Chapter 40 - Acquired Metabolic Flashcards
Normal serum osmolality A. 250-270 mOsm/L B. 260-280 mOsm/L C. 270-290 mOsm/L D. 280-300 mOsm/L
C. 270-290 mOsm/L (p. 1133)
Following cardiac arrest, recovery can be complete if breathing, oxygenation, and cardiac action are restored within A. 3-5 mins B. 5-7 mins C. 6-8 mins D. 7-9 mins
A. 3-5 mins (p. 1134)
Most common early change in imaging studies in cases of severe anoxic-ischemic injury
A. Loss of distinction between the cerebral gray and white matter
B. Watershed infarctions
C. Striatal damage
D. None of the above
A. Loss of distinction between the cerebral gray and white matter (p. 1135)
Plain CT findings in carbon monoxide poisoning*
A. Loss of distinction between the cerebral gray and white matter
B. Watershed infarctions
C. Striatal damage with sparing of the pallidum
D. Decreased attenuation in the pallidum bilaterally
D. Decreased attenuation in the pallidum bilaterally (p. 1138)
Cerebral edema in acute mountain sickness is implicated to overexpression of A. VEGF B. FGF C. EGF D. EPO
A. VEGF (p. 1139)
Main features of chronic mountain sickness or Monge disease EXCEPT A. Coma B. Pulmonary hypertension C. Cor pulmonale D. Secondary polycythemia
A. Coma (p. 1139)
Most effective preventive measure for mountain sickness*
A. Dexamethasone
B. Acetazolamide
C. Dexamethasone and acetazolamide combination
D. Acclimatization by a 2- to 4-day stay at intermediate altitudes
D. Acclimatization by a 2- to 4-day stay at intermediate altitudes (p. 1139)
Chronic hypercapnia can be seen in the following conditions EXCEPT* A. Bronchial asthma B. COPD C. Emphysema D. Fibrosing lung disease E. Myasthenia gravis
A. Bronchial asthma (p. 1139)
Most effective therapeutic measure for hypercapnic pulmonary disease A. Positive pressure ventilation B. Oxygen supplementation C. Phlebotomy D. Antibiotics
A. Positive pressure ventilation (p. 1139)
The patient presents with dehydration, fatigue, weakness, headache, abdominal pain, dryness of the mouth, Kussmaul breathing, and eventually went into coma. He probably has* A. Diabetic acidosis B. Hyperosmolar nonketotic hyperglycemia C. Hepatic coma D. Uremic encephalopathy
A. Diabetic acidosis (p. 1141)
MRI findings in portal-systemic encephalopathy
A. Loss of distinction between the cerebral gray and white matter
B. Watershed infarctions
C. Decreased attenuation in the pallidum bilaterally
D. High signal intensity in the globus pallidus
D. High signal intensity in the globus pallidus (p. 1143)
Neuropathologic findings in hepatic encephalopathy*
A. Alzheimer type I astrocytes
B. Alzheimer type II astrocytes
C. Mild hyperplasia of protoplasmic astrocytes
D. Batwing lesion of the pons
B. Alzheimer type II astrocytes (p. 1143)
Mainstay of treatment in hepatic encephalopathy* A. Restriction of dietary protein B. Neomycin C. Lactulose D. Rifaximin
C. Lactulose (p. 1144)
A patient with SIADH and serum Na less than 120 mEq/Lis treated by restricting fluids to*
A. 500 mL per 24 hours
B. 1000 mL per 24 hours
C. 1500 mL per 24 hours
D. SIADH is not treated with fluid restriction
A. 500 mL per 24 hours (p. 1148)
Batwing lesion of the pons on MRI is attributed to A. Basilar artery occlusion B. Central pontine myelinosis C. Multiple sclerosis D. None of the above
B. Central pontine myelinosis (p. 1150)
Rate of correction of hyponatremia to avoid CPM* A. not more than 10 mEq/L in 24 hours B. not more than 12 mEq/L in 24 hours C. not more than 20 mEq/L in 36 hours D. not more than 30 mEq/L in 36 hours
A. not more than 10 mEq/L in 24 hours (p. 1151)
Which of the following is not seen histopathologically in CPM?* A. Demyelination B. Necrosis C. Reactive glia D. Inflammation
D. Inflammation (p. 1150)
Which among the thyroid encephalopathies is steroid-responsive?
A. Hyperthyroidism-related encephalopathy
B. Hashimoto encephalopathy
C. Myxedema
D. Cretinism
B. Hashimoto encephalopathy (p. 1155)
Cause of non-ischemic hypoxic encephalopathy* A. Lead B. CO C. CO2 D. Arsenic
B. CO (p. 1133)
Which of the following is NOT a predictor of poor neurologic outcome or death at 1 day after cardiac arrest?* A. Absent motor response B. No withdrawal to pain C. Absent pupillary reactivity D. No DTRs E. Absent corneal reflex
D. No DTRs (p. 1137)
After a bout of viral encephalitis, the patient developed liver enlargement with encephalopathy. What is the most likely reason?*
A. Reye syndrome
B. Fluid overload
C. Adverse reaction to antiviral agent
D. Systemic dissemination of viral infection
A. Reye syndrome (p. 1145)
Findings that are reversible on MRI in Cushing disease/ prolonged corticosteroid therapy* A. Thinning of frontal cortex B. Attenuation of basal ganglia C. Ventricular enlargement D. Sulcal widening
C. Ventricular enlargement (p. 1155)
NOT a feature of Hashimoto encephalopathy* A. Multifocal myoclonus B. Stupor C. Seizures D. Ataxia E. Hemiparesis F. Dementia
F. Dementia (p. 1155)
Treatment for Hashimoto encephalopathy* A. Levothyroxine B. RAI C. IVIg D. PTU E. Corticosteroids
E. Corticosteroids (p. 1156)
Galactocerebrosidase deficiency* A. Tay-Sachs disease B. Krabbe disease C. Fabry disease D. Gaucher disease E. Niemann-Pick disease
B. Krabbe disease (Table 37-3, p. 956)
Watershed infarcts are more likely to cause which of the following symptoms?* A. Visual agnosia B. Prosopagnosia C. Tactile hemineglect D. Constructional apraxia
A. Visual agnosia (p. 1136)
What is the pathology in uremic encephalopathy?* A. Cerebral shrinkage B. Microhemorrhages C. Basal ganglia changes D. Cerebral edema
A. Cerebral shrinkage (p. 1146)
NOT true of osmotic demyelination syndrome*
A. A rapid rise in serum osmolality to normal or higher-than-normal levels is an almost obligate antecedent of this process.
B. There is loss of pontine nuclei and axons in the pons.
C. Posteriorly, the lesion may reach and involve the medial lemnisci.
D. Reactive phagocytes and glia cells are in evidence throughout the lesion but oligodendrocytes are depleted.
B. There is loss of pontine nuclei and axons in the pons. (p. 1150)
