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62 Cards in this Set
- Front
- Back
general cerebellar lesions
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Dysmetria: voluntary movements overshoot or undershoot the intended target
Ataxia: erratic gait Intention tremor - tremor during voluntary movement Failure of Progression: complicated or fast movements do not go as intended. |
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Cerebrocerebellar lesions
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Dysarthria: Verbal correlate of dysmetria
Anything that affects the arms or toes Cognative cerebellar syndrome Mental correlates to the physical disorders – e.g., failure of thought progression |
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Spinocerebellar damage contributes
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decreases extensor tone without loss of voluntary strength
Results in the patient falling down when they stop consciously thinking about standing up |
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Vestibulocerebellar lesion
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nystagmus, slow movement of the eyes in one direction followed by rapid movement back
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Corticopontine Tract Lesions
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As the cerebellum tries to execute correction, it is only corrects the part of the pathway it is aware of until it gets efference and proprioceptive input. Then it must correct again. This results in snake-like, writhing movements
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what part of the basal nuclei receives cerebral input ?
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the striatum
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parts of the basal nuclei ?
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The Internal Globus Pallidus (GPi) to strengthen voluntary movement. This is the direct pathway.
The External Globus Pallidus (GPe) to inhibit motor strength. This is the indirect pathway |
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SN
substantia niagra |
emanates from the brainstem and reinforces the strengthening signal while inhibiting the weakening signal of basal nuclei. SN is a functional, but not anatomical, part of the basal nuclei.
Loss of SN in Parkinson's |
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lesion of the cerebral cortex
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leave the medullary reticular formation w/o inhibibitory input
patient is rigid in extension , comatose , hyperthermia , and hypoglycemic |
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medullary reticular formation responible for what ?
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It is essential for governing some of the basic functions of higher organisms, and is one of the oldest portions of the brain.
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patient with cervical stenosis
tractscontributing to patient's symptoms |
numbness - medial lemiscal dorsal column - spinal cord to thalmus
hyperflexia- corticospinal -motor cortex to spinal cord reticulospinal --pons to spine |
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symptoms of Parkinson's
lesion ? |
weakness
mask-like face tremors at rest basal ganglia problem --- substantia nigra loss of direct pathway --- weak stimulus sent out |
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Pontine nuclei found ?
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as part of the communication between the cerebelum and motor cortex
cortocopontine tract goes from motor cortex to pontine --- the intention signal sent to cerebellum |
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spinocerebellar damage
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decreases extensor tone without loss of voluntary strength
patient falls down, when they stop thinking about standing |
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Vestibulocerebellar damage
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slow movement of the eyes
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Lesions of the pons
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As the cerebellum tries to execute correction, it is only corrects the part of the pathway it is aware of until it gets efference and proprioceptive input. Then it must correct again. This results in snake-like, writhing movements
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resting tremors prevented by ?
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basal nuclei
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Striatum
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receives basal input
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GPi (Internal Globus Pallidus)
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strengthen voluntary movement. This is the direct pathway.
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GPe (external Globus Pallidus)
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inhibit motor strength. This is the indirect pathway
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The substantia nigra (SN)
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part of the basal nuclei functionally
emanates from the brainstem and reinforces the strengthening signal while inhibiting the weakening signal of basal nuclei. |
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engage more strength by ?
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disinhibiting lower motor neurons
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what stimulates antigravity extensor muscles ?
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Pontine reticular n. give rise to lateral reticulospinal tracts
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vestibulospinal tracts do what ?
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maintain posture during acceleration
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tectospinal tracts
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mediate eye and auditory reflexes
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when do we observe a V-max ?
what kind of diffusion ? |
facilitated diffusion –there is a transporter involved , can only work so fast ---some point you hit V-Max
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where are antiports found in the body ?
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can rid of hygrogen in the kidney , also in cardiac muscle –transports calc out , for sodium coming in
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Rx to slow down Na pump ?
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Digitalis -used to increase cardiac contractility (it is a positive inotrope) and as an antiarrhythmic agent to control the heart rate, particularly in the irregular (and often fast) atrial fibrillation. It is therefore often prescribed for patients in atrial fibrillation, especially if they have been diagnosed with heart failure.
Calcium sent out during diastole More calcium – more contractile force in a muscle Slowing down this pump , breaks down gradient ---keeping more calcium inside cell ---- cardiac muscle cell is allowed to contract more slowly ! |
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Cell put into a hypotonic solution , what happens ?
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water moves into cell so make solution less dilute -- cell swells , could see lysis
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what determines cell membrane potential Vm ?
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ion flow
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what general information does the Nernst equation give you ?
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what general way things move
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gradients for nerve/skeletal muscle
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Ion Intracellular Extracellular
Na+ 8 mM 140 mM K+ 155 mM 4 mM Cl- 4 mM 100 mM Ca2+ 0.0001 mM 2.4 mM HCO3- 8 mM 24 mM |
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Vm - most neurons
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In most neurons, Vm is -70 to - 85 mV (millivolts)
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Vm (mem. pot. ) of skeletal muscle ?
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In skeletal & cardiac muscle Vm is about -95 mV
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E K+
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is -90 to -95 mV & always more negative then Vm, why ?
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E Na+
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is typically +70 to +80 mV (or more) & always more positive than Vm
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Ionic movement is affected by both electrical fields and chemical gradients
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Resting membrane potential is the electrical field; it attracts cations & repels anions
Concentration gradients favor Na+ & Cl- movement into and K+ movement out of cells. |
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net electrochemical driving force= Ei – Vm
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Ei = is the chemical driving force, converted to an equivalent electrical force by the Nernst equation
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what determines Vm ?
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Ion movement towards equilibrium potential is what determines Vm
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function of a reflex
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opposes sudden changes in muscle length
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Brain Areas for Control of the Gamma
Motor System |
The gamma efferent system is excited specifically by
signals from the bulboreticular facilitatory region of the brain stem and, secondarily, by impulses transmitted into the bulboreticular area from (1) the cerebellum, (2) the basal ganglia, and (3) the cerebral cortex. Little is known about the precise mechanisms of control of the gamma efferent system. However, because the bulboreticular facilitatory area is particularly concerned with antigravity contractions, and because the antigravity muscles have an especially high density of muscle spindles, emphasis is given to the importance of the gamma efferent mechanism for damping the movements of the different body parts during walking and running |
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Clonus
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osicalation of muscle jerks
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patient has been vomitting
what electroltes lost most ? can present with ? |
H+, Cl- (acid) K +
alkylosis lose too much K , hypokalamia (a medical emergency) |
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patient has had a lot of diarrhea
di-arr-hea , how might they present ? |
Loss of HCO3-, as well as water
so lose some base , acidosis |
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what is the average total body water amount ?
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42 Liters for a 70 kg man
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amount of hematocrit ?
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40 % for males
36 % for females .4 , .36 |
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what crosses the cell membrane readily / without a channel ?
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urea, gases, alcohol
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indicator-dilution principle
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Volume = Amt. Injected x [Injected] [Final] (at “equilibrium”)
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antipyrine used for ?
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measurement of total body water
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Inulin used for ?
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Extracellular Fluid Volume (ECFV measurement
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what saline solution is isotonic ?
hypertonic ? hypotonic ? |
0.9%
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what happens if you administer pure water to patients IV ?
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solution becomes hypotonic, can't pull salt out of cell b/c that requires taking water out , plus Na+ likes to be outside of cell ...... water from dilute solution will osmos. into RBC and burst it
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D5W
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D5W enters blood as iso-osmotic solution but becomes hypotonic with time as glucose is consumed.
Results in cell swelling!! |
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if the actual plasma osmolarity is higher than predicted , what could accoutn for this ?
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lactic acid , from diabetics
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acidic solution added to IV to treat alkyosis ? acidic ?
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ammonium chloride
bicarbonate (conjugate of carbonic acid) |
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threshold voltage
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Threshold voltage is roughly -55 to -60 mV
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during the relative refractory peroid , what is needed ?
why ? |
greater depolarization
Until there are as many Na+ channels in the resting state as there were before the action potential, greater depolarization is needed to generate a second action potential |
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the point of refractory period ?
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helps prevent repetetive firing
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Long Q-T syndrome
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Drugs that lengthen the action potential beyond the absolute refractory period are the most common cause of a type of arrhythmia called Long Q-T Syndrome, which can lead to tosade de pointes and ventricular fibrillation, which you’ll learn of later.
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what determines the threshold potential ?
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Threshold potential - the point where an action potential occurs - determined by the number of voltage-gated Na+ channels in the resting state!!!!!
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note on rising phase and conduction
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cells with less negative (more positive ) Vm conduct more slowly
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is hyperkalemia a de-polarizing factor or hyperpolarizing factor ?
causes of ? |
de-polarizing
more positive charge Drugs, kidney failure, severe trauma or burns |