the emergency room with a sudden onset of severe
chest: bac: and abdominal pain that began /@ minutes ago. The pain is described as
being very sharp with a tearing*lie character. Her previous medical history is notable
for hypertension treated with hydrochlorothiaCide. Jhe does not smoe tobacco or
drin alcohol.
9n e#amination: her blood pressure is $%IA?I mm Hg in the right arm and $$?A0I mm
Hg in the left armE pulse: $@I beatsAminuteE temperature: &0.&[+ (??.$[')E and
respirations: $0 breathsAminute. A chest S*ray (+SR) demonstrates a widened
mediastinum: and electrocardiography (E+K) reveals nonspecifc JT and T wave
changes. What is the most appropriate ne#t step in the management of this patient!
A. Aortography
(. Emergent surgery
+. )ntravenous labetalol
,. Thoracic spiral computed tomography (+T)
E. Transesophageal echocardiography (TEE)
-),. &&/@>
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9ption + ()ntravenous labetalol) is correct. Ripping chest pain that radiates into the
bac and stomach: combined with a pulse defcit: previous history of hypertension and
widened mediastinum on chest S*ray (+SR) should be considered an aortic dissection
until proven otherwise. As soon as aortic dissection is suspected: immediate
intravenous ()O) beta*blocer therapy should be started to reduce the pulse and blood
pressure of the patient in an attempt to limit the severity of the dissection.
9ption A (Aortography) is incorrect. Aortography is rarely performed: because it is
invasive and reFuires contrast media into the aorta.
9ption ( (Emergent surgery) is incorrect. Emergent surgery is indicated in cases of
aortic dissection where the pro#imal aorta is involved. The e#act location is
determined using computed tomography (+T) scanning and therefore: surgery would
not be the ne#t step in the management of this patient.
9ption , (Thoracic spiral computed tomography T+TU) is incorrect. Jpiral +T scanning
is e#cellent for maing the diagnosis of aortic dissection. However: the patient can die
in the +T scanner without )O beta*blocer therapy.
9ption E (Transesophageal echocardiography TTEEU) is incorrect. TEE is very useful in
the diagnosis of aortic dissection and is the preferred imaging modality in very
unstable patients. This patient is relatively stable: however and reFuires beta*blocer
therapy.
123456728
+hest #*ray may show widened mediastinum (D/=) and displacement of aortic intimal
calcium.
Transesophageal echocardiography (TEE) is study of choice in unstable patients: but
operator dependent.
LR) has the highest sensitivity and specifcity but limited availabilityE not suitable for
unstable patientsE contraindicated with pacemaers: metal devices.
Helical +T is least operator dependent: involves intravenous contrast.
TEE: LR): helical +T are imaging modalities of choice. Jensitivities (?>= to $@@=) and
specifcities (?I= to ?>=) nearly eFual in silled hands. Test of choice depends on
clinical circumstances and availability.
With medium or high pretest probability: a second diagnostic test should be done if
the frst is negative.
Transthoracic echocardiography has poor sensitivity
Aortography rarely done now.
TREATLEPT
A+;TE KEPERAZ R#
Admit to )+; for monitoring.
Bropanolol $ mg every &*I min or metoprolol I mg )O every I min: followed by
nitroprusside @.&*$@ mgAgAmin: with target J(B $@@*$/@.
)O beta*blocer is cornerstone of treatment.
)O Zabetalol can be used insteadE /@ mg )O: then %@*>@ mg every $@ min.
)O calcium channel blocers with negative inotropy may be used.
Lultiple medications may be needed.
Bro#imal dissections reFuire emergent surgery to prevent rupture or pericardial
eMusion.
,istal dissections are treated medically unless distal organ involvement or impending
rupture occurs.
Evolving role for endovascular stent placement as less invasive treatment for high*ris
surgical patients.
A /?*year*old K/B$@@$ at /> wees] gestation presents for a prenatal oGce visit. Her
pregnancy has been complicated by red cell sensitiCation with an anti*, titer of $.$/>.
;ltrasound reveals an appropriately grown fetus with evidence of fetal hydrops:
including scalp edema and ascites. Which of the following is the most appropriate ne#t
step in patient care!
A. Amniocentesis
(. +esarean delivery
+. 'etal blood sampling
,. )nduction of labor
E. Repeat anti*, titer
-),. /D0$D
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9ption + ('etal blood sampling) is correct. This fetus is demonstrating sonographic
signs of hydrops due to anemia resulting from red cell sensitiCation. At this gestational
age: the plan of management would be fetal blood sampling to confrm anemia and
intrauterine blood transfusion.
9ption A (Amniocentesis) is incorrect. This fetus already demonstrates sonographic
signs of hydropsE an amniocentesis would not add any valuable information.
9ption ( (+esarean delivery) is incorrect. ,ue to the early gestational age: the fetus
should be treated in utero: rather than delivered.
9ption , ()nduction of labor) is incorrect. ,ue to the early gestational age: the fetus
should be treated in utero: rather than delivered.
9ption E (Repeat anti*, titer) is incorrect. This fetus already demonstrates sonographic
signs of hydropsE a repeat anti*, titer would not add any valuable information.
123456728
;ZTRAJ9P)+ ,ETE+T)9P 9' RH JEPJ)T)iAT)9P
Jerial ultrasonic e#aminations of a woman with a fetus at ris for hemolytic disease
can be a useful ad<unct to amniocentesis in confrming fetal well*being and
determining the advent of fetal hydrops. The e#amination should include a routine
fetal assessment plus a determination of placental siCe and thicness and hepatic siCe.
(oth the placenta and the fetal liver are enlarged with hydrops. 'etal hydrops is easily
diagnosed by the characteristic appearance of one or more of the following. ascites:
pleural eMusion: pericardial eMusion: or sin edema. Appearance of any of these
factors during an ultrasonic e#amination eliminates the need for diagnostic
amniocentesis and necessitates therapeutic intervention based on fetal gestational
age.
,oppler assessment of pea velocity in the fetal middle cerebral artery (L+A) may
prove to be the most valuable ultrasonic tool for detecting fetal anemia. A value above
$.I multiples of the median for gestational age is considered predictive. 'or accurate
evaluation: the ,oppler gate is placed over the fetal L+A <ust as it bifurcates from the
carotid siphon. +olor ,oppler is clearly advantageous for this e#amination. After &I
weesX gestation: this test may produce a higher false*positive rate ('igure $D*&).
BER+;TAPE9;J ;L()Z)+AZ (Z99, JALBZ)PK

'igure $D*$ Lodifed Ziley chart used to determine the appropriate management of the
patient with isoimmuniCation. The j9, %I@ nm level in the amniotic fluid at a given
weesX gestation determines whether fetal transfusion or delivery is advisable.

'igure $D*/ -ueenan curve for j9, %I@ values for the management of the patient
with isoimmuniCation. 9,: optical densityE Rh: rhesus. Adapted from -ueenan "T:
Tomai TB: ;ral JH: et al. ,eviations in amniotic Quid optical density at a wavelength of
%I@ nm in Rh*immuniCed pregnancies from $% to %@ weesX gestation. A proposal for
clinical management. Am " 9bstet Kynecol $D>.$&0@*$&0D: $??&.

'igure $D*& Liddle cerebral artery (L+A) ,oppler pea velocities based on gestational
age. LoL: multiples of the median. ,ata from Loise Y": "r. Lanagement of Rhesus
alloisoimmuniCation. 9bstet Kynecol $@@(&).D@@*D$$: /@@/.
Table $D*$. Hematologic values for normal fetusesR
KEJTAT)9PAZ AKE (WY)
Hematologic Oalue $I $D*$0 $>*/@ /$*// /&*/I /D*&@
Hgb: gAdZ $@.? k @.0 $/.I k @.> $$.%> k @.0> $/./? k @.>?
$/.% k @.00 $&.&D k $.$>
R(+s: h $@?AZ /.%& k @./D /.D> k @./$ /.DD k @./? /.?0
k @./0 &.@D k @./0 &.I/ k @.&/
L+O: fZ (k$) $%& k > $%& k $/ $&&.? k >.>& $.$&@ k D.$0
$/D./ k D./& $$>./ k I.0
ROalues are for normal fetuses from $I to &@ weesX estimated gestational age.
,ata from American +ollege of 9bstetricians and Kynecologists. Lanagement of
isoimmuniCation in pregnancy. Technical (ulletin Po. $%>. Washington: ,+: A+9K:
$??@.
Hgb: hemoglobinE R(+s: red blood cellsE L+O: mean corpuscular volume.
Advances in fetal interventional techniFues and high*resolution ultrasonography have
made direct fetal blood sampling the most accurate method for the diagnosis of fetal
hemolytic disease. Bercutaneous umbilical blood sampling (B;(J) can allow
measurement of fetal hemoglobin: hematocrit: blood gases: pH: and bilirubin levels.
The hematologic values for normal fetuses from $I to &@ weesX gestation are listed in
Table $D*$. The techniFue for fetal blood sampling is similar to that described for fetal
intravenous transfusion discussed later in this chapter. 9ne drawbac to this
diagnostic procedure is that it reFuires e#pertise above and beyond that reFuired for
amniocentesis. The ma<or ris is fetal e#sanguination from tears in placental vessels:
but when performed by an e#perienced practitioner: the ris of this complication is
only /= or less. However: there is a greater ris of fetomaternal hemorrhage: reported
to be as high as %@=. Bercutaneous umbilical blood sampling should not be a frst*line
method of assessing fetal status unless clearly indicated.
A /0*year*old woman develops the pictured lesion / days after wearing a new pair of
earrings. What is the most liely diagnosis!
J#t@ID&f$
A. Allergic contact dermatitis
(. Atopic dermatitis
+. )rritant contact dermatitis
,. Pummular dermatitis
E. Jeborrheic dermatitis
-),. &&D$@
123456728
9ption A (Allergic contact dermatitis) is correct. This patient has allergic contact
dermatitis: most liely the result of nicel in her new earrings. Allergic contact
dermatitis should be suspected when there is e#posure to an allergen and a reaction
develops at least %> hours later. As pictured: there is an erythematous base and a
slightly white scale with a defned border.
9ption ( (Atopic dermatitis) is incorrect. Atopic dermatitis is a subacute and chronic
dermatitis that is often called an itch that rashes. )t has dry: scaly: pruritic patches and
plaFues with e#coriations located in the Qe#ural regions.
9ption + ()rritant contact dermatitis) is incorrect. )rritant contact dermatitis is the
result of direct to#ic in<ury to the sin and will occur in any individual given suGcient
e#posure. This is in contrast to allergic contact dermatitis: where individuals with
atopy are more liely to develop it. )rritant contact dermatitis is diMerentiated from
allergic contact dermatitis by the acute speed of the reaction (less than $/ hours
usually): a very sharp border without spread and an absence of papules in the acute
phase.
9ption , (Pummular dermatitis) is incorrect. Pummular dermatitis presents as pruritic:
coin*shaped erythematous plaFues that are dry and scaly.
9ption E (Jeborrheic dermatitis) is incorrect. Jeborrheic dermatitis presents with a
greasy: yellow: erythematous: scaly plaFue primarily in the perioral area or other
areas rich in sebaceous glands: such as the scalp margin and sternum.
123456728
,ermatitis: +ontact (BTK)
(AJ)+ )P'9RLAT)9P
,E')P)T)9P
+ontact dermatitis is an acute or chronic sin inQammation: usually ecCematous
dermatitis resulting from e#posure to substances in the environment. )t can be
subdivided into ^irritant^ contact dermatitis (nonimmunologic physical and chemical
alteration of the epidermis) and ^allergic^ contact dermatitis (delayed hypersensitivity
reaction).
'rom 'erriXs +linical Advisor /@@D by 'erri
BHNJ)+AZ ')P,)PKJ l +Z)P)+AZ BREJEPTAT)9P
)RR)TAPT +9PTA+T ,ERLAT)T)J.
Lild e#posure may result in dryness: erythema: and fssuring of the aMected area (e.g.:
hand involvement in irritant dermatitis caused by e#posure to soap: genital area
involvement in irritant dermatitis caused by prolonged e#posure to wet diapers).
EcCematous inQammation may result from chronic e#posure.
AZZERK)+ +9PTA+T ,ERLAT)T)J.
Boison ivy dermatitis can present with vesicles and blistersE linear lesions (as a result
of dragging of the resins over the surface of the sin by scratching) are a classic
presentation.
The pattern of lesions is asymmetricE itching: burning: and stinging may be present.
The involved areas are erythematous: warm to touch: swollen: and may be confused
with cellulitis.
ET)9Z9KN
)rritant contact dermatitis. cement (construction worers): rubber: ragweed: malathion
(farmers): orange and lemon peels (chefs: bartenders): hair tints: shampoos
(beauticians): rubber gloves (medical: surgical personnel)
Allergic contact dermatitis. poison ivy: poison oa: poison sumac: rubber (shoe
dermatitis): nicel (<ewelry): balsam of Beru (hand and face dermatitis): neomycin:
formaldehyde (cosmetics)
'rom 'erriXs +linical Advisor /@@D by 'erri
,)AKP9J)J
,)''EREPT)AZ ,)AKP9J)J
)mpetigo
Zichen simple# chronicus
Atopic dermatitis
Pummular ecCema
Jeborrheic dermatitis
Bsoriasis
Jcabies
W9RY;B
Ledical history. gradual onset vs. rapid onset: number of e#posures: clinical
presentation: occupational history
Bhysical e#amination. contact dermatitis in the nec may be caused by neclaces:
perfumes: after*shave lotionE involvement of the a#illae is often secondary to
deodorants: clothingE face involvement can occur with cosmetics: airborne allergens:
aftershave lotion
ZA(9RAT9RN TEJTJ
Batch testing is useful to confrm the diagnosis of contact dermatitisE it is indicated
particularly when inQammation persists despite appropriate topical therapy and
avoidance of suspected causative agentE patch testing should not be used for irritant
contact dermatitis because this is a nonimmunologic*mediated inQammatory reaction.
Kram stain and cultures are indicated only in cases of suspected secondary infection
or impetigo.
'rom 'erriXs +linical Advisor /@@D by 'erri
A &I*year*old woman: gravida &: para &: comes to the oGce for a routine annual
gynecologic e#amination. Jhe has no complaints. 9n physical e#amination: multiple
bruises on her left arm are noted. There is no limited range of motion. Jhe does not
have any recent trauma and reports she was unaware of the bruises. Which of the
following is the most appropriate ne#t step in the management of the patient!
A. As about domestic violence
(. 9rder a bleeding time
+. 9rder a coagulation profle
,. 9rder a psychiatric consultation
E. 9rder a radiograph of her arm
-),. /D0%0
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9ption A (As about domestic violence) is correct. Recognition of domestic violence is
the frst and often missed step. )n any case where domestic violence is suspected: it is
critical to as the patient about this issue.
9ption ( (9rder a bleeding time) is incorrect. This would not be the ne#t step in her
managementE but it could be considered if the patient denied domestic violence.
9ption + (9rder a coagulation profle) is incorrect. This would not be the ne#t step in
her managementE but it could be considered if the patient denied domestic violence.
9ption , (9rder a psychiatric consultation) is incorrect. There is no indication for
psychiatric consultation based on the provided information.
9ption E (9rder a radiograph of her arm) is incorrect. This would not be indicated
unless the physical e#amination demonstrated additional fndings: such as limited
range of motion.
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/. What are the characteristics of domestic violence!
Whether the violence is psychological: physical: or se#ual: all violent relationships are
characteriCed by the e#ertion of power and control by the perpetrator against the
victim. 9f particular importance for obstetricianAgynecologists to bear in mind are
tactics such as refusing to permit negotiation of safer se# and contraceptive practices.
Taen from 9bAKyn Jecrets &E by (ader
%. Who needs to be screened!
Jince domestic violence crosses racial: socioeconomic: and cultural lines: and since it
is so common: all women should be screened periodically for violence. While women
do not generally spontaneously disclose abuse: there is ample evidence that they will
respond when ased and that they are grateful for the opportunity.
Lany studies have demonstrated that the incidence of domestic violence increases
during pregnancy and the postpartum period. This fact: along with freFuent doctor
visits during pregnancy and a womanXs concern for the safety and well*being of her
child: mae pregnancy a particularly important time for domestic violence assessment.
A &?*year*old man is seen by the physician: because he is becoming increasingly short
of breath during mild e#ercise. The shortness of breath typically comes on after
waling two to three level city blocs and is associated with moderate diaphoresis. )n
the last month: he has also noticed mild orthopnea. He denies chest pain: chest
tightness: hemoptysis: or changes in weight. His previous medical history is notable
for rheumatic fever in childhood. +urrently: he is not on any medications. Auscultation
of the heart reveals an increased frst heart sound and opening snap following the
second heart sound. Additionally: there is a low*pitched: grade )))AO) middiastolic
murmur that is best heard over the ape# of the heart in the left lateral decubitus
position. What fnding would most liely be detected on investigation of this patient!
A. Elevated left atrioventricular pressure gradient
(. Elevated left ventricular diastolic pressure
+. Zeft ventricle muscle dysfunction
,. Ly#omatous degeneration of mitral valve
E. Right atrial hypertrophy
-),. &&$>/
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9ption A (Elevated left atrioventricular pressure gradient) is correct. This patient has
signs and symptoms consistent with mitral stenosis. The most common cause is
rheumatic fever and presentation is often between the third and ffth decade of life. A
middiastolic rumbling murmur with an opening snap is characteristic of mitral stenosis.
As a result of the stenosis: there is increased pressure in the left atrium: leading to an
increase in the atrioventricular pressure gradient.
9ption ( (Elevated left ventricular diastolic pressure) is incorrect. Zeft ventricular
diastolic pressure is typically normal in patients with mitral stenosis.
9ption + (Zeft ventricle muscle dysfunction) is incorrect. 9ccasionally: there can be
myocardial involvement following rheumatic fever. However: this is much less common
than an elevated left atrial pressure.
9ption , (Ly#omatous degeneration of mitral valve) is incorrect. Ly#omatous
degermation of the mitral valve is the underlying cause of mitral valve prolapse. Litral
valve prolapse often presents with midsystolic clic followed by a murmur.
9ption E (Right atrial hypertrophy) is incorrect. The right atrium is not usually aMected
until very late in the disease. However: right ventricular hypertrophy is a common
conseFuence of mitral stenosis.
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Bathophysiology
The cross section of a normal orifce measures % to D cm/. Parrowing of the valve
orifce causes a pressure gradient across the valve. The obstruction to Qow reduces
flling of the left ventricle: raises left atrial pressure: and causes pulmonary congestion
and reduced cardiac output. A murmur becomes audible when the valve orifce
becomes smaller than / cm/. When the orifce approaches $ cm/: the condition
becomes critical and symptoms become more evident.
'rom Bractical Kuide to the +are of the Ledical Batient DE by 'erri
Bhysical 'indings
Brominent <ugular A waves (in patients with normal sinus rhythm) are present.
9pening snap occurring in early diastoleE a short (`@.@0 second) A/ to opening snap
interval indicates severe mitral stenosis.
The typical murmur of mitral stenosis is a soft: low*pitched: diastolic rumble with
presystolic accentuation best heard at the ape# with the patient in the left lateral
decubitus position.
Accentuated J$ (because of delayed and forceful closure of the valve).
)f pulmonary hypertension is present: there may be an accentuated B/ or a soft: early
diastolic: decrescendo murmur (Kraham JteellXs murmur) caused by pulmonic
regurgitation (it is best heard along the left sternal border and may be confused with
aortic regurgitation).
A palpable right ventricular heave may be present at the left sternal border.
Right ventricular dysfunction in late stages may be manifested by peripheral edema:
enlarged and pulsatile liver: and ascites.
'rom Bractical Kuide to the +are of the Ledical Batient DE by 'erri
,iagnostic Jtudies
Echocardiography. the characteristic fnding on an echocardiogram is a maredly
diminished E to ' slope of the anterior mitral valve leaQet during diastoleE there is also
fusion of the commissures: resulting in anterior movement of the posterior mitral valve
leaQet during diastole (calcifcation in the valve may also be noted). Two*dimensional
echocardiography can accurately establish the valve area.
+hest #*ray.
Jtraightening of the left cardiac border caused by a dilated left atrial appendage.
Zeft atrial enlargement on lateral chest #*ray (appearing as double density on a
posteroanterior chest #*ray).
Brominence of pulmonary arteries.
Bossible pulmonary congestion and edema (Yerley ( lines).
Bossible elevation of left main bronchus as a result of left atrial enlargement.
E+K.
Right ventricular hypertrophy (large R wave in lead O$: and large J wave in OD)E right
a#is deviation caused by pulmonary hypertension.
Zeft atrial enlargement (broad: notched B waves in lead )) and in O$ TB mitraleU).
Atrial fbrillation.
+ardiac catheteriCation helps to establish the severity of mitral stenosis and to
diagnose associated valvular and coronary lesions. )t is also used as a precursor to
balloon valvotomy. 'indings on catheteriCation include normal left ventricular function
and elevated left atrial and pulmonary pressures. Right ventricular and right atrial
pressures are also freFuently elevated.
A $0*year*old female presents to the university health clinic stating she has yet to
e#perience menses despite developing breasts & years ago. Her previous medical
history is unremarable: and she has never been se#ually active. 9n e#amination: her
height is at the DIth percentile: weight is at the I@th percentile: and blood pressure is
$$@A0@ mm Hg. (reasts e#hibit Tanner stage )O development. Oaginal e#amination
demonstrates a short: blind vaginal pouch and pelvic ultrasound fails to locate a
uterus. What is the ne#t best step in the diagnosis of this patient!
A. (rain magnetic resonance imaging (LR))
(. Jerum beta human chorionic gonadotropin (m*H+K)
+. Jerum follicle*stimulating hormone ('JH) and aryotype
,. Jerum progesterone
E. Jerum testosterone and aryotype
-),. &&@?@
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9ption E (Jerum testosterone and aryotype) is correct. )n a patient presenting with
primary amenorrhea (no menses by age $D with some secondary se#ual
characteristics present) and an absent uterus on ultrasound: the most appropriate frst
tests are serum testosterone and aryotype analysis. The diMerential diagnosis in
breast present: uterus absent primary amenorrhea is Lnllerian agenesis and androgen
insensitivity. This patient is e#hibiting characteristics consistent with both. 'emale*
appropriate testosterone levels will suggest a diagnosis of Lnllerian agenesis and a
aryotype of %D SS will confrm the diagnosis. )f this patient had male*appropriate
testosterone: we would consider a diagnosis of androgen insensitivity and a aryotype
of %D SN would confrm the diagnosis.
9ption A ((rain magnetic resonance imaging TLR)U) is incorrect. (rain magnetic
resonance imaging (LR)) would be appropriate in a patient in whom we suspected
Yallmann syndrome or a tumor. )n this patient without a uterus: endocrinologic
evaluation should be performed prior to an LR).
9ption ( (Jerum beta human chorionic gonadotropin Tm*H+KU) is incorrect. )n a patient
who has never been se#ually active: has a blind vagina on e#amination: and does not
have a uterus as demonstrated by ultrasound: a pregnancy test would certainly be
negative.
9ption + (Jerum follicle*stimulating hormone T'JHU and aryotype) is incorrect. Jerum
follicle*stimulating hormone ('JH) and aryotype are the most appropriate ne#t
investigations in a patient with primary amenorrhea when a uterus is present and
pregnancy via beta human chorionic gonadotropin (m*h+K) measurement has been
ruled out. Elevated 'JH suggests primary ovarian failure and maes our diMerential
diagnosis between Turner syndrome: vanishing testes syndrome: or absence of testes
determining factor. Turner syndrome is much more common than the other two and
can be distinguished via aryotyping. Zow 'JH suggests a hypothalamic*pituitary
problem: such as Yallmann syndrome (low gonadotropin*releasing hormone TKnRHU
and anosmia).
9ption , (Jerum progesterone) is incorrect. The rare $0*alpha hydro#ylase defciency
form of congenital adrenal hyperplasia results in androgen and estrogen defciency
with an increase in serum progesterone and blood pressure. This patient has normal
blood pressure.
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BR)LARN ALEP9RRHEA W)TH (REAJT ,EOEZ9BLEPT AP, LoZZER)AP AP9LAZ)EJ
Batients with primary amenorrhea: breast development: and Lnllerian anomalies all
fail to demonstrate a visible or palpable uterine cervi# on physical e#amination. They
fall into two categories. those with complete androgen insensitivity syndrome (%D SN)
and those with a aryotype of %D SS. The distinction can be made by the serum
testosterone level. Batients with complete androgen insensitivity syndrome have male
levels of testosterone.
The aryotype in patients with androgen insensitivity syndrome is %D SN: and they
have testes that are often intraabdominal. (reast development (with smaller nipples
and areolae than normal) is caused by an enCymatic conversion of male levels of
androgen to estrogen. The testes in these patients secrete normal male amounts of
Lnllerian*inhibiting substanceE hence: patients have only a vaginal dimple and no
uterus or tubes. Treatment should consist of gonadal resection to avoid malignant
neoplasia once puberty is complete and the creation of a neovagina when the patient
is prepared to be se#ually active. Bsychological counseling is also an important
component in the care of these patients.
'rom Essentials of 9bstetrics l Kynecology %E by Hacer et al
Batients with primary amenorrhea: breast development: and a aryotype of %D SS with
anatomical anomalies have levels of testosterone appropriate for females. 9ne should
suspect an imperforate hymen in adolescents who report monthly dysmenorrhea in
the absence of menstrual Qow. 9n e#amination: these patients often present with a
vaginal bulge and a midline cystic mass on rectal e#amination. ;ltrasonography
confrms the presence of a normal uterus and ovaries with hematocolpos. These
patients can be successfully treated by hymenectomy.
Alternatively: women may present with similar symptoms but no lower vaginal bulge.
When ultrasonography confrms a normal uterus and ovaries: one should suspect the
possibility of a transverse: obstructing vaginal septum or cervical agenesis. LR) is the
diagnostic method of choice in these patients. )f the LR) scan confrms a transverse
septum: surgical correction is indicated. These procedures can be e#tremely diGcult:
and the surgeon must be prepared to use tissue e#panders: split*thicness sin grafts:
or other techniFues to eMect a functional vagina. Jurgical construction of a functional
cervi# is e#tremely unliely. )n general: it is recommended that these women undergo
hysterectomy.
'rom Essentials of 9bstetrics l Kynecology %E by Hacer et al
'inally: rectal e#amination and ultrasonography may show the absence of a uterus
indicating Leyer*Roitansy*Ynster*Hauser syndrome. This syndrome is characteriCed
by a failure of the Lnllerian ducts to fuse distally and to form the upper genital tract.
These patients usually have bilateral rudimentary uterine tissues (anlagen): fallopian
tubes: and ovaries. )t is uncommon to have functional endometrial tissue within the
anlagen. 9n occasion: the ovaries are not visible on ultrasonography because they
have not descended into the pelvis. )n these cases: computed tomography (+T) or LR)
may identify them well above the pelvic brim.
+reation of a neovagina can be accomplished by using one of two general approaches.
The 'ran method of vaginal dilatation uses dilatation of the vaginal pouch with
vaginal forms (usually thermoplastic acrylic resin TZuciteU dilators) over the course of
wees to months. Alternatively: a Lc)ndoe vaginoplasty: which involves the surgical
creation of a neovaginal space using a split*thicness sin graft: may be performed.
(oth of these methods should be initiated in pro#imity to the time when the patient
anticipates having vaginal intercourse.
A //*year*old K$B@ at &% wees] gestation is involved in a motor vehicle accident. Jhe
was not wearing her seat belt and as she <olted forward: her abdomen hit the steering
wheel. Jhe is brought to labor and delivery for assessment. Jhe is observed for /
hours. The maternal status is stable. 'etal heart trace is reassuring. Po uterine
contractions are noted on e#ternal uterine monitoring. There is no evidence of vaginal
bleeding. The ultrasound e#amination does not detect a placental abruption. Which of
the following is the most appropriate ne#t step in patient care!
A. Administer betamethasone
(. ,eliver by cesarean section
+. ,ischarge home on bed rest
,. )nduce labor
E. 9btain a blood type and Rh status
-),. /D0/$
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9ption E (9btain a blood type and rhesus TRhU status) is correct. A pregnant woman
involved in a motor vehicle accident in which abdominal trauma has occurred should
have blood type and Rh status checed. Those women who are Rh*negative should be
given RhoKAL.
9ption A (Administer betamethasone) is incorrect. (etamethasone is not indicated at
this point because there is no indication of preterm delivery.
9ption ( (,eliver by cesarean section) is incorrect. There is no indication to deliver this
patient in that both she and the fetus are stable.
9ption + (,ischarge home on bed rest) is incorrect. (efore being discharged home: the
patient should have her blood type and Rh status checed because those women who
are Rh*negative should receive RhoKAL.
9ption , ()nduce labor) is incorrect. There is no indication to deliver this patient in that
both she and the fetus are stable.
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BREOEPT)9P 9' RHEJ;J )J9)LL;P)iAT)9P
(ecause Rh isoimmuniCation occurs in response to e#posure of an Rh*negative mother
to the Rh antigen: the mainstay for prevention is the avoidance of maternal e#posure
to the antigen. Rh9*KAL diminishes the availability of the Rh antigen to the maternal
immune system: although the e#act mechanism by which it prevents Rh
isoimmuniCation is not well understood.
Rh9*KAL is prepared from fractionated human plasma obtained from hyperreactive
sensitiCed donors. The plasma is screened for hepatitis ( surface antigen and anti*H)O*
$: the antibody to the acFuired immunodefciency syndrome (A),J) virus. The globulin
is available in several dosages for intramuscular in<ection. Jince the advent of its use
in $?D0: Rh immune globulin has dramatically reduced the incidence of Rh
isoimmuniCation.
(ecause the greatest ris for fetal*to*maternal hemorrhage occurs during labor and
delivery: Rh immune globulin was initially administered only during the immediate
postpartum period. This resulted in a $= to /= failure rate: thought to be due to
e#posure of the mother to fetal red blood cells during the antepartum period. The
indications for the use of Rh immune globulin have therefore been broadened to
include any antepartum event (such as amniocentesis) that may increase the ris of
transplacental hemorrhage. The routine prophylactic administration of Rh immune
globulin at /> weesX gestation is now the standard of care. ,espite adherence to this
suggested Rh immune globulin protocol: @./0= of primiparous Rh*negative patients
still become sensitiCed.
Taen from Essentials of 9bstetrics l Kynecology %E by Hacer et al
)P,)+AT)9PJ '9R A,L)P)JTRAT)9P 9' RH9*KAL
The following provides a practical approach to the administration of Rh immune
globulin to an Rh*negative patient with no Rh antibodies.
,uring a normal pregnancy: &@@ pg of Rh immune globulin is administered at />
weesX gestation: following testing for sensitiCation with an indirect +oombsX test. A
&@@*pg dose is administered following amniocentesis at any gestational age. )f a
fetomaternal hemorrhage is suspected at any time during the pregnancy: a Yleihauer*
(ete test should be performed. )f positive: Rh immune globulin is administered in a
dose of $@ pgAmZ of fetal blood that entered the maternal circulation. 'ollowing an
uncomplicated delivery: &@@ pg of Rh immune globulin is given within 0/ hours. )f a
larger than normal fetal*to*maternal hemorrhage is suspected: such as may occur in
patients with abruptio placentae or those reFuiring cesarean section or manual
removal of the placenta: a Yleihauer*(ete determination should be performed after
delivery and the appropriate dose of the Rh immune globulin determined.
Establishment of fetal circulation occurs at appro#imately % weesX gestation: and the
presence of the Rh9 , antigen has been demonstrated as early as &> days following
conception. +onseFuently: Rh isoimmuniCation can occur at any time during
pregnancy: from the early frst trimester on. (ecause fetal erythrocytes can be readily
detected in the maternal blood following induced or spontaneous abortion: I@ pg of Rh
immune globulin should be given to all Rh*negative women following any type of
abortion.
'etal erythrocytes have been demonstrated in the maternal circulation following
rupture of a tubal pregnancy. +onseFuently: Rh immune globulin should be given to an
Rh*negative woman with an ectopic pregnancy. (ecause chorionic villi in gestational
trophoblastic disease are avascular and are devoid of fetal erythrocytes: Rh immune
globulin is probably not necessary following molar pregnancy. At least one case of
sensitiCation following a molar pregnancy: however: has been reported.
The medical resident on call is reFuested to evaluate a patient for shortness of breath.
9n arrival at the bedside: the resident observes a &?*year*old man sitting up in bed
and leaning forward and supporting himself with his arms. The patient complains of
severe shortness of breath. He is in his frst hospital day for acute pancreatitis. The
resident starts the patient on $@@= o#ygen by facemas: and orders a stat upright
portable chest radiograph (see fgure). An arterial blood gas is obtained I minutes
later and shows a Ba9/ of /@@ mm Hg. Which of the following is the most liely cause
of the patient]s current condition!
"#f@/>f$
A. Acute pulmonary embolism
(. +ongestive heart failure
+. ,iMuse alveolar in<ury
,. ,isseminated intravascular coagulation (,)+)
E. Zegionella pneumonia
-),. /0//?
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9ption + (,iMuse alveolar in<ury) is correct. The patient]s chest radiograph shows
bilateral diMuse alveolar shadowing with air bronchograms and no cardiac
enlargement. This is the appearance of AR,J: which is defned by the acute onset of
bilateral pulmonary infltrates and severe hypo#emia in the absence of evidence of
cardiogenic pulmonary edema. The patient]s Ba9/A')9/ is /@@: which along with the
appearance of his chest radiograph: maes the diagnosis of AR,J a virtual certainty.
AR,J is the result of diMuse alveolar in<ury.
9ption A (Acute pulmonary embolism) is incorrect. AR,J is defned by the acute onset
of bilateral pulmonary infltrates and severe hypo#emia in the absence of evidence of
cardiogenic pulmonary edema. A pulmonary embolism can result in AR,J. This may in
fact have been the precipitating event for this patient. Lany other events could have
triggered the actual cause of the condition: which is diMuse alveolar in<ury.
9ption ( (+ongestive heart failure) is incorrect. There is no cardiac enlargement seen
in the patient]s chest radiograph. AR,J is defned by the acute onset of bilateral
pulmonary infltrates and severe hypo#emia in the absence of evidence of cardiogenic
pulmonary edema.
9ption , (,isseminated intravascular coagulation (,)+)) is incorrect. AR,J occurring in
a patient with sepsis or ,)+ would not be surprising. The common pathway for the
development of the disorder is diMuse alveolar in<ury.
9ption E (Zegionella pneumonia) is incorrect. (ilateral diMuse alveolar shadowing with
air bronchograms is seen in the patient]s chest radiograph. Zegionella pneumonia may
have a similar radiographic appearance and hypo#emia: but considering the patient]s
entire clinical picture of the acute onset of bilateral pulmonary infltrates and severe
hypo#emia and concurrent acute pancreatitis: the patient almost certainly has AR,J.
The cause of AR,J is diMuse alveolar in<ury.
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Jystemic )nQammatory Response Jyndrome: Jepsis: Lultiple 9rgan ,ysfunction
Jyndrome: and Adult Respiratory ,istress Jyndrome
The systemic inQammatory response syndrome (J)RJ) is a constellation of clinical
signs and symptoms resulting from the host response to various insults. When caused
by infection: J)RJ is called sepsis. The diagnosis of J)RJ reFuires at least two of the
following. temperature greater than &>[+ or less than &D[+: tachycardia greater than
?@ beatsAmin: tachypnea greater than /@ breathsAmin or Ba+9/ less than &/ mm Hg:
and white blood cell count greater than $/:@@@ApZ or less than %@@@ApZ. This systemic
response to inQammation may result in dysfunction of multiple organs (usually lung:
liver: idneys: cardiovascular system: or central nervous system): and this clinical
situation is called multiple organ dysfunction syndrome or multiple organ system
failure. Lortality of patients with J)RJ increases with the number of organs failing:
from a low of &@= to %@= for two failing organs to greater than ?@= with fve or more
failing organs.
Zung dysfunction occurs often and early in J)RJ and is termed the adult respiratory
distress syndrome. The usual criteria defning this syndrome are Ba9/ to ')9/
(commonly called the BA' ratio) of /@@ or less and bilateral pulmonary infltrates
evident on the chest radiograph in the absence of volume overload. )f a pulmonary
artery catheter is in place: the pulmonary artery wedge pressure must be less than or
eFual to $> mm Hg. There is no specifc therapy for the adult respiratory distress
syndrome that has been shown to be eGcaciousE thus: treatment is supportive.
Lechanical ventilation using low tidal volumes of D mZAg ideal body weight is the
principal form of supportive therapy in these patients. )t is possible to ventilate the
lungs with liFuid perQuorocarbons: which have a very high capacity for dissolving and
distribute o#ygen evenly in in<ured lungs. Bartial liFuid ventilation with these chemicals
is being evaluated as a method of treating patients who cannot be adeFuately
o#ygenated despite use of the optimal available ventilatory strategies. E#tracorporeal
membrane o#ygenation and <et ventilation have been successfully used in infants but
have not proved benefcial in adults.
A %0*year*old man presents to the emergency room &@ minutes after the sudden onset
of chest pain is located more prominently over the left hemithora# and does not
radiate elsewhere. )t is sharp in Fuality: notably more severe on inspiration: and does
not change with position. He has been previously well and is not on any current
medications. His blood pressure is $&@A>I mm HgE pulse: $@0 beatsAminuteE
temperature: &>.D[+ ($@$.%[')E and respirations: /% breathsAminute. Auscultation
reveals a fourth heart sound and rales over the left posterior hemithora#.
Electrocardiography (E+K) demonstrates a right bundle branch bloc that was not
present on his previous electrocardiogram performed $ month ago. What is the most
appropriate ne#t step in the management of this patient!
A. Echocardiography
(. Zeg ultrasonography
+. PebuliCed salbutamol
,. Bulmonary arteriography
E. Oentilation*perfusion (OA-) scan
-),. &&$>I
123456728
9ption E (Oentilation*perfusion TOA-U scan) is correct. This patient has a liely
pulmonary embolism (BE). The diagnosis is suspected because of the fnding of
pleuritic chest pain (pain that changes with respiration): dyspnea: tachypnea:
tachycardia: and new onset right bundle branch bloc. Batients can also be febrile with
a BE. At present: ventilation*perfusion scan (OA- scan) or spiral computed tomography
(+T) scan are considered the frst diagnostic steps in patients with an intermediate to
high probability of having a pulmonary embolism. )f the options had included
anticoagulant therapy: that would have been the frst step in the management of this
patient: because of the reasonably high probability of this patient having a BE.
9ption A (Echocardiography) is incorrect. Echocardiography is a rapid method of
evaluating for the possibility of pulmonary embolism (BE) via right ventricular siCe or
function. However: these fndings are nonspecifc and cannot be used to diagnose a
BE. )ts role in the management of patients with BE is largely confned after diagnosis to
determine which patients can beneft from thrombolytic therapy.
9ption ( (Zeg ultrasonography) is incorrect. ,uple# ultrasonography of the lower
e#tremities is useful if the ventilationAperfusion (OA-) scan or spiral computed
tomography (+T) scan fndings are nondiagnostic for pulmonary embolism (BE).
9ption + (PebuliCed salbutamol) is incorrect. PebuliCed salbutamol could possibly
alleviate some of this patientXs shortness of breath: but the issue causing the
shortness of breath is delivery of blood to the lung: not o#ygen into the alveoli. This
would not be the frst step in the management of this patient. The most appropriate
frst pharmacotherapy would be anticoagulation.
9ption , (Bulmonary arteriography) is incorrect. Bulmonary arteriography is the gold
standard for the diagnosis of pulmonary embolism (BE). However: there is a %= ris of
having a ma<or complication during the procedure: including death: cardiac
arrhythmias: bleeding: and cardiac perforation. As such: this is not the frst diagnostic
step.
123456728
+linical features
,yspnea is the most freFuent symptom: and tachypnea is the most freFuent sign in
pulmonary embolism (BE). ,yspnea: syncope: hypotension: or cyanosis indicates a
massive BE: while pleuritic pain: cough: or hemoptysis often suggests a small
embolism located near the pleura. 9n e#amination: young or previously healthy
individuals may simply appear an#ious but otherwise seem well: even with a large BE.
Lany drugs interact with warfarin to enhance or diminish its eMect. As the patient to
report any changes in treatment.
)nvestigations
)nvestigations supporting the diagnosis of BE include the following.
Electrocardiogram. tachycardia or the ^typical^ J$ -& T& pattern.
,*dimer: EJR: Z,H: AJT.
A(Ks. hypo#emia.
+SR. usually normal but may show atelectasis or a small wedge shadow.
OA- scan. unmatched OA- defects.
BE protocol +T scan.
)f these investigations are negative but the clinical suspicion remains high: a search
for corroborative evidence of thromboembolism is instigated by measuring ,*dimer
and looing for the presence of deep vein thrombosis with ultrasound or venography.
Batients who have a negative ,*dimer and low probability of having BE are eMectively
ruled out with this test.
'rom +rash +ourse. )nternal Ledicine by (aliga
A &/D@*g (0 lb / oC) male infant is born at &> wees] gestation to a healthy: /D*year*
old woman. The only abnormality noted during the course of the pregnancy was that
the woman]s fundal height measured consistently Vlarge for dateW of gestation. The
infant is delivered via spontaneous: vaginal delivery and has Apgar scores of ? and $@
at one and fve minutes: respectively. 9n the frst day postpartum: the mother calls for
help as she is feeding the infantE the infant e<ects formula from the nose and mouth
and then begins to cough: choe: and turn blue as soon as the mother begins to feed
him. Which of the following is the most liely reason for the mother]s abnormal uterine
fundal height during the pregnancy!
A. Abnormal esophageal development: inhibiting the fetus from
swallowing amniotic Quid
(. Abnormal renal development: causing oligohydramnios
+. Abnormal renal development: causing polyhydramnios
,. 'etal macrosomia: which accounted for large uterine fundal siCe
E. Hyperglycemia: causing the fetus to produce more urine than
normal
-),. /0I?0
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9ption A (Abnormal esophageal development: inhibiting the fetus from swallowing
amniotic Quid) is correct. The history of large fundal height and choing on frst
feeding is consistent with tracheoesophageal fstula. )nability of the fetus to swallow
amniotic Quid results in polyhydramnios and large fundal height: and the opening
between the esophagus and trachea results in choing and aspiration on feeding.
9ption ( (Abnormal renal development: causing oligohydramnios) is incorrect.
9ligohydramnios would cause a smaller than e#pected fundal height.
9ption + (Abnormal renal development: causing polyhydramnios) is incorrect.
Pormally: maldevelopment of the idneys causes oligohydramnios and results in a
smaller uterine fundal height. Also: a renal problem alone would not e#plain the
choing while feeding.
9ption , ('etal macrosomia: which accounted for large uterine fundal siCe) is
incorrect. At &/D@ g (0 lb / oC): this infant is not considered macrosomic and would not
have been so as a fetus.
9ption E (Hyperglycemia: causing the fetus to produce more urine than normal) is
incorrect. Laternal hyperglycemia does cause polyuria in the fetus: much as it does in
diabetic individuals. However: the Fuestion stem states that the mother is healthy.
Also: a fetus continually e#posed to high blood glucose levels is liely to develop either
macrosomia or intrauterine growth restriction.
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E#amination of the pregnant uterus is vital. The fundal height is measured in
centimeters from the symphysis pubis to the top of the uterus. Jerial measurements
over the course of pregnancy provide an e#cellent assessment of fetal growth with a
rough appro#imation between centimeters and wees: gestation from $>*&% wees in
a patient with a normal body habitus. 'etal heart tones should be auscultated: and
fetal position and estimated weight determined during the last trimester. Zastly:
uterine contractions can be easily palpated during a routine e#am and: if freFuent and
many wees before term: may point to the possibility of preterm labor.
A /*wee*old male infant presents to the emergency room (ER) because of crying
episodes. He had an uneventful hospital stay and has received all his immuniCations.
He appears well with stable vital signs. He is crying non*stop and diGcult to console.
Oitals are stable and he is afebrile. His e#am is nonfocal. The pediatrician cannot see
any hair tourniFuets and both testicles are in the scrotum.The pediatrician also
reaches for the Qorescence strip to rule out which abnormality!
A. +orneal abrasion
(. Hemoccult*positive stool
+. Binworm infection
,. Broteinuria
E. ;rinary tract infection (;T))
-),. &/>>I
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9ption A (+orneal abrasion) is correct. A Qorescence strip can be wet with sterile saline
and a drop of the Quid placed in the eye. A WoodXs lamp or other Vblac lightWcan be
used to illuminate the eye. )f an abrasion is seen: it will glow green in the blac light.
Treatment is with topical antibiotics.
9ption ( (Hemoccult*positive stool) is incorrect. A stool guaiac may be helpful if there
is worry about intussusception. The crying spells in this abnormality are more cyclic
and rarely are seen with Vcurrent <elly stoolsW.
9ption + (Binworm infection) is incorrect. Bin worm infection is diagnosed with the
Vscotch tape testWand classically presents with anal itching that is worse at night.
9ption , (Broteinuria) is incorrect. Broteinuria is seen with glomerulonephritis and
other idney abnormalities: but this diagnosis usually does not cause crying spells.
9ption E (;rinary tract infection (;T))) is incorrect. A ;T) could cause crying spells
fever: nausea: and vomiting. A urinalysis (;AA) can be ordered to rule out this
infection.
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E-;)BLEPT
+entimeter ruler (Qe#ible: clear)
WoodXs lamp (to view Quorescing lesions)
'lashlight with transilluminator
Handheld magnifying lens (optional)
A 0&*year*old woman is brought to the emergency room because this morning she was
found by her daughter to be acutely confused. Jhe has otherwise been in e#cellent
health and does not tae any regular medication. The daughter reports that her
motherXs mental status was normal yesterday. 9n arrival in the emergency room: she
is disorientated to person: place: and time. Jhe is diaphoretic and tremulous. Her
blood pressure is $/IA>I mm HgE pulse: >> beatsAminuteE temperature: &0.%[+
(??.&[')E and respirations: $% breathsAminute. 9ccasional ectopic heart beats are
detected during auscultation of the heart. There is bilaterally symmetrical %AI muscle
strength in the upper and lower e#tremities. Zaboratory evaluation following an
overnight fast demonstrates the following.
Jerum
Jodium $&D mEFAZ
+hloride ?0 mEFAZ
Botassium%.$ mEFAZ
(icarbonate // mEFAZ
Lagnesium $.D mEFAZ
+alcium >.% mgAdZ
;rea nitrogen ((;P) $$ mgAdZ
+reatinine@.D mgAdZ
Klucose %@ mgAdZ
)nsulin $I micro*;AmZ (Pormal `? micro*;AZ)
Bro*insulin $/ micro*;AmZ (Pormal `/@= total insulin)
+*peptide &.@$ ngAmZ (Pormal @.0> d $.>? ngAZ)
What is the most liely cause of this patientXs fndings!
A. Alpha*cell pancreatic endocrine neoplasm
(. (eta*cell pancreatic endocrine neoplasm
+. ,elta*cell pancreatic endocrine neoplasm
,. E#ogenous insulin
E. Julfonylurea use
-),. &&//@
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9ption ( ((eta*cell pancreatic endocrine neoplasm) is correct. This patient has an
insulinoma: the most common pancreatic endocrine neoplasm. The diagnosis is based
on symptoms of hypoglycemia (confusion: palpitations: diaphoresis) and laboratory
evaluation showing blood glucose less than I@ mgAdZ: elevated insulin: pro*insulin and
+*peptide.
9ption A (Alpha*cell pancreatic endocrine neoplasm) is incorrect. Alpha*cell tumors are
glucagonomas and result more commonly in hyperglycemia. There is a characteristic
rash associated with alpha*cell tumors nown as necrolytic migratory erythema. There
is often an associated anemia.
9ption + (,elta*cell pancreatic endocrine neoplasm) is incorrect. These neoplasms are
also nown as somatostatinomas and typically cause cholelithiasis: steatorrhea: and
hypochlorhydria. There would be elevated somatostatins.
9ption , (E#ogenous insulin) is incorrect. E#ogenous insulin suggests that insulin is
being in<ected. Juch insulin would not have the +*peptide in it: and as a result: +*
peptide would not be elevated.
9ption E (Julfonylurea use) is incorrect. Julfonylureas result in increased insulin
output: but not increased insulin production. +onseFuently: although there can be
elevated insulin and +*peptide: pro*insulin should be normal if the cause were
sulfonylurea administration.
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0. What are the symptoms of hypoglycemia!
Hypoglycemic symptoms are classifed according to the their type and their timing in
relation to meals. Jymptoms: such as confusion: slurred speech: blurred vision:
seiCures: and coma: result from inadeFuate delivery of glucose to the brain
(neuroglycopenia). Jymptoms: such as tremors: sweating: palpitations: and nausea:
result from a counter*regulatory discharge of catecholamines (adrenergic). When
symptoms occur within I hours of the previous meal: they are considered to be
^postprandial^E if they occur more than I hours after a meal they are considered to be
^fasting.^ )nsulinomas most commonly cause fasting neuroglycopenic symptoms:
although postprandial and adrenergic symptoms may also occur.
'rom Endocrine Jecrets %E by Lc,ermott
>. How is the diagnosis of an insulinoma made!
The diagnosis reFuires documentation of symptomatic hypoglycemia and endogenous
hyperinsulinemia. Hyperinsulinemic hypoglycemia is defned as hypoglycemia with a
insulin.glucose ratio of e @.&&. Jome patients present to the provider during a
symptomatic episode: but more commonly the physician must attempt to provoe
hypoglycemia when the diagnosis is suspected. This often reFuires a prolonged fast
(up to %> hours) with blood sampling for glucose: insulin and +*peptide levels every D
hours and during any symptoms that occur. Jince proinsulin is normally cleaved into
insulin and +*peptide within the pancreas: both +*peptide and proinsulin are marers
of endogenous insulin secretion. A drug screen for sulfonylurea and meglitinide use is
also recommended.
?. How can insulinomas be distinguished from other causes of hyperinsulinemic
hypoglycemia!
Hyperinsulinemic hypoglycemia can be due to insulinomas: surreptitious insulin
administration: and medication use. Table II*$ illustrates how these entities can be
distinguished.
'rom Endocrine Jecrets %E by Lc,ermott
Table II*$. )PJ;Z)P9LAJ OERJ;J 9THER +A;JEJ 9' HNBER)PJ;Z)PEL)+
HNB9KZN+EL)A
Test )nsulinoma Jurreptitious
)nsulin ;se Julfonylurea or
Leglitinide ;se
)nsulin r r r
+*peptide r s r
Broinsulin r s Pl
,rug screen Peg Peg Bos
A &/*year*old man presents to the physician: because he noticed a large amount of
blood in the toilet bowl whist defecating this morning. The blood was bright red in
color and located primarily in the bowl. The stool was brown*colored and did not have
an unusual smell. He denies any abdominal pain: nausea: vomiting: or passage of
mucus. Two years ago: he e#perienced an isolated episode of vomiting bright red
blood. He is currently employed as an aircraft mechanic: smoes $ pac of cigarettes a
day for the last $@ years: and drins &@ to %@ g of ethanol weely. His father and
brother have also had several episodes of bright red blood per rectum: but he denies
any nowledge of a family history of colon cancer. 9n e#amination: his vital signs are
as follows. blood pressure: $$>A0I mm HgE pulse: 00 beatsAminuteE temperature:
&0.D[+ (??.0[')E and respirations: $& breathsAminute. There are multiple
telangiectasias on the face: inside the nose: on the oral mucosa: and upper thora#.
The abdomen is tympanic to percussion: and normal bowel sounds are auscultated. )t
is soft and nontender to palpation: and there is no organomegaly or masses. Rectal
e#amination reveals a normal anal reQe# and bright red blood on the glove. There is
no mucus or palpable hemorrhoids. What is the most liely diagnosis!
A. 'amilial colonic polyposis syndrome
(. Kardner syndrome
+. Lecel diverticulum
,. 9sler*Rendu*Weber syndrome
E. BeutC*"eghers syndrome
-),. &&/D>
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9ption , (9sler*Rendu*Weber syndrome) is correct. (right red BR bleeding that is
associated with multiple telangiectasias on the sin: lungs: brain: or mucosa combined
with a family history is strongly suggestive of 9sler*Rendu*Weber syndrome. (leeding
results from rupture of the telangiectasias in the gastrointestinal (K)) tract. Therefore:
treatment is with endoscopic in<ection therapy.
9ption A ('amilial colonic polyposis syndrome) is incorrect. Also nown as polyposis
coli: this familial polyposis syndrome results in thousands of adenomatous polyps and
carries a $@@= ris of developing colon cancer if prophylactic total colectomy is not
performed.
9ption ( (Kardner syndrome) is incorrect. Kardner syndrome is a constellation of
adenomatous polyps (therefore: they have malignant potential): soft tissue: and bony
tumors.
9ption + (Lecel diverticulum) is incorrect. Lecel diverticulum also presents with
painless bright red rectal bleeding. However: this diagnosis is less liely: because of
the family history of per rectum (BR) bleeding and the numerous telangiectasias found
on e#amination. Lecel diverticulum would be diagnosed with a technetium*uptae
scan (also called a Lecel scan).
9ption E (BeutC*"eghers syndrome) is incorrect. BeutC*"eghers syndrome is one of the
familial polyposis syndromes but fortunately produces only hamartomas polyps: which
do not have malignant potential. The polyps are found throughout the large and small
intestine. There is typically mucocutaneous pigmentation: most commonly around the
lips. These pigmentations are not telangiectasias.
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0. )s e#amination of the sin helpful in identifying the source of an upper K) bleed!
The sin e#amination can be helpful for suggesting a potential source if certain
stigmata are present. Zymphadenopathy or abdominal masses may suggest sources
for intra*abdominal pathology (Table I*$).
Table I*$. JY)P ')P,)PKJ )P +9P,)T)9PJ THAT +A;JE K) (ZEE,)PK
,isease Associated sin fndings
BeutC*"eghers Bigmented macules on lips: palms: soles
Lalignant melanoma Lelanoma
Hereditary hemorrhagic telangiectasias Telangiectasias on lips: mouth: palms: soles
(9sler*Weber*Rendu)
(lue rubber bleb nevus ,ar: blue soft nodules
(ullous pemphigoid 9ral and sin bullae
Peurofbromatosis +aft*au*lait spots: a#illary frecles: neurofbromas
+ronhite*+anada AlopeciaE hyperpigmentation of creases: hands: and face
+irrhosis Jpider angiomata: ,upuytrenXs contracture
PeoplasmAcanthosis nigricans
YaposiXs sarcoma +utaneous YaposiXs sarcoma
Ehlers*,anlos Jin fragility: eloids: paper thin scars
Bseudo#anthoma elasticum Nellow ^chicen fat^ papules and plaFues in Qe#ural
areas
TurnerXs Webbing of nec: purpura: sin nodules