Term
A health condition that involves the Nervous System |
|
Definition
|
|
Term
|
Definition
|
“disease of the brain” generally in its entirety (both cerebral hemispheres). i.e., metabolic encephalopathy
|
|
|
Term
|
Definition
|
“disease of the spinal cord” i.e, compressive myelopathy (tumor, disc, etc causing weakness, sensory loss, spasticity below the level of compression)
|
|
|
Term
|
Definition
|
: “disease of the nerve root(s)” i.e., any process affecting a single or multiple nerve roots at cervical, thoracic or lumbar or sacral level
|
|
|
Term
|
Definition
|
“disease of a nerve” (one is mononeuropathy or neuropathy, several individual is mononeuropathy multiplex, and many/diffuse is polyneuropathy peripheral nerves. Dysfunction of a single cranial nerve = cranial mononeuropathy)
|
|
|
Term
|
Definition
|
“primary disease of muscle”
|
|
|
Term
|
Definition
|
|
Term
________: Implies a group of mental processes that includes attention, memory, learning, reasoning, problem solving,, decision making (processing, applying knowledge and adjusting).
Is generally bi-hemispheric in nature
Critical task it to separate
reversible from irreversible
causes
|
|
Definition
|
|
Term
| What are mental status changes? |
|
Definition
| altered content of consciousness or level of consciousness |
|
|
Term
|
Definition
| muscle weakness but not complete paralysis |
|
|
Term
|
Definition
|
|
Term
|
Definition
| dealing with brachial/lumbosacral plexus |
|
|
Term
| If the pt has weakness where are you thinking there may be damage? |
|
Definition
| Precentral gyrus or corticospinal tract |
|
|
Term
|
Definition
|
|
Term
| Where will thalmis lesions cause numbness? |
|
Definition
|
|
Term
| Where would cortical lesions cause parasthesias? |
|
Definition
|
|
Term
|
CHARACTERIZED BY DIFFICULY WITH INITIATION OF GAIT (FEET “GLUED TO THE FLOOR”)
|
|
Definition
|
|
Term
|
BASAL GANGLION DYSFUNCTION (PARKINSON DISEASE); GAIT IS CHARACTERISTICALLY SLOW, SHUFFLING, FLEXED POSTURE, BRADYKINETIC… TURNING 180 DEGREES TAKES EXTRA STEPS.
FESTINATION (CAN’T STOP FORWARD PROGRESS ONCE ENGAGED |
|
Definition
|
|
Term
|
WIDE-BASED UNSTEADY GAIT (LOOKS LIKE A PERSON ENEBRIATED)
|
|
Definition
|
|
Term
|
HEMIPARETIC GAIT (STIFF, CIRCUMDUCTION, OVEREXTENDED LEG)
|
|
Definition
| UNILATATERAL CORTICOSPINAL TRACT DISEASE |
|
|
Term
|
(Ex:MYELOPATHY); both legs stiff, spastic gait, sometimes with scissoring motion of each leg around the other
|
|
Definition
| Bilateral corticospinal tract disease |
|
|
Term
|
Definition
| walk around without looking and if u fall u have a positive romberg sign |
|
|
Term
|
A 50 year old man presents to your emergency room with a 6 day history of numbness and tingling from his mid chest area down both legs. When he flexes his neck forward he perceives an electrical shock like sensation down his back and into his arms.
Exam shows mild weakness in both legs generally (4.5/5) and decreased sensation to pinprick below his nipples, and in his lower chest, abdomen and legs. Reflexes are brisk in his legs , and planter responses are extencasorbilaterally.
Which of the following best describes his clinical syndrome?
A.Encephalopathy
B.Myelopathy
C.Radiculopathy
D.Neuropathy
E.Myopathy
|
|
Definition
|
|
Term
|
A 76 year old woman, with 6 year history of diabetes mellitus comes to your clinic because of severe pain.
The pain is sharp and burning, begins in her medial scapular region, radiates around her trunk to beneath her right breast.
The pain is not exacerbated with breathing, but is uncomfortable, in this area, to touch
She takes oral hypoglycemic medication. She has seen several specialists, including a cardiologist and gastroenterologist, but no diagnosis was forthcoming.
On your examination, her general examination is unremarkable, and there is no skin rash.
Neurologic exam is normal except for severe discomfort to touch under her right breast and below her right scapula (about 2-3 cm. in height from mid thoracic spine posteriorly to the lower sternum anteriorly.
What best describes the localization of her pain syndrome?
A.Encephalopathy
B.Myelopathy
C.Radiculopathy
D.Neuropathy
E.Plexopathy
|
|
Definition
|
|
Term
| What is Gerstmann Syndrome? what are the symptoms? |
|
Definition
Left posterior hemispheric lesion
R-L confusion
Inability to recognize fingers
Agraphia (inability to write)
Acalculia (Inability to write) |
|
|
Term
|
Definition
Olfaction
test each nostril for smell fragrance |
|
|
Term
|
Definition
Optic nerve
Check visual fields and acuity. fundoscopic exam |
|
|
Term
|
Definition
Asymmetric pupils
Anisocoriaindicates a lesion in the efferent fibers (away from the brain) supplying the pupillary sphincter muscles.
can indicate problem with CN III
|
|
|
Term
| How do you tell which pupil has the problem when they are asymetric? |
|
Definition
|
The smaller pupil is abnormal when the degree of anisocoria is greatest in darkened settings, while the larger pupil is abnormal when the degree of anisocoria is greatest in bright light.
|
|
|
Term
|
Definition
|
droopy eyelid (ptosis) plus constriction of pupil of eye; SMALL pupil is the abnormal one and due to lesion of Sympathetic tract
|
|
|
Term
| What nerves does the pupillary light reflex test? |
|
Definition
|
|
Term
| An eye movement abnormality in which the two eyes move conjugatelybut have limited movement in one direction is called a _____ |
|
Definition
|
|
Term
|
Definition
| neurons are not activated by voluntary or reflexes. |
|
|
Term
|
Definition
| voluntary gaze is impaired but reflexes can still activate neurons. |
|
|
Term
|
_______ lesion is manifest by impaired adduction on affected side, accompanied by nystagmus in the other, abducting eye. one eye cant look one way.
|
|
Definition
|
|
Term
|
Definition
test facial sensation by touching with cotton. 3 branches, ophthalmic, maxillary, and mandibular
also involved in the muscles of mastication |
|
|
Term
| What does cranial nerve VII do? |
|
Definition
| controls fascial muscles and taste of tongue |
|
|
Term
|
________: a peripheral weakness or paralysis of one side of the face causing a facial droop; drooling, eye issues with tearing (excessive, dry eye); loss of taste, pain behind ear, increase sensitivity to sound
A facial nerve (Cr N VII) lesion
|
|
Definition
|
|
Term
| What does cranial nerve VIII do? |
|
Definition
Vestibular nerve
hearing, balance |
|
|
Term
| Unilateral weakness of muscles of the palate, pharynx, or larynx indicates a _______ |
|
Definition
|
|
Term
|
______ can result from any condition that damages motor control of the structures necessary for speech production, including cerebellar or basal ganglia disorders, and the specific characteristics of the ______ may be useful in localization and differential diagnosis.
|
|
Definition
|
|
Term
|
Definition
| head rotation or shoulder elevation |
|
|
Term
| What is tongue weakness a sign of? |
|
Definition
|
|
Term
|
Definition
|
= weakness of BOTH LOWER extremities
|
|
|
Term
|
DTR’s _______ in Central nervous system (CNS) lesions
DTR’s _______ or absent in Peripheral Nervous System
Options: increase or decrease
DTR= deep tendon reflex
|
|
Definition
|
|
Term
| Often distal weakness suggests a disease of _______ |
|
Definition
|
|
Term
_______ maneuver is distracting patient in order to achieve relaxation and better facilitate the reaction
|
|
Definition
|
|
Term
| What are the main causes of status epilepticus? |
|
Definition
| Medication or drug withdrawl or stroke. |
|
|
Term
|
Definition
|
|
Term
|
PATIENT WITH HEAD TRAUMA PLUS HEADACHE OR ALTERED MENTAL STATUS OR FOCAL FINDING ON EXAM
what do u do?
|
|
Definition
| order enhanced CT followed by frequent neurological evaluations. |
|
|
Term
Chronic Alcohol Abuse Patients with Poor Nutritional Intake; need to give __1___. They will present with :
1. Apathetic – confused state
2. Ophthalmoplegia (eye paralysis); or Nystagmus
3. Gait ataxia
This triad of symptoms is known as ___2____
|
|
Definition
Thiamine
Wernicke's encephalopathy |
|
|
Term
|
Definition
| When myesthenia gravis causes muscle weakness that interferes with vital functions like breathing and swallowing. |
|
|
Term
|
Definition
|
Acute inflammatory demyelinating polyneuropathy
Rapidly progressive demyelinating polyneuropathy |
|
|
Term
|
Definition
Image of the ventricular system within the brain by draining the cerebrospinal fluid (CSF) out of the subarachnoid space by Lumbar Puncture, and replacing it with air |
|
|
Term
|
Definition
CONTRAST MATERIAL INJECTED INTO THE SPINAL SUBARACHNOID CANAL |
|
|
Term
|
Definition
direct injection of contrast
material into the carotid artery |
|
|
Term
| What does PET scan measure? |
|
Definition
| glucose metabolism at the cellular level. |
|
|
Term
| What artery supplies the Broca speech area? |
|
Definition
|
|
Term
| What artery supplies the lower limb sensorimotor cortex? |
|
Definition
|
|
Term
| What artery supplies the visual cortex? |
|
Definition
|
|
Term
| What artery supplies the posterior limb of internal capsule? |
|
Definition
| Medial cerebral artery and ventral part of anterior choroidal |
|
|
Term
| What artery supplies the dorsolateral part of rostral medulla? |
|
Definition
| ventral or posterior inferior cerebellar artery |
|
|
Term
| What artery supplies the anterior and lateral funiculi of spinal cord? |
|
Definition
|
|
Term
| Why does the brain use so much energy? |
|
Definition
| maintaining ionic gradients |
|
|
Term
| What is the normal blood glucose range? |
|
Definition
|
|
Term
| _____ signals to store glucose |
|
Definition
|
|
Term
| _____ signals to use glucose. |
|
Definition
|
|
Term
| How does glucose enter cells? |
|
Definition
| GLUTs that allow for facilitated difussion. |
|
|
Term
| An enzyme with a high Km has a ____ affinity for the substrate |
|
Definition
|
|
Term
| An enzyme with a low Km has a ____ affinity for the substrate |
|
Definition
|
|
Term
| What tissue type in GLUT2 seen in and what is its Km? |
|
Definition
|
|
Term
| What tissue type in GLUT1 seen in and what is its Km? |
|
Definition
|
|
Term
| What tissue type in GLUT4 seen in and what is its Km? |
|
Definition
|
|
Term
| What tissue type in GLUT3 seen in and what is its Km? |
|
Definition
|
|
Term
| GLUT_ is regulated by insulin |
|
Definition
| 4, since it is in muscle and fat cells |
|
|
Term
| _____ can replace 75% of glucose in the brain during starvation. |
|
Definition
|
|
Term
| Ketone bodies are produced from _____ |
|
Definition
|
|
Term
| (T/F) fat can be converted to glucose? |
|
Definition
| F. Fat is turned into ketone bodies to run metabolism. |
|
|
Term
| What organ turns Acetyl-CoA into ketone bodies? Why not send the Acetyl-CoA to the brain? |
|
Definition
| Liver. Too big to get through BBB. |
|
|
Term
| Venous sinuses all drain into ______ |
|
Definition
|
|
Term
| ________ is a division of the autonomic nervous system that controls gastrointestinal motility and secretions. Functions independently of CNS usually. |
|
Definition
|
|
Term
The parasympathetic NS has a ____ preganglionic and a ____ postganlionic neuron
choices :Long or short |
|
Definition
The parasympathetic NS has a long preganglionic and a short postganlionic neuron
|
|
|
Term
The sympathetic NS has a ____ preganglionic and a ____ postganlionic neuron
choices :Long or short |
|
Definition
The parasympathetic NS has a short preganglionic and a long postganlionic neuron
|
|
|
Term
| in parasympathetic NS what is the neurotransmitter used in the preganglionic and postganglionic synapses. |
|
Definition
|
|
Term
| in sympathetic NS what is the neurotransmitter used in the preganglionic and postganglionic synapses. |
|
Definition
Acetylcholine neurotransmiFer at preganglionic synapse, norepinephrine at postganglionic synapse because its faster |
|
|
Term
| What are splanchnic nerves? |
|
Definition
| nerves that innervate organs. most but not all are sympathetic. |
|
|
Term
| what are the only splanchnic nerves that carry parasympathetic fibers? |
|
Definition
|
|
Term
Lower motor cellbodies for the head and neck are located in the ______ |
|
Definition
|
|
Term
Lower motor cellbodies for the body are located within the ______ |
|
Definition
| ventral horn of the spinal cord |
|
|
Term
| What enzyme takes choline + acetyl-CoA-> Acetylcholine |
|
Definition
|
|
Term
How is the formation of acetylcholine powered? |
|
Definition
| The thioester bond in Acetyl-CoA is broken giving off energy. |
|
|
Term
Deficiency of choline interferes with lipid processing and leads to _______ |
|
Definition
|
|
Term
| 90% of the bodies serotonic is found in the ______ |
|
Definition
|
|
Term
| What enzymes makes seratonin? What is the building block? |
|
Definition
Tryptophan hydroxylase (Adds OH) and 5-hydroxytryptophan decarboxylase (Removes CO2)
Tryptophan |
|
|
Term
What type of synapse is this?
Gap junctions
Fast bidirectional
group control
Channels are large and unselective |
|
Definition
|
|
Term
| Where are vessicles made? |
|
Definition
|
|
Term
| What happens when a synapsin is non-phosphorylated? |
|
Definition
| the synapsins bind the vessicles to actin filaments keeping them in the cytosol. |
|
|
Term
| What happens when a synapsin is phosphorylated? |
|
Definition
| the synapsins release vessicles allowing them to move into the active zone and be released. |
|
|
Term
| What causes synapsins to be phosphorylated? |
|
Definition
| Ca entry into presynaptic cell. |
|
|
Term
|
Definition
| help the vessicles target the docking sites. |
|
|
Term
| What is the SNARE complex used for? |
|
Definition
| docking and priming of the vessicles |
|
|
Term
| _____ and ______ are used to dock the vessicle to the presynaptic membrane. |
|
Definition
| Synaptobrevin (VAMP) , SNAP-25 and syntaxin |
|
|
Term
| _____ is required for exoxytosis of synaptic vesicles. Elimination of this will prevent vesicle fusion. |
|
Definition
|
|
Term
| Clostridial neurotoxins cleave _____ proteins. |
|
Definition
|
|
Term
| Tetanus targets and cleaves _____ |
|
Definition
|
|
Term
| Botulimum toxin A cleaves ______ |
|
Definition
|
|
Term
| Botulimum toxin B cleaves ______ |
|
Definition
|
|
Term
| Botulimum toxin C cleaves ______ |
|
Definition
|
|
Term
|
Definition
A spider toxin that generates massive vesicle depletion and transmitter release by binding to neurexin, which is a similar to syntaxin. vessicles get stuck and it depletes the terminal. |
|
|
Term
The binding of Ca2+ and ______ triggers the fusion with the terminal membrane and release of the neurotransmitter for fast synaptic transmission. |
|
Definition
|
|
Term
|
Definition
|
|
Term
| Uptake of glutamate uses _____ exchange |
|
Definition
|
|
Term
| Neurotransmitters other than gluamate use ______ exchange for uptake. |
|
Definition
|
|
Term
| Seratonin is degraded by ___ |
|
Definition
|
|
Term
| What is Lambert-Eaton syndrome? |
|
Definition
| autoimmune disease where you make antibodies against voltage gated Ca channels in the presynaptic terminals. Neurotransmitter is not released. |
|
|
Term
|
Definition
• Ligand-gated: a molecule binds to the receptor and opens the channel that is part of the receptor.
• The neuromuscular junction is the classic example. |
|
|
Term
|
Definition
• The receptor is a separate protein from the ion channel.
• The receptor activates a G-protein that will work directly or through an intermediate effector to change the ion channel. |
|
|
Term
|
Definition
| stimulates (increases) cAMP |
|
|
Term
|
Definition
| Inhibits (decreases) cAMP |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
| Signals the release of Ca from the ER that binds to calmodulin and can activate enzymes. |
|
|
Term
Is this Ionotropic or Metabotropic?
– Much slower
– Activate diffusable second messengers
– More widespread action
– Can open or close channels.
– Usually does not lead directly to action potentials
– Modulatory effect on synaptic action |
|
Definition
|
|
Term
Ionotropic or metabotropic?
– Simpleon/offs witch for opening channels
– Excite or inhibit neuronal firing
– Local action |
|
Definition
|
|
Term
| What type of receptors are muscarinic? |
|
Definition
| G-protein coupled receptors |
|
|
Term
ACh activates muscarinic receptors to stimulate a G- protein that activates the ____ channel. |
|
Definition
GIRK (G-protein inward rectifier K channel)
Opening this allows K to leave the cell and it hyperpolarizes. Used to slow the heart. |
|
|
Term
| What is the formula for calculating membrane length constant? |
|
Definition
|
|
Term
| How do u calculate the membrane time constant? |
|
Definition
|
|
Term
| What is the membrane time constant? |
|
Definition
| Time required to charge the membrane |
|
|
Term
For the best nerve condution you want a __1__length constant and a __2___ time consant.
Choices: big, small |
|
Definition
|
|
Term
How does myelination affect neurons in terms of :
Rm, Ri, Cm |
|
Definition
| Myelination increases the Rm and reduces the Cm. |
|
|
Term
How does thick axons affect neurons in terms of :
Rm, Ri, Cm |
|
Definition
|
|
Term
| What cells produce myelin in the periphery? |
|
Definition
|
|
Term
| What cells produce myelin in the CNS? |
|
Definition
|
|
Term
| What is saltatory conduction? |
|
Definition
| gaps in myelin where there is lots of Na channels that acts as booster stations. |
|
|
Term
What are the gaps between the myelin called?
These are used in saltatory conduction |
|
Definition
|
|
Term
| What happens in a demyelinating disease to the action potentials? |
|
Definition
| K channels get exposed and it allows for the membrane potential to be hyperpolarized. |
|
|
Term
| What is the vertical sheet of dura called that separates the hemispheres of the cerebrum? |
|
Definition
|
|
Term
| What is the horizontal sheet of dura separating the cerebrum and the cerebellum called? |
|
Definition
|
|
Term
|
Definition
|
|
Term
| What is the path called that connects the lateral ventricles to the third ventricle? |
|
Definition
|
|
Term
| What is the name of the path that connects the third ventricle to the fourth? |
|
Definition
|
|
Term
|
Definition
| Arachnoid Villi superior sagital sinus |
|
|
Term
| What is the major difference between CSF and plasma? |
|
Definition
| CSF has less large proteins due to the Blood-CSF barrier. |
|
|
Term
| What type of epithelium is the BBB? |
|
Definition
| Tight junction endothelium |
|
|
Term
| does an epidural hematoma involve a vein or artery? |
|
Definition
|
|
Term
| Does a subdural hematoma involve an artery or vein? |
|
Definition
|
|
Term
| Does a subarachnoid hematoma involve an artery or vein? |
|
Definition
|
|
Term
__ system amino acid transporter moves large neutral AA with branced or ringed side chains through the BBB.
Choices: ASC, A, L |
|
Definition
|
|
Term
___ system moves glycine and other neutral amino acids with short linear or polar side chains through the BBB. Energy dependent, Na+ dependent. Limits glycine within spinal cord and glutamate within brain. Powered by Na+/K+ -ATPase
Choices: ASC, A, L |
|
Definition
|
|
Term
ASC system is also energy dependent and moves alanine, serine, and cysteine.
Choices: ASC, A, L |
|
Definition
| ASC because it moves Alanine, Serine and Cysteine |
|
|
Term
|
Definition
an increase in volume of brain Issue, blood, CSF or other brain fluids will produce an increase in intracranial pressure because the bony calvarium fixes the total cranial volume. |
|
|
Term
| What is vasogenic brain edema? |
|
Definition
• This is caused by increased permeability of brain capillary endothelial cells which leads to increased volume of extracellular fluid.
• More swelling occurs around white maZer than gray maZer because fluid tends to accumulate along fiber tracts which are hydrophobic. |
|
|
Term
|
Definition
| injured neurons, glia, or endothelial cells swell. |
|
|
Term
| What is hydrocephalus and what are the 3 ways it is caused? |
|
Definition
increase in volume of thecerebral ventricles.
Oversecretion of CSF
impaired absorption of CSF
obstruction of CSF pathways |
|
|
Term
| The dura above the tentorium is innervated by the _____ nerve |
|
Definition
|
|
Term
| What are afferent signals? |
|
Definition
|
|
Term
|
Definition
| folding of neural plate into a closed tube of ectoderm |
|
|
Term
| When is the formation of neural plate? |
|
Definition
|
|
Term
| when do the neural folds elevate? |
|
Definition
|
|
Term
| when is the fusion of neural folds? |
|
Definition
|
|
Term
| when does the cranial neuropore close? |
|
Definition
|
|
Term
| when does the caudal neuropore close? |
|
Definition
|
|
Term
| what is anencephaly and what causes it? |
|
Definition
failure to develop brain
Results from failure to close anterior neuropore |
|
|
Term
| What causes spine bifida? |
|
Definition
| incomplete closure of the embryonic neural tube. |
|
|
Term
|
Definition
| form of spina bifida with protrusion of meninges |
|
|
Term
|
Definition
| form of spina bifida with protrusion of meninges and spinal cord |
|
|
Term
|
Definition
| form of spina bifida with an open neural tube. |
|
|
Term
| Neural tube defects can be prevented with ______ |
|
Definition
|
|
Term
| What regions of the brain does the Diencephalon develop into? |
|
Definition
|
|
Term
| What regions of the brain does the Telencephalon develop into? |
|
Definition
|
|
Term
| What regions of the brain does the mesencephalon develop into? |
|
Definition
|
|
Term
| What regions of the brain does the Metencephalon develop into? |
|
Definition
|
|
Term
| What regions of the brain does the Myelencephalon develop into? |
|
Definition
|
|
Term
|
Definition
| incomplete closure of the choroid fissure. presents as fucked up pupils that are like pear shaped. |
|
|
Term
| what is the anterior part of the spinal cord called during development? |
|
Definition
|
|
Term
| what is the posterior part of the spinal cord called during development? |
|
Definition
|
|
Term
| What separates the alar and basal plates in the developing spinal cord? |
|
Definition
|
|
Term
| When do the Sulci and Gyru form in the cortex? |
|
Definition
|
|
Term
| The PNS develops from ______ |
|
Definition
|
|
Term
| What are neurocristopathies? |
|
Definition
| pathologies arising from tissues derived from neural crest cells. |
|
|
Term
| Innervation of the heart is from what spinal nerves? |
|
Definition
|
|
Term
|
Definition
results from a failure of neural crest migration
newborn has constipation without physical
obstruction |
|
|
Term
| Which type of MRI has a high fat signal and a low water signal? |
|
Definition
|
|
Term
| Which type of MRI has a low fat signal and a high water signal? |
|
Definition
|
|
Term
| What does a Trans Cranial Ultrasound Doppler (TCD) look at? |
|
Definition
| Looks at flow to assess vasculature |
|
|
Term
| What do u inject for a MR-angiography? (MRA) |
|
Definition
|
|
Term
| What do u inject for a 3-D CT angiogram? |
|
Definition
|
|
Term
| Where do bacteria that cause meningitis localize? |
|
Definition
| Leptomeninges (arachnoid and pia) |
|
|
Term
| Where do Polio that cause meningitis localize? |
|
Definition
| motor neurons of the spinal cord and bulbar area |
|
|
Term
|
Definition
| inflamation of the arachnoid and pia mater |
|
|
Term
|
Definition
| Inflamation of the dura mater. usually from chronic infections like chronic sinusitis or mastoiditis |
|
|
Term
| How does acute meningitis look? |
|
Definition
| creamy like someone blew their load on the brain. |
|
|
Term
| If a neonate has meningitis what bugs do you suspect? |
|
Definition
| E. Coli and group B Strept |
|
|
Term
| If a infant, 3mo-3yo, has meningitis what bug(s) do you suspect? |
|
Definition
|
|
Term
| If a adult has meningitis what bug(s) do you suspect? |
|
Definition
|
|
Term
| If a person living in a tight living space with many other people has meningitis what bug(s) do you suspect? |
|
Definition
|
|
Term
| _____ are the halmark cell of an acute infection |
|
Definition
|
|
Term
| How do u diagnose meningitis? |
|
Definition
|
|
Term
| What does it mean if the pt has lymphocytes in their CSF? |
|
Definition
| meningitis caused by TB or a fungal infection |
|
|
Term
|
Definition
| TB of the spine. Produces epidural granulomatous mass that frequently causes destruction of spinal cord from compression. |
|
|
Term
| Pick one: (Bacterial/viral) meningitis decreases the glucose levels in the CSF |
|
Definition
|
|
Term
| What is cryptococcal meningitis? |
|
Definition
| oportunistic infection in people with AIDS or a fucked up immune system. Get it from bird shit being inhaled. |
|
|
Term
| What labs would u do to test for Cryptococcal meningitis? |
|
Definition
latex cryptococcal agglutination test
encapsulated spheres with a gelatinous capsule that shows a clear halo with
India Ink stain |
|
|
Term
|
Definition
| motor neurons of the spinal cord |
|
|
Term
| where does Rabies affect? |
|
Definition
|
|
Term
| where does herpes simplex affect? |
|
Definition
|
|
Term
| where does SSPE and PML affect? |
|
Definition
|
|
Term
The classic hallmark of viral infections of the CNS is the presence of ______ involving small arteries and arterioles. |
|
Definition
| perivascular cuffs of lymphocytes |
|
|
Term
| Which is the only virus with inclusion bodies in the cytoplasm? |
|
Definition
|
|
Term
| What bug(s) has eosinophilic intranucles inclusions? |
|
Definition
|
|
Term
| What virus(s) has basophilic intranuclear inclusions? |
|
Definition
|
|
Term
| What virus(s) has basophilic intranuclear inclusions? |
|
Definition
|
|
Term
| What virus(s) has intranuclear inclusions with a ground glass appearance? Destroys oligodendrocytes |
|
Definition
|
|
Term
| How can u prevent Streptococcus pneumoniae? |
|
Definition
|
|
Term
| How do most neonates contract Streptococcus agalactae? |
|
Definition
| Contract during vaginal delivery. Women should undergo screening to check. Can be prevented by intrapartum antibiotic prophylaxis |
|
|
Term
| What diesease causes meningitis with a purplish rash? |
|
Definition
|
|
Term
| How does one usually contract Listeria monocytogenes? |
|
Definition
| Contaminated food, can grow in the fridge. Can also be passed in utero. |
|
|
Term
| How does Listeria monocytogenes move around? |
|
Definition
| ActA polymerizes actin behind the bacteria pushing it through the cytoplasm and plasma membrane. |
|
|
Term
| What should be used as an acute treatment for migraines? |
|
Definition
|
|
Term
| What is the mechanism of triptan drugs? |
|
Definition
1.Stimulate 5-HT1B receptors causing vasoconstriction
2.Reduce excitability of trigeminal nuclei in the brainstem by stimulating 5-HT1B/1D
3. inhibit inflamation by targeting pre-synaptic 5-HT1D receptors.
AKA:
1. vasoconstriction
2. trigeminal inhibition
3. decreased pain transmission. |
|
|
Term
| What is the mechanism of Ergot Alkaloids? |
|
Definition
vasoconstriction
Targets 5-HT alpha-1-adrenergic receptor. |
|
|
Term
| Explain the function of a presynaptic autoreceptor |
|
Definition
5-HTR gets stimulated which blocks the release of the neurotransmitter 5-HT
|
|
|
Term
| all triptans end in _____. |
|
Definition
|
|
Term
| Which triptan has the longest half life? |
|
Definition
|
|
Term
| which triptan has the fastest onset? |
|
Definition
rizatriptan (oral 1 hr)
sumatriptan (subcutaneous 15 mins) |
|
|
Term
| generic triptan is called? |
|
Definition
| sumatriptan, only one that can be given subcutaneously as well as oral or nasal |
|
|
Term
| What are the adverse side effects of triptans? |
|
Definition
including paresthesias, flushing, and mild, transient neck tightness or chest pressure
|
|
|
Term
| When should you not give a triptan? |
|
Definition
vascular condition like arterial vasospasm
HTN
hemiplegic or basilar migraine |
|
|
Term
| what drugs to triptans interact with? |
|
Definition
SSRIs, SNRIs
Dont give if they are on a MAO-A inhibitor |
|
|
Term
| What are the side effects of Ergot Alkaloids? |
|
Definition
nausea vomiting,
MAJOR: arterial vasoconstriction |
|
|
Term
| How long should u have between giving a triptan and an Ergot alkaloid? |
|
Definition
|
|
Term
| What drugs can you not mix Ergot alkaloids with? |
|
Definition
CYP 3A4 inibitors
anything ending in: -vir, -conazole, -romycin |
|
|
Term
| What happens if you stimulate the Beta-1 receptor? |
|
Definition
| increased heart rate and contraction force |
|
|
Term
| What happens if you stimulate the Beta-2 receptor? |
|
Definition
| relaxes/dialates the lungs uterus and blood vessels |
|
|
Term
| What happens if you stimulate the Beta-3 receptor? |
|
Definition
|
|
Term
| What do Beta-1 blockers do? |
|
Definition
| Decrease heart rate and contractions |
|
|
Term
| What do Beta-2 blockers do? |
|
Definition
| constricts lungs and arterial smooth muscle |
|
|
Term
| What do u need for a migraine? |
|
Definition
Need 2 of these 3:
Limiting activity, causea, photophobia |
|
|
Term
| What does calcitonin gene related peptide (CGRP) do? |
|
Definition
| induces headaches. Triptans reduces levels of this. |
|
|
Term
| What is central sensitization? |
|
Definition
| makes it so after one pain the next pain stimulus is easier to trigger and get a headache |
|
|
Term
Which of these is an alpha adrenergic receptor agonist?
Truptans or Ergots |
|
Definition
|
|
Term
Inhibition of neurons causes ______.
Choices: depolarization or hyperpolarization |
|
Definition
|
|
Term
| Does glutamate cause inhibition or excitation? |
|
Definition
| main excitatory neurotransmitter of the CNS. |
|
|
Term
| What uptakes glutamate out of the synaptic cleft? |
|
Definition
|
|
Term
| What happens when the NDMA glutamate channel gets stimulated? |
|
Definition
| allows Ca2+ to enter the cell. The calcium can make the postsynaptic cell release NO which can make the presynaptic cell change how much it releases. |
|
|
Term
| What happens when there is hypercalcemia in the synapse? |
|
Definition
| depreased neuromuscular excitability because Ca2+ blocks the voltage gated Na+ channels. |
|
|
Term
| What does Ca2+ do to voltage sensitive K+ channels? |
|
Definition
| When Ca2+ enters the cell, it opens them allowing K+ to leave. |
|
|
Term
| What happens when there is hypocalcemia? |
|
Definition
| increased excitability of nerve and muscle cells. |
|
|
Term
| What happens during hyperkalemia? |
|
Definition
| lots of K+ in the synapse. Voltage gated Na+ channels remain inactivated (Blocked inactivation gate) in the cell is not allowed to hyperpolarize. |
|
|
Term
|
Definition
| overactive area of the brain. |
|
|
Term
|
Definition
|
|
Term
| What are the 4 branches of generalized acute neurological events? |
|
Definition
| Toxic iscemic, complex seizure, encephalitis |
|
|
Term
|
Definition
| Transient Ischemia Attack, aka mini stroke |
|
|
Term
| What disease processes can present as a focal neurological event? |
|
Definition
| Partial seizures, strokes, TIA |
|
|
Term
| What processes can present as generalized neurological events? |
|
Definition
|
|
Term
| What is Cerebral Perfusion Pressure and what is the formula to calculate it? |
|
Definition
The driving force across the brain capillaries.
CPP=MAP-ICP
MAP=mean arterial pressure
ICP= intracranial pressure |
|
|
Term
| What happens if your arterial pressure is too low in the brain? |
|
Definition
|
|
Term
Brain arterioles ___1___ with increased blood pressure and ___2____ with lowered blood pressure.
Choices: dilate and constrict |
|
Definition
|
|
Term
Raised arterial CO2 causes brain arterioles to ___1___ and cerebral blood flow will ___2____.
1 choices: dilate or constrict
2 choices: Increase or decrease |
|
Definition
|
|
Term
Low arterial CO2 causes brain arterioles to ___1___ and cerebral blood flow will ___2____.
1 choices: dilate or constrict
2 choices: Increase or decrease |
|
Definition
|
|
Term
| What does Hypercapnia (High CO2) and acidosis do to blood flow in the brain? |
|
Definition
|
|
Term
| What does hyperventilation do to CO2 levels? |
|
Definition
| Lowers the CO2 levels which lowers the blood pressure and decrease blood flow. |
|
|
Term
Which affects blood flow to the brain more?
O2 or CO2 concentration |
|
Definition
| CO2, brain is more sensitive to CO2 |
|
|
Term
| What controls cerebral blood flow autoregulation? |
|
Definition
|
|
Term
| What controls cerebral blood flow active hyperemia? |
|
Definition
| blood flow controlled by metabolic demand |
|
|
Term
| What controls cerebral blood flow reactive hyperemia? |
|
Definition
| increased flow following a period of occlusion |
|
|
Term
| What does the law of Laplace deal with? |
|
Definition
Wall tension
Tension=(pressure)*(radius) |
|
|
Term
| What is the myogenic hypotesis? |
|
Definition
| Vascular smooth muscle around arterioles contracts when stretched. |
|
|
Term
Increase in metabolites leads to ______.
Choices dilation or contraction |
|
Definition
|
|
Term
| How does Ischemia lead to excitotoxicity? |
|
Definition
| Lack of blood means lack of O2 and glucose in the cells. This stops the Na/K ATPase and causes Na+ to build up in cells. |
|
|
Term
| How does Excitotoxicity damage neurons? |
|
Definition
| O2 deprived cells release tons of glutamate. Overactivates NMDA glutamate receptors lets in tons of Ca2+ that causes the cell to degrade. |
|
|
Term
| What does Lipid peroxidation do? |
|
Definition
| leads to free radicals that fuck up the cell and kill it. |
|
|
Term
| What is Neighborhood decay? |
|
Definition
| neighboring partially ischemic cells are unable to maintain their Na+ gradients. Without the Na+ gradient glutamate uptake doesnt work which causes excitotoxic damage and cell death. |
|
|
Term
| What is the Cushing reaction? |
|
Definition
| high intracranial pressure leads to high CO2 that increases blood flow and raises pressure even more. spiral effect. |
|
|
Term
| Pt presents with right arm and face weak. what cerebral vessel and structure are most likely affected? |
|
Definition
| Left MCA and left lateral motor cortex. |
|
|
Term
| Pt presents with aphasia and right visual field deficit. what cerebral vessel and structure are most likely affected? |
|
Definition
| Left MCA. Wernicke's area and left parietal cortex. |
|
|
Term
| Pt presents with right pure hemiparesis. what cerebral vessel and structure are most likely affected? |
|
Definition
| Left MCA. Left corticospinal tracts |
|
|
Term
| Pt presents with right leg weakness. what cerebral vessel and structure are most likely affected? |
|
Definition
| Left ACA. left Medial motor cortex |
|
|
Term
| Pt presents with right homonymous hemianopia. what cerebral vessel and structure are most likely affected? |
|
Definition
| left PCA. left visual cortex |
|
|
Term
| What is Arteriovenous Malformation? |
|
Definition
| Dilated vascular channels in the brain, these can rupture and cause subarachnoid hemorrhage |
|
|
Term
| What is a cavernous angioma? |
|
Definition
| benign neoplasia composed of large vascular spaces compartmentalized by prominent fibrous walls. |
|
|
Term
|
Definition
| focal aggregation of small vessels with innervening neural parenchyma. |
|
|
Term
| What is a venous angioma? |
|
Definition
| few large veins distributed randomly in the brain or spinal cord. |
|
|
Term
| What causes berry aneurysms? |
|
Definition
| missing tunica media in part of the blood vessel when it bifurcates. |
|
|
Term
| In __% of cases, multiple berry aneurysms are present. |
|
Definition
|
|
Term
| What are Atherosclerotic aneurysms? |
|
Definition
| biggest aneurysms seen in the brain, located in larger vessels. Atherosclerosis causes fibrous replacement of the tunica media and destruction of the internal elastic membrane. |
|
|
Term
| What is a mycotic aneurysm? |
|
Definition
| bacteria grow in an artery in the cardiac valve and it lodges itself in the middle cerebral artery where the bacteria grow and fuck up the arterial wall causing an aneurysm. |
|
|
Term
| What are Charcot-Bouchard aneurysms? |
|
Definition
| weakened walls deep inside the brain in vessel trunks (not on bifurcations) caused by HTN. Can lead to hypertensive cerebral hemorrhage. |
|
|
Term
| Where do Charcot-Bouchard aneurysms and Hypertensive intercerebral hemorrhages occur? |
|
Definition
mostly the basal ganglia thalmus
also pons and cerebellum. |
|
|
Term
| What is transtentorial herniation? |
|
Definition
| hernia causes part of one hemisphere to go into the other. |
|
|
Term
| What is an interventricular hemorrhage? |
|
Definition
| rupture of small vessel into a ventricle. |
|
|
Term
| How does a pt with a cerebellar hemorrhage present? |
|
Definition
| Bleeding into the cerebellum causes abrupt ataxia, usually severe headache and vomiting. |
|
|
Term
| red neurons are indicitive of _____ |
|
Definition
|
|
Term
Cerebral infarcts caused by embolization are ____
Choices: bland or hemorrhagic |
|
Definition
|
|
Term
cerebral infarcts caused by thrombic occlusions are chronic, largely ischemic and ____
Choices: bland or hemorrhagic |
|
Definition
|
|
Term
|
Definition
| detatched traveling mass in the blood circulation |
|
|
Term
| How are infarctions healed? |
|
Definition
| astrocytes perform astrogliosis and clean up the area creating a cyst. |
|
|
Term
| Where are the striate arteries and what happens if they get blocked? |
|
Definition
| go superior from the middle cerebral artery into the deep brain to the capsule. If blocked can cause hemiparesis or hemiplegia. |
|
|
Term
|
Definition
| inability to talk or understand language. |
|
|
Term
| what happens if there is an infarction of the trifurcation of the middle cerebral artery? |
|
Definition
| causes motor and sensory problems. If it is the dominant hemisphere (usually left) then it produces aphasias. |
|
|
Term
|
Definition
| mini strokes, getting multiple ones leads to dementia and loss of brain tissue. |
|
|
Term
What are parenchymal cells more predisosed to having damage them?
choices: atherosclerosis or HTN? |
|
Definition
|
|
Term
| what is petechiae? what causes it? |
|
Definition
| swelling of the optic nerve. malignant hypertension resulting in hypertensive encephalopathy. |
|
|
Term
| young black male presents with vomiting and is going into coma. Cell sample shows an onion skin looking arteries what is wrong? |
|
Definition
| fibrinoid necrosis from hypertensive encephalopathy. |
|
|
Term
| what normally causes fat embolism syndrome. |
|
Definition
| get a traumatic leg bone fracture then later the fat goes to the brain and occlides capillaries. |
|
|
Term
| what are subfalcine herniations? |
|
Definition
| cerebral hemisphere expannds and compresses the anterior cerebral artery. |
|
|
Term
| what is a tonsilar herniation? |
|
Definition
| pushes brainstem through foramen magnum killing you. |
|
|
Term
| what are transtential herniations? |
|
Definition
| hippocampus is pressed against the tentorium cerebelli. compresses the 3rd cranial nerve and fixes pupil dilation on the side of the lesion. |
|
|
Term
| What is a Duret hemorrhage? |
|
Definition
| lesions in the midbrain and pons usually caused by a transtentorial herniation. caused by compression of vasculature in brain stem. |
|
|
Term
|
Definition
|
|
Term
|
Definition
| formation of a blood clot |
|
|
Term
|
Definition
| mass traveling in the blood |
|
|
Term
|
Definition
|
|
Term
| list the 4 steps of hemostasis in order |
|
Definition
1. Vasoconstriction
2. Platelet actions
3. coagulation (clot formation)
4.Fibrinolysis |
|
|
Term
| what are the 4 major components of the hemostatic system? |
|
Definition
Vascular endothelium
platelets
coagulation system
fibrinolytic system |
|
|
Term
| Where is NO synthesized and what role does it play in hemostasis? |
|
Definition
| endothelial cells. Inhibits platelet adhesion and aggregation by increasing levels of cAMP |
|
|
Term
| Where is Prostacyclin (PGI2) synthesized and what role does it play in hemostasis? What inhibits its formation? |
|
Definition
| endothelial cells. vasodilator that inhibits platelet aggregation and adhesion by increasing cAMP. Same mechanism as NO. Blocked by NSAIDs and cox inhibitors. |
|
|
Term
| Where is Thrombomodulin synthesized and what role does it play in hemostasis? |
|
Definition
| endothelial cells. Binds thrombin which activates protein C that works with protein S to degrade factors V and VIII. |
|
|
Term
| Where is Tissue plasminogen activator (t-pa) synthesized and what role does it play in hemostasis? |
|
Definition
| endothelial cells. Activates fibrinolysis by turning plasminogen into plasmin which digests fibrin. |
|
|
Term
| what role does ADP play in hemostasis? |
|
Definition
| inhibits patelet aggregaion |
|
|
Term
| Describe primary hemostasis |
|
Definition
primary is dealing with platelets
vWF causes platelets to adhere to the vessel wall.
platelets release ADP and TXA2 granules that recruit more platelets. |
|
|
Term
| Describe secondary hemostasis |
|
Definition
Secondary deals with fibrin.
Tissue factor is released that causes phospholipic complex expression. Then there is thrombin generation which causes fibrin polymerization. |
|
|
Term
| describe the steps in the common coagulation pathway |
|
Definition
| Thrombin activates factor V that combines with factor X to make even more thrombin. This thrombin turns fibrinogen into fibrin, which forms a fibrin polymer, and activates factor XIII. Factor XIII causes the fibrin polymers to crosslink forming a clot. |
|
|
Term
| how does platelet adhesion work? |
|
Definition
| platelets bind to collagen once vWF is secreted. |
|
|
Term
| What do α-granules contain? |
|
Definition
| Fibrinogen, factor V, factor VIII |
|
|
Term
| What are the 2 types of granules in platelets? |
|
Definition
|
|
Term
| What do dense granules contain? |
|
Definition
|
|
Term
| What does activation of the Gp IIB/IIIA receptor do? |
|
Definition
| causes the platelet to undergo conformational change so the clump up and become not smooth and form a wall. |
|
|
Term
| What releases TXA-2 and what does it do? |
|
Definition
| Stimulation of the GPIIB/IIIA receptor causes platelet activation which releases TXA-2 along with the 2 types of granules. The TXA-2 causes vasoconstriction. |
|
|
Term
| Describe platelet aggregation. |
|
Definition
| fibrinogen binds to the GpIIB/IIIA receptor in activated platelets. thrombin converts fibrinogen to fibrin causing it to cement. |
|
|
Term
| If a person had a defect in GPlb what would be the effects? |
|
Definition
| platelets would be unable to bind to collagen |
|
|
Term
| What are the main inhibitors of fibrinolysis? |
|
Definition
Plasminogen activator inhibitors (PAI)= inactivates tPA.
α2-antiplasmin= binds free plasmin. |
|
|
Term
|
Definition
|
|
Term
| Describe the Fibrinolytic pathway |
|
Definition
breaking a clot/
t-PA turns plasminogen into plasmin that breaks the clot by splitting the fibrins. |
|
|
Term
| Why is fibrinolytics less effective in busting older clots? |
|
Definition
| older clots have more fibrin cross linking. |
|
|
Term
| how long afer a stroke can u give a fibrinolytic drug and still have benefits outweigh the costs? |
|
Definition
|
|
Term
| When can you not give a thrombic therapy for a stroke (Contraindications)? |
|
Definition
if there is an increased chance of bleeding.
hemmorhage, anticoagulate or antiplatelets in last 24 hrs, seizure during stroke. different stroke in the last 3 months, head injury. |
|
|
Term
| what is the common fibrolytic drug used for stroke treatment? |
|
Definition
|
|
Term
| What are the 2 targets you can give oral drugs for to inhibit platelet aggregation? What drugs block them? |
|
Definition
Block COX-1 with asprin
Block ADP receptor with clopidogrel |
|
|
Term
| What is the target of the IV treatment for inhibiting platelet aggregation? |
|
Definition
| Block the IIB/IIIA receptor |
|
|
Term
| how much asprin should a person be taking to inhibit the COX-1 receptors and inhibit platelet aggregation? |
|
Definition
| small amounts, 81-325 mg/day |
|
|
Term
| _____ is the primary excitatory neurotransmitter in the CNS. |
|
Definition
|
|
Term
| where is glutamate synthesized? |
|
Definition
|
|
Term
| What enzyme converts glutamine -> glutamate |
|
Definition
|
|
Term
| What enzyme converts glutamate -> glutamine? |
|
Definition
|
|
Term
| What enzyme converts glutamate into α-keto glutarate? |
|
Definition
|
|
Term
| What enzyme converts α-keto glutarate into glutamate |
|
Definition
|
|
Term
| What cells remove glutamate from the synapse and how? |
|
Definition
| astrocytes do it actively using a Na/glutamate symporter called the excitatory amino acid transporter. |
|
|
Term
| what happens to the glutamate once it is in the astrocyte? |
|
Definition
| it is converted to glutamine and sent back to the presynaptic neuron to be converted back into glutamate to be released again. |
|
|
Term
| why is some glutamate converted into α-ketoglutarate? |
|
Definition
| dont want free glutamate and it can be used as an intermediate in the citric acid cycle. |
|
|
Term
| what cells contain glutamine synthetase? |
|
Definition
|
|
Term
| which cells contain glutaminase? |
|
Definition
|
|
Term
| how does glycogen in astrocytes affect presynaptic neurons? |
|
Definition
makes glucose that makes ATP that is used for:
glutamate -> glutamine so that the high energy glutamine can travel to the presynaptic neuron to be converted to glutamate without needing energy. |
|
|
Term
| ___ is the more important inhibitory transmitter in the brain. |
|
Definition
|
|
Term
| what enzyme is missing that wont allow astrocytes to send glucose to neurons? |
|
Definition
|
|
Term
| what is hypoxia? what happens? |
|
Definition
| Short term reduced O2-> reduced oxidative phosphorylation -> reduced ATP-> lactate production -> angiogenesis |
|
|
Term
| What is Ischemia? what happens? |
|
Definition
long term lack of O2-> no oxidative phosphorylation -> depleted ATP -> shutting down of active transports -> Ca2+ entering cells -> cells swell and lyse
->phospholipases and proteases digesting the cell. |
|
|
Term
| Reperfusion (reintroduction of O2) after ischemia causes _____. |
|
Definition
| reactive oxygen species (ROS aka free radicals) because there was a build up of electrons and NADH. |
|
|
Term
| Superoxide anion gets converted to H2O2 which can be turned into water and O2 by catalase but if there is sone of electrons what is the major thing that can go wrong? |
|
Definition
| H2O2 picks up an electron to form a hydroxyl radical which is the most reactive type of radical. |
|
|
Term
| What happens with glutamatergic excitotoxicity? |
|
Definition
| excessive glutamate released from presynaptic neuron. Ca2+ rushes into cell and causes even more Ca2+ to be released leads to oxygen radicals damaging DNA causing cell death. |
|
|
Term
| If there is no cell lysis is there inflamation? |
|
Definition
no, Individual cells delete themselves by an intrinsic mechanism - there is no rupture of the cell membrane and thus no inflammation |
|
|
Term
| is there inflamation in necrosis? |
|
Definition
|
|
Term
| what happens if you are deficient in Bcl-2? |
|
Definition
|
|
Term
| What does cytocgrome C do? |
|
Definition
| turns procaspase -> caspase which cleavs stuff and causes apoptosis |
|
|
Term
|
Definition
|
|
Term
| what does Bax do? what inhibits it? |
|
Definition
| puts a hole in the mitochondria letting cytochrome C come out. Inhibited by bcl-2. |
|
|
Term
| describe the extrinsic cell death pathway: |
|
Definition
| microglia, T-cell or NK cell binds and releases a ligand that activates caspase 8. Caspase 8 activates Procaspas-3 into caspase-3 which chews up the cell. Faster than intrinsic cell death. |
|
|
Term
| what is the trophic factor hypothesis? |
|
Definition
| neurons that dont have a target die |
|
|
Term
|
Definition
| loss of pyramidal neurons in the hippocampus |
|
|
Term
|
Definition
| loss of dopaminergic neurons in the substantia nigra. |
|
|
Term
| Amyotropic lateral sclerosis |
|
Definition
|
|
Term
| alzheimers has the presence of extracellular __1__ and inclusions of ___2___. |
|
Definition
1. β-amyloid
2. hyperphosphorylated tau protein |
|
|
Term
| alzheimers contains Lewy bodies that contain _____ |
|
Definition
|
|
Term
| 10% of patients with ALS have a problem with what gene? |
|
Definition
| mitochondrial enzyme superoxide dismutase (SOD1) |
|
|