AIPGMEE 2014 - 2015

An 8-year-old male is admitted to the hospital with a drooping right eyelid (ptosis). The initial diagnosis is Horner’s syndrome (See image). Which of the following additional signs on the right side would confirm the diagnosis?

• Constricted pupil
• Dry eye
• Exophthalmos
• Pale, blanched face
• Sweaty face

Horner’s syndrome involves interruption of sympathetic supply to the face. This results in ptosis (drooping eyelid), miosis (constricted pupil), and anhydrosis (lack of sweating) of the face. The eye is lubricated by the lacrimal gland, which secretes in response to parasympathetic stimulation, and would be unaffected. Exophthalmos (protrusion of the globe) is frequently caused by hyperthyroidism and is not present in Horner’s syndrome. Loss of sympathetic innervation leads to unopposed vasodilatation of the vessels to the face, leading to flushing rather than paleness.

AIPGMEE 2014-2015

A 45-year-old woman is admitted to the hospital for severe ear pain. Physical examination reveals chronic infection of the mastoid air cells (mastoiditis). The infection can erode the thin layer of the bone between the mastoid air cells and the posterior cranial fossa and spread most commonly into which of the following venous structures?

• Superior sagittal sinus
• Inferior sagittal sinus
• Straight sinus
• Cavernous sinus
• Sigmoid sinus

The sigmoid venous sinus empties into the internal jugular vein and drains the cranial vault. It runs along the posterior cranial fossa near the suture between the temporal and occipital bones. The superior sagittal sinus lies within the superior aspect of the longitudinal fissure, between the two cerebral hemispheres. The inferior sagittal sinus runs inferior to the superior sagittal sinus within the falx cerebri and joins the great cerebral vein (of Galen) to form the straight sinus. The straight sinus drains the great cerebral vein (of Galen) into the confluence of sinuses. The cavernous sinus is located within the middle cranial fossa and receives the ophthalmic veins, the greater petrosal sinus, and other venous vessels.

GAS 842-844; GA 445

AIPGMEE 2014-2015

A 55-year-old man is admitted to the hospital after an injury sustained at work in a factory. He presents with severe scalp lacerations, which were sutured. After three days the wound is inflamed, swollen, and painful. Between which tissue layers is the infection most likely located?

• The periosteum and bone
• The aponeurosis and the periosteum
• The dense connective tissue and the aponeurosis
• The dense connective tissue and the skin
• The dermis and the epidermis

The scalp is divided into five layers: skin, dense connective tissue, aponeurosis, loose connective tissue, and periosteum. Typically, infections will be located in the loose connective tissue because of the ease with which infectious agents spread via the many veins located in this region. This area is usually referred to as the “danger zone” of the scalp mainly because scalp infections here can be transmitted into the skull via emissary veins, then via diploic veins of the bone to the cranial cavity. The periosteum and bone are almost inseparable; thus, it is not likely to find infections between these layers. The areas between the dense connective tissue and aponeurosis and between the connective tissue and the skin layers do not include connecting veins but mainly superficial veins of the head. The skin provides a very strong barrier against infections; the epidermis and dermis layers are rarely seen separated, and thus the likelihood of an infection between these areas would be rare.

GAS 797, 874-878; GA 442

AIPGMEE 2014- 2015

An unconscious 48-year-old woman is admitted to the hospital. CT scan reveals a tumor in her brain. When she regains consciousness, her right eye is directed laterally and downward, with complete ptosis of her upper eyelid, and her pupil is dilated. Which of the following structures was most likely affected by the tumor to result in these symptoms?

• Oculomotor nerve
• Optic nerve
• Facial nerve
• Ciliary ganglion
• Superior cervical ganglion

An injury to the oculomotor nerve would cause the eye to point downward and laterally due to the unopposed contractions of the trochlear and abducens nerves. The oculomotor nerve also provides innervation to the levator palpebrae superioris; thus, any injury would cause complete ptosis or drooping of the eyelid. The constriction of the pupil is provided by parasympathetic nerves via the oculomotor nerve. The optic nerve is responsible only for the sensory aspect of light via the retina in the eye. The facial nerve innervates the facial muscles, including the orbicularis oculi, which supplies the blink reflex. The ciliary ganglion could be damaged in this patient, but the loss of parasympathetic supply would not adequately explain the ptosis of the eyelid. The superior cervical ganglion provides sympathetic innervation to the head and neck, but no loss of sympathetics is evident in this patient.

GAS 855, 1075; GA 450-451, 465, 469, 536

AIPGMEE 2014 - 2015

A 50-year-old woman complained of pain over her chin and lower lip. A few days later small vesicles appeared over the same area and soon began erupting. She was diagnosed with a dermatomal herpes zoster inflammation (shingles). Which of the following nerves was most likely responsible for the transmission of the virus in this case?

• Auriculotemporal
• Buccal
• Lesser petrosal
• Mental
• Infraorbital

The chin and lower lip area are supplied by the mental nerve, a branch of the inferior alveolar nerve, which in turn is a branch of the mandibular division of the trigeminal nerve. The auriculotemporal nerve supplies the TMJ, the temporal region, the parotid gland, and the ear. The buccal nerve is sensory to the internal surface of the cheek. The lesser petrosal nerve is a parasympathetic nerve and would not be affected by herpes zoster, a disease of the dorsal root ganglia. The infraorbital nerve provides sensory innervation to the upper lip.

Meningitis

Meningitis
It is an inflammation of the leptomeninges and underlying
subarachnoid cerebrospinal fluid (CSF). Symptom onset
can be divided into acute (< 1 day), subacute (1-7 days),
and chronic (> 7 days) categories. Unlike subacute or
chronic meningitis, which have myriad infectious and
noninfectious etiologies, acute meningitis is almost always
a bacterial infection.
Table 2.1
Scenario Common etiological
agent
Neonatal age Group B streptococci
Beyond neonatal Streptococcus
age (over all) pneumoniae
Adolescents Neisseria meningitidis
Immune deficient patients, very Listeria
young, very old patients
HIV (< 100 CD4 cells) Cryptococcus
Tick exposure Mid Atlantic area- rocky
mountain spotted fever
(RMSF)North eastern
area- Lyme disease
COMMON ETIOLOGICAL AGENTS
The spread of the organism into the CNS can be by sporadic
(unknown) mechanisms or by means of contiguous local
infection (otitis media, sinusitis, mastoiditis, and dental
infections) or by hematogenous spread (endocarditis and
pneumonia).
Aseptic Meningitis
It is a broad term that denotes a nonpyogenic cellular
response. Patients characteristically have an acute onset
of meningeal symptoms, fever, and cerebrospinal
pleocytosis that is usually prominently lymphocytic.
Viruses cause most cases of aseptic meningitis; it can also
be caused by bacterial, fungal, mycobacterial, and parasitic
agents.
Clinical Features
Classic symptoms may not be evident in infants and
elderly) include the following:
• Headache
• Nuchal rigidity (generally not present in children
< 1year or in patients with altered mental status)
• Fever and chills
• Photophobia
• Vomiting
• Prodromal upper respiratory infection (URI)
symptoms (viral and bacterial)
• Seizures (30-40% in children, 20-30% in adults)
• Altered sensorium (confusion may be sole presenting
complaint, especially in elderly)
• Focal neurologic deficits can also occur, the most
common being visual field and cranial nerve deficits.
• Rash:
– Petechial rash: Neisseria.
– On wrists and ankles with centripetal spread
toward the body: Rocky Mountain Spotted Fever
– Target-like erythema migrans rash: Lyme
Fungal Meningitis
Headache, low-grade fever, and lethargy are the primary
symptoms; the course may be mild with fluctuating
symptoms, especially in immunocompromised patients.
Tuberculous Meningitis
Fever, weight loss, night sweats, and malaise, with or
without headache and meningismus are common
symptoms; this infection may follow a protracted course
with vague, nonspecific presentation.
Signs
• Kernig sign: In a supine patient, flex the hip to 90°
while the knee is flexed at 90°. An attempt to further
extend the knee produces pain in the hamstrings and
resistance to further extension.
• Brudzinski sign: Passively flex the neck while the
patient is in a supine position with extremities
extended. This maneuver produces flexion of the hips
in patients with meningeal irritation.
Symptoms in Infants
• Fever
• Lethargy and/or change in level of alertness
• Poor feeding and/or vomiting
• Respiratory distress, apnea, cyanosis
‘99er’- The most common long-term neurologic deficit
is damage to the 8th cranial nerve. Facial nerve palsy is
suggestive of Lyme.
Diagnosis
The cornerstone in the diagnosis of meningitis is
examination of the CSF. CT scan of the brain may be
performed prior to lumbar puncture in some patient groups
with a higher risk of herniation, which include those with:
• newly onset seizures
• an immunocompromised state
• signs suspicious for space-occupying lesions (such
as papilledema and focal neurologic signs)
• moderate-to-severe impairment in consciousness
If the lumbar puncture is delayed more than 20-30
minutes for any reason, then the best initial step is to give
an empiric dose of antibiotics with ceftriaxone or
cefotaxime. Also begin empiric therapy prior to head CT
scan if a focal neurologic deficit is present.
Treatment
Table 2.3
Predisposing feature Common pathogens
Age 0-4 weeks Group B or D streptococci, E. coli,
Listeria
Age 1-3 months From both above and below group
Age 3 months to S. pneumoniae, N meningitidis, and
50 years H influenzae.
Older than 50 years S. pneumoniae, H. influenzae,
Listeria species, Pseudomonas
aeruginosa, and N. meningitidis.
Impaired cellular Cryptococci, Mycobacterium
immunity tuberculosis, syphilis, HIV aseptic
meningitis, and Listeria species
Neurosurgery, head Staphylococcus epidermidis,
trauma, or CSF shunt S. aureus, coliforms, Propionibacterium
acnes.
Table 2.4
Pathogen Treatment
S. pneumoniae Vancomycin + III generation cephalosporin
(+dexamethasone- not always)
L. monocytogenes Ampicillin
S. agalactiae Ampicillin
N. meningitides Ampicillin/ III generation cephalosporin
H. influenzae III generation cephalosporin
General Principle in Treatment
• Suspected meningitis should be treated immediately,
and do not wait for LP results.
Table 2.2
WBC count/μL Glucose (mg/dL) Protein (mg/dL) Confirmatory test
Normal 0-5; lymphocytes 50-75 15-40
Bacterial 100-5000;>80% PMNs <40 >100 Gram stain, culture (better results)
Viral 10-300;lymphocytes Normal, reduced in Normal, but may be Viral isolation, PCR analysis
mumps, Lassa virus slightly elevated
Tuberculous 100-500; lymphocytes Reduced; <40 Elevated;>100 AFB staining, culture, PCR
Cryptococcal 100-200; lymphocytes Reduced 50-200 India ink, cryptococcal
antigen.
Aseptic 100-300;lymphocytes Normal Normal; may be
slightly elevated
• Empiric therapy of bacterial meningitis is best
achieved with ceftriaxone or cefotaxime.
• Ampicillin is added to those with immune defects to
cover Listeria. Listeria is resistant to all forms of
cephalosporins.
• Lyme disease: ceftriaxone.
• Cryptococcus: initially with amphotericin; lifelong
fluconazole therapy in HIV-positive patients.
• Syphilis- penicillin.
• TB meningitis: in the same fashion as you would use
for pulmonary TB. Steroid use in adult meningitis is
only appropriate for TB meningitis.
• Viral (or aseptic) meningitis: no treatment currently
proven useful for.
Prophylaxis
For close contacts of patients with (suspected)
N. meningitides by rifampin (same for suspected
H. influenzae). Indicated for those at increased risk, such as
those who were in close contact with patient for at least
4 hours during the week before onset or were exposed to
patient’s nasopharyngeal secretions.

AIPGMEE 2014- 2015

Question 1

Each of the following treatments might be useful in restoring a prolonged prothrombin time (PT) to the normal range EXCEPT

• Recombinant factor VIII
• Vitamin K
• Fresh frozen plasma
• Stopping warfarin (Coumadin)
• Cryoprecipitate

The PT and the activated partial thromboplastin time (aPTT) are common tests used to evaluate coagulation factors. The PT primarily tests for factor VII in the extrinsic pathway, as well as factors I, II, V, and X of the common pathway. The aPTT primarily tests for factors VIII and IX of the intrinsic pathway, as well as factors I, II, V, and X of the common pathway. Although the PT is prolonged with deficient function of factors I, II, V, VII, or X, it is more sensitive to deficiencies of factor VII and less so with deficiencies of factor I or II. In fact, the PT is not prolonged until the level of fibrinogen (factor I) is less than 100 mg/dL and may only be prolonged 2 seconds when the level of factor II (prothrombin) is 10% of normal. Factors II, VII, IX, and X are vitamin-K-dependent factors and their formation is blocked with Coumadin therapy. Administering factor VIII will not help a prolonged PT (Barash: Clinical Anesthesia, ed 5, pp 222-224, 228).

Question 2

Proper processing of platelet concentrates (to avoid future hemolytic transfusion reactions) before administration involves

• Type and crossmatch
• ABO and Rh matching
• Rh matching only
• ABO matching only
• Platelets can be administered without regard to any antigen system

Platelet concentrates contain a fair amount of plasma and white blood cells (WBCs) but relatively few RBCs. Although ABO-compatible platelet transfusions are preferred (platelets survive better and crossmatching for subsequent RBCs is easier), in emergencies it has been noted that platelets often give adequate hemostasis without regard to ABO compatibility. Even though there are only small quantities of RBCs in platelets, the RBCs present can cause Rh immunization if Rh-positive platelet concentrates are injected into Rh-negative patients. Thus, until childbirth is no longer possible, Rh-negative females should only receive Rh-negative platelets (Miller: Anesthesia, ed 6, pp 1822-1823; Stoelting: Pharmacology and Physiology in Anesthetic Practice, ed 4, p 625).

Question 3

The most common inherited coagulopathy is

• Hemophilia A
• Hemophilia B
• von Willebrand disease
• Factor V deficiency
• Factor II deficiency

Coagulopathies can be inherited or acquired. Of the inherited coagulopathies, von Willebrand’s disease is the most common, affecting 1 in 100 to 500 people. Both hemophilia A (Factor VIII) deficiency and hemophilia B (Factor IX or Christmas disease) are X-linked recessive disorders. Hemophilia A occurs in 1 to 2 per 10,000 males and hemophilia B occurs in 1 per 100,000 males. Factor V, Factor VII, Factor X, and prothrombin (Factor II) are exceedingly rare autosomal recessive disorders. (Kasper: Harrison’s Principles of Internal Medicine, ed 16, pp 680-682; Stoelting: Anesthesia and Co-Existing Disease, ed 4, pp 490-493).

Question 4

In a 70-kg patient, 1 unit of platelet concentrate should increase the platelet count by

• 2000 to 5000/mm³
• 5000 to 10,000/mm³
• 15,000 to 20,000/mm³
• 20,000 to 25,000/mm³
• Greater than 25,000/mm³

Platelet count is increased about 5000 to 10,000/mm³ per unit of platelet concentrate in the typical 70-kg patient. Each unit contains greater than 5.5 × 1010 platelets (Barash: Clinical Anesthesia, ed 5, p 216; Harmening: Modern Blood Banking and Transfusion Practices, ed 5, pp 14-15; Miller: Anesthesia, ed 6, pp 1822-1823).

Question 5

A 68-year-old patient receives a one unit transfusion of packed red blood cells (RBCs) in the recovery room after a laparoscopic prostatectomy. As the blood is slowly dripping into his peripheral IV, the patient complains of itching on his chest and arms, but his vital signs remain stable. The antibody most likely responsible for this is directed against

• Rh
• ABO
• MN, P & Lewis
• Kell, Duffy & Kidd
• None of the above

This is an example of a typical allergic reaction. All of the other choices in this question may be involved in hemolytic reactions. Allergic reactions are a form of nonhemolytic transfusion reactions, which are thought to be caused by foreign proteins in the transfused blood. The reactions occur in about 3% of all transfusions and present with urticaria, erythema, pruritus, fever and sometimes respiratory symptoms. When it occurs, the transfusion is stopped and supportive therapy including antihistamines is administered. If the symptoms resolve and there are no signs of a hemolytic reaction (no free hemoglobin in the plasma or urine) or a severe anaphylactic reaction, the transfusion can be resumed (Lobato: Complications in Anesthesiology, p 512; Miller: Anesthesia, ed 6, p 1817; Stoelting: Basics of Anesthesia, ed 5, p 361).

AIPGMEE 2014 - 2015

A 15 yr old boy is noted to have enlarged kidneys with macrocysts seen bilaterally on a renal
ultrasound study after developing gross hematuria while playing hockey. His mother is 40 yr of
age and demonstrates similar findings on renal ultrasound examination. What is the most
appropriate next step in this patient's management?
□Evaluate the patient for kidney transplantation
■Check the blood pressure
□Obtain a cystogram to evaluate for vesicoureteral reflux
□Start the patient on an antibiotic for prevention of urinary tract infection
□Obtain a renal ultrasound study of all siblings
description: Treatment of ADPKD is primarily supportive. Control of blood pressure is critical because
the rate of disease progression in ADPKD correlates with the presence of hypertension. Angiotensinconverting
enzyme inhibitors and/or angiotensin II receptor antagonists are agents of choice. Obesity,
caffeine ingestion, smoking, multiple pregnancies, male sex, and possibly the use of calcium channel
blockers appear to accelerate disease progression. Older patients with a family history of intracranial
aneurysm rupture may be considered candidates for screening for aneurysms. (See Chapter 515, page
1798.Nelson Pediatrics 19th edn)

AIPGMEE 2014 - 2015

A 46-year-old woman presents with menorrhagia and dysmenorrhoea. Which one of these is the probable cause?

• Adenomyosis of the uterus
• Dysfunctional uterine bleeding
• Pelvic endometriosis
• None of the above

Adenomyosis of the uterus is the probable diagnosis. Pelvic endometriosis occurs during childbearing period, and dysfunctional uterine bleeding should be painless bleeding.

AIPGMEE 2014- 2015

Characteristics of choroidal melanoma include all of the following except
a. choroidal excavation
b. high internal reflectivity
c. double circulation
d. orbital shadowing
Ans=b. high internal reflectivity
Ref-(thanks to the publisher)

Retina

by Stephen J. Ryan

5th edition published by Elsevier

Gross appearance of choroidal melanoma

The gross examination of intraocular tumors is the basis for clinicopathologic correlations as it allows for a detailed macroscopic evaluation and measurement of the tumor size including the prognostically relevant largest basal diameter.^5,6 The largest basal diameter can be reliably assessed on gross examination, although the tumor size may be underestimated when measured after fixation due to tumor shrinkage.⁷Choroidal melanomas exhibit an oval or fusiform shape (Fig. 142.2) when confined by Bruch’s membrane or a collar-button/mushroom configuration (Fig. 142.3) when the tumor has broken through Bruch’s membrane.

FIG.142.2 

(A) Oval-shaped, heavily pigmented choroidal melanoma (molecular profile class I) in a 66-year-old man. (B) Histologically, a mixed-cell type melanoma (asterisk) is present within the uvea (H&E, ×40). Bruch’s membrane (arrow) is intact, the overlying RPE and retina display atrophic changes.

FIG.142.3 

(A) Collar-button shaped pigmented choroidal melanoma in a 70-year-old woman. (B) Histologic examination shows the tumor breaking through Bruch’s membrane (arrow) (H&E, ×40).

Ocular structures may be invaded by choroidal melanomas. Invasion into the ciliary body may be detected macroscopically, whereas invasion into the sclera, retina, and optic nerve as well as invasion into the vitreous, iris, and anterior chamber is usually detected by microscopic examination. Extraocular extension (Fig. 142.4) usually occurs along vortex veins or emissary canals and, dependent on the extent, may be diagnosed clinically or on gross examination.

FIG.142.4 

An 86-year-old woman presented with (A) extraocular extension of a uveal melanoma (molecular profile class II). (B) On gross examination, extraocular extension (arrow) of a mildly pigmented bilobulated tumor was detected that invades the choroid and the ciliary body. (C) Histologic examination (H&E, ×10) shows the extraocular part of the tumor (asterisk) composed of epithelioid cells. The patient died from liver metastasis less than 1 year after enucleation.

The amount of pigmentation of uveal melanomas varies from tumor to tumor or even within a single tumor and may be related to overall survival.^5,8 Most tumors exhibit mild to moderate pigmentation, although heavily or non-pigmented (amelanotic) choroidal melanomas (Fig. 142.5) may be observed.