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Systems Pathology: week 1
Pathologies of the CNS
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Tuesday
Dr. Taylor mentioned that there will be a few changes to his course that he is trying this trimester. First from 10% to 20% of the tests will be based on material cover in class only. Also he is asking that people who contribute to class hand in note cards at the end of class. The cards will then be tallied up and contributing students will be given 5 bonus points added to their final exam score.
Old tests are of course permitted for this class if you didn't already know and I would very much encourage that.
Wednesday
Age group ----------- Classification
Neonate ---- birth to 1 month
Infant ----- 1 month to 2 years
Child ------ 2 years to puberty
Adolescent - 10 years to maturity (19 years)
Adult ------ beyond age 19
The CNS has 11 listed unique featurtes:
Neurons don't regenerate.
Intolerance for low O2 and glucose.
Localization of function.
Absense of Lymphatic drainage.
Uniqu circulatory pattern.
presence of blood brain barrier.
Presence of CSF.
Muted immune response.
specialized cell injury function.
limited known cortical function.
CNS encasement within bone. The fact that the skull is encased in bone allows for a great deal of protection as well as unique pathologies. Being encased in bone is the most unique factor and is the reason for many pathologies.
The number one factor in CNS pathologies is space occupying lesions. The top three space occupying lesions are:
Edema
Hemorrhage
Abnormal tissue growth - tumors
Thursday
Neurons reaction to injury
Liquefactive Necrosis - the fluid remains of necrotic tissue that was digested by enzymes.
Pyknosis - Nuclear contraction and clumping of the chromasomes.
Karyorrhexis - a degenerative cellular process involving fragmentation of the nucleus and the breakup of the chromatin into unstructured granules.
vasogenic edema - the accumulation of extracellular fluid.
Whenever there is damage in the brain there is inevitably inflamation leading to edema. Because the brain is encased in bone edema is vary serious and often lethal. In the brain there is no aerobic glycolisis therefore there is no change in PH when a neuron is damaged. This means that when the proteins breakdown a neuron there is no change in the PH to limit the breakdown by the enzymes of the damaged neurons. This leads to increased edema. The process of neuron degradation begins with a healthy cell. Next the cell undergoes pyknosis, then karyorrhexis, then, finally, karyolysis which is the dissolution of the nucleus of the cell.
Clinical indications of increased ICP (intracranial pressure).
vomiting - this is projectile and often comes without warning or injury. This is often an indication of medullary injury.
Headache - variable symptamology. This is often an indication of blood vessel injury or meningeal inflamation.
Papilledema - Visual disturbance. May indicate optic disc formation.
Loss of consciousness.
Friday
Signs and symptoms of brain damage.
- focal deficits - This is often seen in very localized functional impairment. For example there may be loos of sensation over one dermatome or another. There may be loss of vision or a hand that is spasming.
- non-localizing deficits - the effects of the damage are located throughout the body and not limited to just one place.
- Decorticate Posturing - There is lack of cortical activity. The patients legs are straight, but their hands are balled into fists and their arms are bunched up to their chests.
- High brain injury - there is extreme spasm. The hands and feet are spayed out and the back and neck are arched back.
- Opisthotonus - the neck and back are arched and the heals are bent back.
The brain is made up of three different volumes. the brain is 80%, CSF is 8%, and blood is 12%. There is a lot of cushioning in the skull for increased pressure. When there is increased pressure the brain is not displaced, but the blood volume in the brain is the first to be displaced to some degree to accomodate the increase of volume and to help alleviate pressure. However, when the ICP of the brain continues to 4x normal the Cushing reflex begins to take effect.
Cushing reflex
The Cushing Reflex is characterized by
Systemic hypertension
Bradycardia (slower heart rate)
Apnea Cheyne Stokes crescendo (a cyclic form of breathing whereby the person will start inhaling and exhaling more and more rapidly for about 30 seconds to a minute and then stop. There will be a pause and then the person will take in a deep breath and start the cycle over again).
The cushing reflex can be summarized as follows:
increased ICP
cerebral blood flow then decreases leading to Ischemia
Ischemia stimulates the vasomoter center located in the brainstem
there is an increase in systemic blood pressure. The cardioinhibatory center of the brain is stimulated to slow the heart rate.
Bradycardia ensues and the respiratory rate increases. There is then an increase in systemic cerebral blood pressure.
The respiratory rate decreases leading to Hypocapnia (deficiency of CO2 in the blood.
cerebral systemic vasodilation to increase oxygen to the brain. The total fluid flow in the brain then collapses leading to global ischemia, which is then fatal very soon after.
Decreased blood flow decreases PH. The vascular system is controlled localy adn therefore overrides any neurological control. Lactic acid formation from decreased blood flow stimulates vasodilation at the local level.
Frank Starling Law of the Heart - the force of contraction of the cardiac muscle is proportional to its initial length. The energy set free at each contraction is a simple function of cardiac filling. When the diastolic filling of the heart is increased or decreased with a given volume, the displacement of the heart increases or decreases with this volume. | |