The American Board of Pathology (ABP) recently published their pass rates for the Spring 2017 administration. After maintaining a 100% pass rate for the previous four administrations of the exam over two years, the Spring 2017 exam pass rate has dipped to an appalling 97.7%!
A total of 265 individuals took the exam (at $700 per examinee, the ABP brought in a paultry $185,000 from this administration). Included in this number is probably the few like me who only took the neuropathology exam, with the majority likely taking the AP/CP exam.
Bottom line: No need to worry about either your likelihood of passing the MOC exam or the financial well-being of the ABP.
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Showing posts with label MOC. Show all posts
Showing posts with label MOC. Show all posts
Friday, September 8, 2017
Friday, August 25, 2017
I took the American Board of Pathology Neuropathology Maintenence of Certification Exam
I took the American Board of Pathology neuropathology maintenance of certification exam this week. Given that the ABP goal is virtually a 100% pass rate, I found the test more difficult than I anticipated. I suppose I shouldn't have been surprised by the level of difficulty of some of the questions, given that the ABP publishes the topics covered. But in some cases knowing the topic does not really help with preparation. For example, one topic listed is: "abnormal corticospinal tracts/pyramids". In any case, I am sure the cut-off score for passing is relatively low. Results, which only entail whether or not one has passed, will be released in October.
Tuesday, November 22, 2016
MOC Exam Topic: Acute Hemorrhagic Leukoencephalopathy
First recognized as a discrete entity by Weston Hurst in 1941, acute hemorrhagic leukoencephalopathy (AHL) is a usually fatal disease characterized clinically by an abrupt onset of fever, neck stiffness, and neurological deficits, often progressing rapidly to seizures and coma. The presenting clinical picture is similar to that of acute disseminated encephalomyelitis (ADEM) but with a more fulminant course. At autopsy, the brain is swollen with multiple petechial hemorrhages centered in the white matter. Large foci of necrosis with cavitation may be present. The cerebral cortex and basal ganglia usually appear intact. Histologically, perivascular demyelinating lesions consist of ball or ring hemorrhages surrounding necrotic venules. There are cuffs of mononuclear cells and neutrophils. There is also substantial axonal injury in the affected areas. The lesions are indistinguishable from ADEM, but the extent of microvascular damage and therefore hemorrhage is is greater. An allergic mechanism is postulated.
| FIGURE 3. A (H&E, 100×), B (LFB/PAS, 100×), and C (HAM-56 IHC, 400×). Light microscopic studies revealed thin sleeves of pallor surrounding small-caliber parenchymal blood vessels (A) which correspond to areas of demyelination on special stain (B). Macrophages stain strongly positive for macrophage marker HAM-56 (C). From Lann MA, et al. Am J Forensic Med Pathol. 2010 Mar;31(1):7-11. |
Tuesday, November 15, 2016
MOC Exam Topic: Status Marmoratus
The neurons of the infant caudate, putamen, thalamus, and globus pallidus are susceptible to damage by hypoxia-ischemia. In some extensive injuries, a marked gliosis occurs and, if the brain is actively forming myelin in that region, there is hypermyelination of the area with aberrant myelination of astrocytic processes. There is frequently also neuronal loss and mineralization of residual neurons. The resulting white, firm, marbled-appearing lesion is called status mamoratus. Thought to occur if a hypoxic insult happens before the age of 6 to 9 months, status marmoratus has been associated with complicated parturitions and acute febrile illness during the first year of life. Lesions in the basal ganglia occurring after the period of active myelination exhibit only gliosis associated with neuronal loss. (Source: Greenfield's Neuropathology, 8th Edition)
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| status marmoratus involving thalamus and basal ganglia |
Tuesday, November 8, 2016
MOC Exam Topic: More on Aquaporin-4
My last post elicited two important comments on aquaporin-4. Since not all readers necessarily look at the comments, I am publishing them as a separate post here:
Maria said...
Maria said...
Worth mentioning that [aquaporin-4] is the most well known target in Neuromyelitis Optica (NMO) and NMO spectrum disorders, since about 80% of patients with this syndrome will have circulating anti-aquaporin 4 antibodies. The IHC is useful when considering active NMOSD on a biopsy specimen by showing loss of staining (Neurology. 2015 Jan 13;84(2):148-58)
Agent86 said...
And one can only get so far without mentioning the glymphatic pathway..
Genetic knock-out of the gene encoding the astroglial water channel aquaporin-4, which is importantly involved in paravascular interstitial solute clearance, exacerbated glymphatic pathway dysfunction after TBI and promoted the development of neurofibrillary pathology and neurodegeneration in the post-traumatic brain. These findings suggest that chronic impairment of glymphatic pathway function after TBI may be a key factor that renders the post-traumatic brain vulnerable to tau aggregation and the onset of neurodegeneration.
Iliff JJ, Chen MJ, Plog BA, Zeppenfeld DM, Soltero M, Yang L, Singh I, Deane
R, Nedergaard M. Impairment of glymphatic pathway function promotes tau pathology
after traumatic brain injury. J Neurosci. 2014 Dec 3;34(49):16180-93.
Genetic knock-out of the gene encoding the astroglial water channel aquaporin-4, which is importantly involved in paravascular interstitial solute clearance, exacerbated glymphatic pathway dysfunction after TBI and promoted the development of neurofibrillary pathology and neurodegeneration in the post-traumatic brain. These findings suggest that chronic impairment of glymphatic pathway function after TBI may be a key factor that renders the post-traumatic brain vulnerable to tau aggregation and the onset of neurodegeneration.
Iliff JJ, Chen MJ, Plog BA, Zeppenfeld DM, Soltero M, Yang L, Singh I, Deane
R, Nedergaard M. Impairment of glymphatic pathway function promotes tau pathology
after traumatic brain injury. J Neurosci. 2014 Dec 3;34(49):16180-93.
Monday, November 7, 2016
MOC Exam Topic: Aquaporin-4
Among the topics for the neuropathology maintenance of certification examination is aquaporin-4 (AQP-4). An important regulatory molecule in the maintenance of the proper flow of water across the blood-brain barrier, AQP-4 is the major water channel expressed within CNS astrocytic foot processes. Water flux across AQP4 is bidirectional.
Wednesday, November 2, 2016
Neuropathology Maintenance of Certification Topics
For those taking the maintenance of certification (MOC) examination at some point in the next few years, the American Board of Pathology (ABP) has published topics that may be covered in the examination. The examination consists of 150 multiple-choice questions, 50 of which are required to be in the a category designated "general neuropathology I". The remaining 100 questions can be from various categories which the examinee chooses (general neuropathology II, degenerative I & II, developmental/pediatric/congenital I & II, neoplastic I & II, and neuromuscular I & II). The ABP provides an MOC examination study guide to help examinees prepare for the exam. The following list is copied from the study guide and includes possible topics in the mandatory general neuropathology 50-question module:
abnormal corticospinal tracts/pyramids
leptomeningeal opacifications
acute hemorrhagic leukoencephalopathy
leukodystrophies
anaplastic astrocytoma
motor cortex; smear prep
aquaporin-4
multicystic encephalopathy
astrocytomas; chemotherapeutic resistance
multiple system atrophy
axonal injury; IHC
myxopapillary ependymoma
borderzone hypoxic-ischemic damage
orbital plate fractures
cervical spinal cord tracts
Pick disease
CNS cysts
pituitary gland histology
CNS neoplasms; loss of heterozygosity
postmortem artifacts
CSF; metastatic tumors
primary angiitis of the CNS
deep (basal) nuclei; tracts
ragged red fibers
dermatomyositis
retinal hemorrhage
dysembryoplastic neuroepithelial tumor
retinoblastoma
fetal developmental; neuroanatomy
skeletal muscle ultrastructure
fibrillary astrocytoma
spinal cord anatomy
glioblastoma
status marmoratus
GM1 and GM2 gangliosidoses
Steele-Richardson-Olszewski syndrome
hereditary sensory-motor neuropathies
substantia nigra
Huntington disease
tauopathies
hypoxic injury
TORCH infections
infant developmental neuropathology; cerebellum
tract degeneration
infant spinal cord; sequence of myelination
trinucleotide repeat disorders
Lafora progressive myoclonic epilepsy
vascular malformations
abnormal corticospinal tracts/pyramids
leptomeningeal opacifications
acute hemorrhagic leukoencephalopathy
leukodystrophies
anaplastic astrocytoma
motor cortex; smear prep
aquaporin-4
multicystic encephalopathy
astrocytomas; chemotherapeutic resistance
multiple system atrophy
axonal injury; IHC
myxopapillary ependymoma
borderzone hypoxic-ischemic damage
orbital plate fractures
cervical spinal cord tracts
Pick disease
CNS cysts
pituitary gland histology
CNS neoplasms; loss of heterozygosity
postmortem artifacts
CSF; metastatic tumors
primary angiitis of the CNS
deep (basal) nuclei; tracts
ragged red fibers
dermatomyositis
retinal hemorrhage
dysembryoplastic neuroepithelial tumor
retinoblastoma
fetal developmental; neuroanatomy
skeletal muscle ultrastructure
fibrillary astrocytoma
spinal cord anatomy
glioblastoma
status marmoratus
GM1 and GM2 gangliosidoses
Steele-Richardson-Olszewski syndrome
hereditary sensory-motor neuropathies
substantia nigra
Huntington disease
tauopathies
hypoxic injury
TORCH infections
infant developmental neuropathology; cerebellum
tract degeneration
infant spinal cord; sequence of myelination
trinucleotide repeat disorders
Lafora progressive myoclonic epilepsy
vascular malformations
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