Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
87 Cards in this Set
- Front
- Back
|
What are the four possible form of brain tumors?
|
Encapsulated
Infultrating Benign Malignant |
|
|
What are the two types of tumors that is determined by its origin?
|
Primary CNS tumor
Metastatic |
|
|
Encapsulated Tumors
|
Tumor cells that grow within their own membrane. They are almost always benign tumors and affects the brain by exerting pressure on it. Particularly easy to identify on a CT scan
|
|
|
Meningiomas
|
Tumors that grow between the meninges. All meningiomas are encapsulated tumors and therefore are mostly benign tumors.
|
|
|
Benign tumors
|
Tumors that can be removed surgicaly with little risk of further growth in the body.
|
|
|
Infiltrating tumors
|
Most brain tumors are infiltrating; they grow diffusely through surrounding tissue. They are usually Malignant tumors.
|
|
|
Malignant tumors
|
These are usually infiltrating tumors that are difficult to surgically remove or destroy them completely. Any cancerous tissue that remains after surgery continues to grow.
|
|
|
Metastatic tumors
|
metastasis refers to the transmission of disease from one organ to another.
About 10% of brain tumors do not originate in the brain. They grow from infiltrating tumor fragments carried to the brain by the bloodstream from some other part of the body. the brain is a particularly fertile ground for tumor growth. |
|
|
Neuromas
|
Tumors that grow on nerves or tracts. Acoustic neuroma is the kind of tumor that Dr. P has.
|
|
|
Glioma
|
Brain tumors are usually formed from glial cells caled Glioma.
|
|
|
What is a cerebrovascular disorder discussed in class?
|
strokes
|
|
|
What are the two types of strokes?
|
Cerebral Hemorrhage
Cerebral Ischemia |
|
|
What is stroke?
|
A sudden-onsest cerebroascular disorder that cause brain damge.
|
|
|
what are some common consequences of stroke?
|
amnesia, aphasia (language difficulty), paralysis, coma.
|
|
|
What is an infarct?
|
The area of dead or dying tissue produced by a stroke.
|
|
|
What is the Penumbra?
|
The dysfunctional area that surrounds the infarct. The cells in this area may recover or die; the goal of treatment is to try to save them.
|
|
|
Cerebral hemorrhage
|
Bleeding in the Brain
Occurs when a cerebral blood vessel ruptrues and blood seeps into the surrounding neural tissue and damages it. |
|
|
What are two dangers of cerebral hemorrhage?
|
1) Blood that leaks out is toxic to neurons.
2) Hematoma can form |
|
|
Hematoma
|
This is a solid blood clot that forms after a stroke. It damages the brain by building up pressure and compress brain.
|
|
|
What happens after cell death in a stroke?
|
The cavity is build-in by astrocytes. This is called glial scarring - form a hard layer.
|
|
|
What are two risk factors for strokes?
|
Hypertension
Aneurysm |
|
|
What is aneurysm?
|
A pathological balloonlike dilation that forms in teh wall of an artery at a point where teh elasticity of the artery wall is defective. Aneurysms can occur in any part of the body other than the brain. Can be congenital or caused by exposure to vascular poisons or infection.
|
|
|
What is another form of stroke other than Cerebral Hemorrhage?
|
Cerebral Ischemia
|
|
|
What is Cerebral Ischemia? and the result of it?
|
This is a disruption of blood supply to an area of the brain.
Cells end up deprived of oxygen and glucose. Waste removal disrupted Neurotransmitters release too much glutamate. and brain tissue dies eventually (infarction) |
|
|
What are three causes of Cerebral ischemia?
|
1) Thrombosis
2) Embolism 3) Arteriosclerosis |
|
|
What is thrombosis?
|
This can be formed by blood clot, fat, oil air bubble, tumor, cells or any combination there of. These material forms a clog and blocks blodd flow at the site of its formation.
|
|
|
What is Embolism?
|
This is like a thrombosis (vessel clog) that traveled from site of product to site of disruption. This plug is now called a embolus. Usually formed in big vessel and travel to clog a smaller vessel.
|
|
|
What is arteriosclerosis?
|
Often result from fat deposits. Teh walls of blood vessels thicken and the channels narrow. This narrowing can eventually lead to complete blockage of the blood vessels.
|
|
|
What is responsible for most of the damage caused by stroke?
|
Excitoxicity.
Prolonged ischemia causes an excessive release of excitatory amino acid neurotransmitters - particularly GLUTAMATE - the brain's most prevalent ecitatory neurotransmitter. |
|
|
Describe the mechanism of glutamate release in a brain ischemia.
|
1) Neurons deprived of blood supply are overactive, and release excessive glutamate.
2) Glutamate overactivates glutamate receptors in poastsynaptic neurons 3) Glutamate binds to NMDA receptors 4) Large amount of Na+ and Ca++ ions enter postsynaptic neurons. 5) Internal concentration of NA+ and CA++ increases 6) Trigger more release of glutamate to affect other neurons, and/or eventually trigger apoptosis. |
|
|
What are three properties of Ischemia-induced brain damage?
|
1) Damage takes a while to be detected; usually after a day or two later.
2) Damage does not occur equally in all parts of the brain. Most susceptible neurons are located in hippocampus. 3) Mechanism of ischemia-induced damage vary from structure to structure in the brain; astrocytes have been implicated in some cases. |
|
|
Knowing that the over release of glutamate leads to more damage, what is a potential treatment to minimize brain damage?
|
the use of glutamate antagonist
|
|
|
What are some standard treatments to brain trauma?
|
1) Medication to dissolve obstruction such as tPA - tissue plasminogen activator. This can be toxic if it doesn't stay in blood vessels but leak into tissue.
2) Cooling the brain can slows down brain activity by counteracting hyperactivity. |
|
|
What are some potential treatments to brain trauma that are under clinical trails or research?
|
1) Vampire Bat Saliva, anticoagulant
2) Apply neurotrophins to help neurons survive 3) Apoptosis blockers |
|
|
What does TIA stands for and what is it?
|
Transient Ischemic Attack
- "mini-stroke" - ischemia is short lived (temporary) - damage is not permanent |
|
|
What are the symptoms of TIA?
|
partial paralysis
language difficulties - aphasia confusion sensory loss most symptoms depends on the area of brain disruption. |
|
|
What is penetrating head injury?
|
This occurs when objects penetrate the brain through the skull
E.g. Gun shot wounds, iron rod into brain (Phineas Gage), rare cases of deliberate self-injury. |
|
|
What is closed head injury?
|
Brain injuries produced by blows that do not penetrate the skull are called this.
|
|
|
Describe how the protection of the brain can serves as an enemy to the brain.
|
The CSF that surrounds the skull acts as a cushion that allows the brain to bounces back and forth. Allowing the brain to accelerates inside the skull.
|
|
|
What did Holbourn found in 1940?
|
He discovered the phenomenon of wax+jello brain.
|
|
|
What are contusions?
|
They are closed-head injuries that involve damage to the cerebral circulatory system. These damages can produce internal hemorrhaging, which results in a hematoma.
|
|
|
How are contusions formed?
|
They are typically formed when the brain slams against the inside of the skull. Blood from such injries can accumulate in the subdural space and severely distort the surrounding neural tissue.
|
|
|
What is the subdural space?
|
The space between the dura mater and arachnoid membrane.
|
|
|
What is a contrecoup injury?
|
The phenomenon where contusions occur frequently on the side of the brain opposite the side struck by a blow between the blow causes the brain to strike the inside of the skull on the other side of the head.
|
|
|
What forms a diagnosis of concussion?
|
This is diagnosed when there is a disturbance of consciousness following a blow to the head and there is no evidence of a contusion or other structural damage.
Symptoms often includes loss of consciousness, headaches, dizzy, nausea, amnesia, and confusion. |
|
|
It is commonly assumed that concussions entail a temporary disruption of normal cerebral function with no long-term damage. What shows that this is false?
|
The punch-drunk syndrome.
|
|
|
What is Punch-drunk syndrome?
|
This is the dementia and cerebral scarring that is observed in boxers and other individuals who experience repeated concussions. E.g. boxers who experience many hard blows on the head can later develop this syndrome signifies by general intellectual deterioration.
|
|
|
Most people recover from a concussion just fine, however, there are the unlucky 15%. What happens to them?
|
This 15% of the population can experience what is called the post-concussive syndrome. Its symptoms include headaches, lethargy, mental dullness (cannot think as clearly), depression. This usually occurs several months after the initial concussion.
|
|
|
What happens during a head injury?
|
1) Shearing and stretching of white matter.
2) Holbourn suggests that layers of brain slide over each other 3) axons twisted, torn, broken, cell bodies disrupted, blood vessel damage 4) Loss of consciousness 5) Strain tissue in brain stem (ANS disrupted) 6) RAS dysfunction |
|
|
What are the two main types of brain infections? and what is the brain's typical response?
|
Bacterial infections
Viral infections Inflammation of the brain is common - encephalitis |
|
|
What happens when ones brain is infected by bacteria?
|
Formation of cerebral abscesses - pockets of pus in the brain.
Often attack and inflame the meninges - meningitis. |
|
|
What is Syphilis?
|
This is one bacterial brain infection that is passed by contact of genital sores. Infectin bacteria go into a dormant stage for several years, then become virulent after several years. Causes insanity and dementia that is called general paresis.
|
|
|
What are the two types of viral brain infections?`
|
1) Viruses that have a particular affinity for neural tissue
2) Viruses that attack neural tissue but has no greater affinity for it than for other tissues. |
|
|
What is an example of retrovirus?
|
Rabies
This is a virus in saliva of animals and they travel cell-by-cell via peripheral nerves to the brain. |
|
|
What is West Nile Virus?
|
a virus that is spread by mosquito bites, especially mosquitoes that has bitten a bird.
|
|
|
What are mumps and herpes?
|
These are examples of viruses that can attack the nervous system but has no special affinity for it. They usually attack other tissues of the body.
|
|
|
What is toxoplasmosis?
|
This is a parasitic brain infection that is also caused by a parasite called toxoplasma gondii. It mainly resides in cat and cats feces. Eating uncooked meat can also be infected. IT is usually dormant in an individual, but activated when immune system is weak such as HIV. This parasite formulates why "pregnant women should not clean kitty's litter box". This parasite forms cysts in the brain.
|
|
|
What is Cysticerosis?
|
This is a parasitic brain infection caused by the larvae of Taenia solium in uncooked pork. This tapeworm larvae migrate and form cysts in the brain and leave calcifications behind called "brain sand". Symptoms involves seizures, headaches, encephalitis, swelling and confusions once parasites die.
|
|
|
What are the symptoms of Parkinson's Disease?
|
resting tremor, slurred speech, facial dullness, regidity (causes shuffling gait), brady kinesia (slow movements). and less commonly, dementia.
|
|
|
What is the pathology of Parkinson's Disease?
|
Degeneration of neurons in the brain specifically severe in the substantia nigra that projects via the nigrostriatal pathways to the striatum of the basal ganglia. These neurons mostly produce dopamine. Brain can make up for low dopamine level until 80% of those neurons are lost, symptoms appears.
|
|
|
What is the treatment for Parkinson's Disease??
|
The treatment involves administration of levodopa (L-dopa), which is dopamine precursor. They can cross the BBB while pure dopamine cannot. However, L-dopa only helps for a while, prolonged usage does not cure Parkinson's and patients eventually do not respond to L-Dopa.
|
|
|
What are the side effects of L-Dopa?
|
freezing (unable to move)
dyskinesia (involuntary movement) On-off phenomenon - alternating state between the two. |
|
|
When L-Dopa doesn't help, what other treatments are given to Parkinson's patient?
|
1) lesion of the globus pallidus or subthalamic nucleus (helps movement, and reduce tremors) - pallidotomy
2) electrode implantation - which can be turned on/off with a switch. This is also called Deep Brain Stimulation, helps to reduce tremor-like symptoms. |
|
|
What are Lewy Bodies?
|
These are clumps of protein found during autopsy of Parkinson Patients. They are found in the surviving dopaminergic neurons of the substantia nigra
|
|
|
Describe the MPTP model of Parkinson's Disease
|
A street drug (new heroin) caused parkinson's-like symptoms overnight in young adults. This drug was contaminated with chemicals that selects specific neurons in brain the kill - selective neurotoxin. This drug allows us to develop animal models of parkinson's to test for potential treatments, such as MPTP monkeys.
One MPTP victim had dopamine neurons grafted into nigrostriatal pathway and his symptoms improved. |
|
|
How is the MPTP patients different from natural Parkinson' patients?
|
MPTP causes' for Parkinsons invovles externally administering selective neurotoxins, whereas natural Parkinson's patients cause is some internal disruption in neuro-mechanics.
|
|
|
Comment of the genetics of Huntington's Disease
|
It is 100% genetics related. It is passed on from generation to generation by a single dominant gene. Therefore, all individuals who carry the gene develop the disorder.
|
|
|
Comment on the inheritance of Huntington's Disease
|
This disease can be easily passed on because the age of onset is about 40 years old, often just passed the reproductive years.
|
|
|
Comment on the course of Huntington's Disease
|
The first motor signs of Huntington's disease are often increased fidgetiness. Often develops into rapid complex jerky movements of entire limbs. This is followed by motor and intellectual deterioration (dementia) and disables the individual to perform self care (feeding, bowel control).
There is no cure and death is typical after 15 years of first symptom onset. |
|
|
Comment on the brain damage in Huntington's Disease
|
The mutated that cause Huntington is called huntingtin and it makes Huntingtin protein. Huntingtin protein is found all over the brain but specifically damage to the striatum and cerebral cortex.
Striatum for movement. and Cortex for cognition. |
|
|
What is Multiple sclerosis?
|
An autoimmune disorder in which the body's immune system attacks the myelin of axons, causing scarring or hardening (sclerosis) of the brain. Symptoms involves sensory disturbances, ataxia, tremor, numbness, weakness etc.lo
|
|
|
Who is Alois Alzheimer?
|
In 1906, he presented a case of a 51 years old woman with severe memory loss and behavioral disturbances.
|
|
|
What did Alois Alzheimer find in the "interesting patient's" brain?
|
Intracellular: found neurofibrillary tangles - threads of "tau protein" in neural cytoplasm
Extracellular: found amyloid plaques - deposits of "beta-amyloid protein" and scar tissue in degenerating neurons |
|
|
Comment on the diagnosis of Alzheimer's Disease
|
Patients are typically only diagnosed with "dementia" because Alzheimer's can only be diagnosed during autopsy with the presence of the following:
1) Neurofibrillary tangles - thread |
|
|
What are the symptoms of Alzheimers?
|
It is progressive and is characterized by a selective decline in memory initially. Its intermediate stage involves confusion, irritability, anxiety and deterioration of speech.
|
|
|
Where are the neurofibrillary tangles and amyloid plaques found most in an Alzheimer's patient's brain?
|
They are particularly prevalent in medial temporal lobe structures such as the entorhinal cortex, anygdala, hippocampus. Structures that are involved in various aspects of memory. Also prevalent in the inferior temporal cortex, posterior parietal cortex and prefrontal cortex - areas that mediate complex cognitive functions.
|
|
|
What is the primary hypothetical cause of Alzheimer's disease?
|
The cholinergic hypothesis states that Alzheimer's disease is caused by a decreased in acetylcholine levels because this declines is one of the earliest neurochemical changes appearing in patients, typically in middle and late stages (not the cause). Current treatment includes Ach agonist (Aricept)
|
|
|
What are the current researches on Alzheimers Disease focus on?
|
why do Tau proteins (neurofibrillary tangles) and amyloid plaques form? which one forms first?
|
|
|
What is anterograde degeneration?
|
The degeneration of neuron in the distal segment - the cut and the synaptic terminal.
Occurs quickly after axotomy, distal segment becomes badly swollen in a few hours, removed from metabolic center, breaks into fragments within a few days. |
|
|
What is retrograde degeneration?
|
The degeneration of neuron in the proximal segment - the segment of a cut axon between the cut and the cell body.
Degeneration progresses back to the cell body. In 2 or 3 days major changes takes place. Increase in size means regenerative, decrease means degenerative changes (apoptosis and/or necrosis). |
|
|
What is transneuronal degeneration?
|
Degeneration of neurons that spreads from damaged neurons to neurons that are linked to them by synapses
|
|
|
Name the three stages of neuron degeneration followed by Axotomy
|
1) Axotomy
2) Anterograde Degeneration 3) Retrograde Degeneration 4) Transneuronal Degeneration |
|
|
What is retrograde transneuronal degeneration?
|
The degeneration of a neuron that synapsed onto a damaged neuron.
|
|
|
What is anterograde transneuronal degeneration?
|
The degeneration of a neuron that was synapsed onto by a damaged neuron.
|
|
|
What kind of damage of nerves in the PNS gives the best prognosis?
|
When a nerve is damaged without severing the Schwann cell sheaths e.g. by crushing, individual axons can follow the myelin to their original targets at a rate of a few mm per day.
|
|
|
What kind of damage of nerves in the PNS gives the worse prognosis?
|
When a nerve is damaged and the severed ends of the Schwann cell sheaths are widely separated, there is typically no functional regeneration, only a tangled mass around the proximal stump where the neuron ultimately die.
|
|
|
What kind of damage of nerves in the PNS often leads to the connection of incorrect nerves?
|
When a nerve is damaged and the severed ends of teh Schwann cell sheaths are slightly separated, individual axons often regenerate up incorrect sheaths and reach incorrect targets.
|
