Pathophys exam 2 nervous and random cardio

inhibitory neurotransmitters do what

open CL channels and generate inhibitory postsynaptc potential, keeping postsynaptic membrane near equilibrium

this type of nerve tissue supports neurons and is non-excitable.

glia

this type of nerve tissue is involved in the cells that are excitable.

neruons

your CNS consists of what things

brain and spinal cord

Your PNS consists of 

nervous tissue connecting to the CNS. Afferent dividions are “accepting”/sensory, efferent nerves are “exciting”/motor.

motor edplate, many parts of the brain, excitatory or inhibitory, involved in memory. this neurotransmitter is

class I ACh

epinephrine, norepi, dopamine, serotonin, histamine are what neurotransmitter class

class II amines

CNS; glutamate- excitatory, GABA and glycine - inhibitory in the brain.l tis neurotransmitter class is

class III AA

these neurotrans open cation channels that allow influx of na aor ca2+ and generate a depoalrizing excitatory postsynaptic potential.

excitatory

these neurotrans like GABA and glycine , open Cl channels and generate an inhibitory postsynaptic potential, keeping the postsynaptic membrane near equilibrium

inhibitory

astrocytes do what

make connection between neurons and blood vessels, fill the spaces b/w the neurons. they also stop neuronal repsonses to glutamate, the most abundant excitatory neurotrans.

astrocytes reapond rto brain injury by increasing in size and sometimes number in a process called

reactive astrocytosis

myelin in the peripheral ns is produced by what cell

schwann cells

myelin in the CNS is produced by what cell

oligodendrocytes

this cell is an immune effector cell. derived from bone marrow precursors of macrophage monocyte lineage and invade CNS during perinatal period. remove dead tissue and destroy invading organisms but can contribute to CNS damage, like in inflammatory and degenerative CNS diseases.

microglia

damage to the lower motor neurons results in

loss of all voluntary mtoor action and reflexes

pyramidal tracks control

all voluntary actions

extrapyramidal tracsk control

involuntary injury

pyramidal tracks originate from and carry what type of signals

cerebral cortex, motor cells

extrapyramidal tracks originate from where and carry what

all involuntary

a motor unit is made up by

alpha mtoor neuron and 200  muscle fibers

if there is damage to the lower motor neurons paralysis is

flaccid. muscle tone or resistance to passive movement is reduced, and deep tendon reflexes are lost/

tendon reflexes and muscle tone depend on what 3 things

alpha motor neurons, muscle spindles, and smaller gamma motor neurons whose axons innervate the spindles.

upper motor neuron damage is

spastic paralysis

tapping on the tendon to stretch the spindles, causing them to send impulses that activate alpha motor neuron. a brief muscle contraction is observed during the

myotactic stretch reflex

each point of contact b/w nerve terminal and skeletal muscle forms specialized synapse aka

neuromuscular junction

neuromuscular junction composed of

presynaptic motor nerve temrinal (stores synpatic vesicles that rleease ACh) and post synaptic mtoor end palte

antibodies block influx of calcium and block ca channels that go into the nerve temrinal and reduce neurotrans release. no muscle contracton = paralysis. this dz is

Lambert eaton myasthenic syndrome

in a pt with lambert eaton myasthenic syndrome, repetitive nerve stimulation does what to the body

releases calcium but it accumulates in the nerve terminal and inc ACh release

this pt has weakness, blurred vision, diplopia, ptosis, and large unreactive pupils as a result of a bacterial infection

botulism

this toxin cleaves certain presynaptic proteins, preventing neurotransmitter release at both neuromuscular and parasympathetic cholinergic synapses

clostridium botulinum

how to stimulate the muscle fibers to reduce labert eaton effects

repetitive nerve stimulation, because it inc calcium in the presynaptic cell so more ACh is produced, producing a stronger muscle signal

this medication impairs calcium channel function and causes similar sx to Lambert eaton myasthenic syndrome

aminoglycoside abx

this bacteria cleave certain presynaptic proteins preventing neurotransmitter release at neuromuscular and parasympathetic cholinergic synapses.

clostridium botulinum

autoantibodies to the nicotinic ach receptor (AChR) block neurotransmission by inhibiting receptor function and activates complement mediated lysis of postsynaptic membrane

MG

what happens to denervated muscles over time

atrophy due to lack of signals to the part

when muscle fibers in a denervated motor unit discharge spontaneously what happens

a visible twitch called a fasciculation

when do fibrillations usually occur and how do you visualize them

7-21 days post trauma of the lower motor neuron and can be seen via electromyography

upper motor neuron pathways can be destroyed where

cortex, subcorticla white amtter, internal cpasule, brainstem, spinal cord.

unilateral upper motor neuron lesions spare muscles innervated by lower motor neurons like

eyes, jaw, upper face, pharynx, larynx, neck, thorax, abdoen

paralysis from upper motor neuron lesions is different than lower MN in that

it is rarely complete for a long period of time.

spinal shock is

damage to the upper MN. period of flaccid paralysis that then develops into spastic paralysis. also babinksi and hyperreflexia

in humans lesions of the cerebral peduncles also cause what effect

mild paralysis w/o spasticity

lesions above the pons do what 

impair movements of contralateral lower face, arm, leg.

lesions below the pons spare what part of the body

the face

weakness, spasticity of cranial, trunk, and limb muscles, leading to dysarthria (slurred speech), dysphonia (hoarseness), dysphagia, bifacial paresis, reflexive crying and laughing (pseudobulbar palsy). this lesion is

bilateral cerebral lesions

receives proprioceptive input from muscles and tendons and influences posture, muscle tone, and gait. what part of the brain is responsible for these things

anterior lobe of the cerebellum

receives input from cerebral cortex via pontine nuclei and middle cerebellar peduncles. important for voluntary skilled movement initiated by the cerebral cortex. what part of the brain does this.

posterior lobe cerebellum

what part of the brain is responsible for control of posture and eye movement

flocculonodular lobe, which is the flocculus and nodulus of the vermis

this part of the brain controls movement thru connections with cerebral motor cortex and brainstem nuclei.

cerebellum

damage to this part of the brain interferes with the performance of motor tasks

cerebellum

ataxia is where simple movements are delayed in onset and their rates of acceleration and deceleration are dec, resulting in an intention tremor and dysmetria (overshooting). most often associated with hypotonia bc of dec activity of alpha and gamma motor neurons. this is a manifestation of what neuro dz

cerebellar

cerebellar hemisphere lesions affect what part of the body

the limbs causing limb ataxia

midline cerebellar lesions affect what part of the body

axial muscles , causing truncal and gait ataxia and d/o of eye movement

if a lesion of the cerebellum/cerebellar peduncles is unilateral, the signs of limb ataxia are on what side of the lesion

the same side

if a lesions lies beyond the decussation (nerve split) of efferent cerebellar fibers in the midbrain, the clinical signs are on the

opposite side of the lesion

dopamine is synthesized by neurons of what part of the brain

substantia nigra.

sx of bradykinesia, akinesia, loss of postural reflexes or abnormal activation of the motor system, = reigidity, tremor, and involuntary movements like chorea, athetosis, ballismus, and dystonia. the part of the brain affected causing these sx is the 

basal ganglia

degeneration of nigral neurons leads to loss of dopaminergic inhibition and relative excess of cholinergic activity. this dz is

parkinsons

how to tx parkinsons

anticholenergic and dopamine agonists

huntington’s dz is what form of inheritance

AD

this dz happens later in life where pts develop rapid jerking movements called chorea and slow writhing movements of limbs and trunk (athetosis).

huntington dz late onset

pts show more signs of parkinsonism like intention tremor and cogwheel rigidity

huntington dz early onset

why do pts with huntigon’s have psych d/o and cognitive defecits

bc the neurons deep in the cerebral cortex also degenerate early in the dz including the hippocampus and hypothalamus. 

gene for huntintton dz is on what chromosome and encodes for what AA protein

4, 3144 AA protein = huntingtin

somatosensory pathways provide information about what movements

touch, pressure, temrpeature, pain, vibraton, and position and movement of body

free nerve endings of unmyelinated fibers and small diameter myelinated fibers in skin do what

convey sensory information in response to chemical thermal and mechanical stimuli.

Intense stimulation of free nerve endings of unmyelinated fibers and small diameter myelinated fibers produces what type of sensation

pain

inflammatory conditions do what to deep tissues

sensitize afferents to evoke pain on mechanical stimulation

damage to sensory afferents in the deep tissues causes what

a deficit in pain and temperature discrimination. also painful sensations aka dysesthesias, usually in area or sensory loss. aka neuropathic pain. burning, tingling, electric shock like quality.

lesions in multiple peripheral nerves, dorsal columns, medial lemniscus, or thalamus, but not single nerve lesions creates what deficit

cant feel vibration

in pts with damage to the sensory cortex or its projections from the thalamus what feeling(s) are preserved?

touch, pain, temp, vibration senses all preserved.

in pts with damage to the sensory cortex or its projections from the thalamus what feeling(s) are impaired?

complex tasks needing integration of multiple somatosensory stimuli and of somatosensory stimuli with auditory or visual information are impaired. ex like distinguishing two points from one when touched on skin (two point discrimination), localize tactile stimuli, perceive position of the body parts in space, recognize letters or numbers drawn on skin (graphesthesia) and identify objects by their shape, size, and texture (stereognosis)

symmetric distal sensory loss in the libs affecting the legs more than the arms signifies a generalizedd/o of what

multiple peripheral nerves aka polyneuropathy

sensory sx and deficits may be restricted to the distribution of what

a single peripheral nerve (mononeuropathy) or two or more peripheral nerves (mononeuropathy multiplex).

sx linked to dermatome indicate what

spinal root lesion aka radiculopathy

what nerve innervates ipsilateral medial, superior, and inferior rectus muscles and the inferior oblique muscles. also supplies the ipsilateral levator palpebrae, which elevates the eyelid. also carries parasympathetic fibers that mediate pupillary constriction

oculomotor

what nerve decussates before leaving brainstem, supplying contralateral superior oblique muscle.

trochlear

what nerve innervates the lateral rectus muscle of the same side

abducens

what nerve innervates the extraocular motor nuclei and provide supranuclear control of gaze; vertical, lateral, etc

cortical and brainstem

damage to the tarsal muscles of the eyelids causes

Horner syndrome, which is miosis, ptosis, and sometimes impaired sweating ipsilateral to the lesion

this type of deafness results from diseases of external or middle ear that impair conduction and amplification of sound from air to cochlea

conductive deafness

this type of deafness results from dz of cochlea or eighth cranial nerve

sensorineural deafness

this type of deafness results from dz affecting cochlear nuclei or auditory pathways in the CNS

central deafness

transient episodes of tinnitus occur in individuals and are not associated with dz. when its persistent, tinnitus is associated with hearing loss. this dz is 

Meniere dz

what lesion produces a disturbed vestibular function

small brainstem lesions

pts with diseases of vestibular system complain of

disequilibrium and dizziness

how is a vestibular dz and cerebellar dz different

cerebellar dz is described as a problem with coordination instead of dizziness in the head

dz of the labyrinth or vestibular nerve causes what sx

peripheral vertigo

dysfunction of brainstem and CNS pathways causes what sx

central vertigo

this type of vertigo is more severe and associated w n/v esp with acute onset.

peripheral vertigo

what dz causes rotational vertigo

dz of semicircular canal neurons or their fibers

what dz causes sensations of tilting or listing similar to a boat

dz of utricle or saccule

brainstem ischemia, brainstem tumors, and multiple sclerosis cause what sx

central vertigo

activation of cells in ipsilateral hypothalamus triggers trigeminal autonomic vascular system. also paired with sx of severe unilateral periorbital pain for days or weeks, ipsilateral nasal congestion, rhinorrhea, lacrimation, redness of the eye, Horner syndrome (ptosis, pupillary meiosis, facial anhidrosis/hypohydrosis. episodes occur at night, awaken the pt, and last b/w 15 mins and 3 hrs. alcohol, stress, glare, or ingestion of food triggers an attack.

cluster headache

what are the trigeminal autonomic cephalgias

hemicrania continua, paroxysmal hemicrania, and short lasting neuralgiform headache attacks

how to tx cluster headaches

subcu or intranasal sumatriptan or inhalation of oxygen, zolmitriptan, dihydroergotamine or viscous lidocaine.

how to prophylax for a cluster headache

oral meds like verapamil, lithium carb, topiramate, and galcanezumab.

this pain begins unilaterally in the temple but spreads to the entire head. pt also has preceded visual disturbances and dizziness, nausea, and abdominal discomfort, and fatigue

migraine

how to tx mild migraines

NSAIDs