Physiology

Front 1

general cerebellar lesions

Back 1

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.

Front 2

Cerebrocerebellar lesions

Back 2

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

Front 3

Spinocerebellar damage contributes

Back 3

decreases extensor tone without loss of voluntary strength

Results in the patient falling down when they stop consciously thinking about standing up

Front 4

Vestibulocerebellar lesion

Back 4

nystagmus, slow movement of the eyes in one direction followed by rapid movement back

Front 5

Corticopontine Tract Lesions

Back 5

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

Front 6

what part of the basal nuclei receives cerebral input ?

Back 6

the striatum

Front 7

parts of the basal nuclei ?

Back 7

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

Front 8

SN
substantia niagra

Back 8

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

Front 9

lesion of the cerebral cortex

Back 9

leave the medullary reticular formation w/o inhibibitory input

patient is rigid in extension , comatose , hyperthermia , and hypoglycemic

Front 10

medullary reticular formation responible for what ?

Back 10

It is essential for governing some of the basic functions of higher organisms, and is one of the oldest portions of the brain.

Front 11

patient with cervical stenosis

tractscontributing to patient's symptoms

Back 11

numbness - medial lemiscal dorsal column - spinal cord to thalmus

hyperflexia- corticospinal -motor cortex to spinal cord
reticulospinal --pons to spine

Front 12

symptoms of Parkinson's

lesion ?

Back 12

weakness
mask-like face
tremors at rest

basal ganglia problem --- substantia nigra
loss of direct pathway --- weak stimulus sent out

Front 13

Pontine nuclei found ?

Back 13

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

Front 14

spinocerebellar damage

Back 14

decreases extensor tone without loss of voluntary strength

patient falls down, when they stop thinking about standing

Front 15

Vestibulocerebellar damage

Back 15

slow movement of the eyes

Front 16

Lesions of the pons

Back 16

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

Front 17

resting tremors prevented by ?

Back 17

basal nuclei

Front 18

Striatum

Back 18

receives basal input

Front 19

GPi (Internal Globus Pallidus)

Back 19

strengthen voluntary movement. This is the direct pathway.

Front 20

GPe (external Globus Pallidus)

Back 20

inhibit motor strength. This is the indirect pathway

Front 21

The substantia nigra (SN)

Back 21

part of the basal nuclei functionally
emanates from the brainstem and reinforces the strengthening signal while inhibiting the weakening signal of basal nuclei.

Front 22

engage more strength by ?

Back 22

disinhibiting lower motor neurons

Front 23

what stimulates antigravity extensor muscles ?

Back 23

Pontine reticular n. give rise to lateral reticulospinal tracts

Front 24

vestibulospinal tracts do what ?

Back 24

maintain posture during acceleration

Front 25

tectospinal tracts

Back 25

mediate eye and auditory reflexes

Front 26

when do we observe a V-max ?
what kind of diffusion ?

Back 26

facilitated diffusion –there is a transporter involved , can only work so fast ---some point you hit V-Max

Front 27

where are antiports found in the body ?

Back 27

can rid of hygrogen in the kidney , also in cardiac muscle –transports calc out , for sodium coming in

Front 28

Rx to slow down Na pump ?

Back 28

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 !

Front 29

Cell put into a hypotonic solution , what happens ?

Back 29

water moves into cell so make solution less dilute -- cell swells , could see lysis

Front 30

what determines cell membrane potential Vm ?

Back 30

ion flow

Front 31

what general information does the Nernst equation give you ?

Back 31

what general way things move

Front 32

gradients for nerve/skeletal muscle

Back 32

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

Front 33

Vm - most neurons

Back 33

In most neurons, Vm is -70 to - 85 mV (millivolts)‏

Front 34

Vm (mem. pot. ) of skeletal muscle ?

Back 34

In skeletal & cardiac muscle Vm is about -95 mV

Front 35

E K+

Back 35

is -90 to -95 mV & always more negative then Vm, why ?

Front 36

E Na+

Back 36

is typically +70 to +80 mV (or more) & always more positive than Vm

Front 37

Ionic movement is affected by both electrical fields and chemical gradients

Back 37

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.

Front 38

net electrochemical driving force= Ei – Vm

Back 38

Ei = is the chemical driving force, converted to an equivalent electrical force by the Nernst equation

Front 39

what determines Vm ?

Back 39

Ion movement towards equilibrium potential is what determines Vm

Front 40

function of a reflex

Back 40

opposes sudden changes in muscle length

Front 41

Brain Areas for Control of the Gamma
Motor System

Back 41

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

Front 42

Clonus

Back 42

osicalation of muscle jerks

Front 43

patient has been vomitting
what electroltes lost most ?
can present with ?

Back 43

H+, Cl- (acid) K +
alkylosis
lose too much K , hypokalamia (a medical emergency)

Front 44

patient has had a lot of diarrhea
di-arr-hea , how might they present ?

Back 44

Loss of HCO3-, as well as water
so lose some base , acidosis

Front 45

what is the average total body water amount ?

Back 45

42 Liters for a 70 kg man

Front 46

amount of hematocrit ?

Back 46

40 % for males
36 % for females

.4 , .36

Front 47

what crosses the cell membrane readily / without a channel ?

Back 47

urea, gases, alcohol

Front 48

indicator-dilution principle

Back 48

Volume = Amt. Injected x [Injected] [Final] (at “equilibrium”)

Front 49

antipyrine used for ?

Back 49

measurement of total body water

Front 50

Inulin used for ?

Back 50

Extracellular Fluid Volume (ECFV measurement

Front 51

what saline solution is isotonic ?
hypertonic ?
hypotonic ?

Back 51

0.9%

Front 52

what happens if you administer pure water to patients IV ?

Back 52

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

Front 53

D5W

Back 53

D5W enters blood as iso-osmotic solution but becomes hypotonic with time as glucose is consumed.
Results in cell swelling!!

Front 54

if the actual plasma osmolarity is higher than predicted , what could accoutn for this ?

Back 54

lactic acid , from diabetics

Front 55

acidic solution added to IV to treat alkyosis ? acidic ?

Back 55

ammonium chloride
bicarbonate (conjugate of carbonic acid)

Front 56

threshold voltage

Back 56

Threshold voltage is roughly -55 to -60 mV

Front 57

during the relative refractory peroid , what is needed ?

why ?

Back 57

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

Front 58

the point of refractory period ?

Back 58

helps prevent repetetive firing

Front 59

Long Q-T syndrome

Back 59

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.

Front 60

what determines the threshold potential ?

Back 60

Threshold potential - the point where an action potential occurs - determined by the number of voltage-gated Na+ channels in the resting state!!!!!

Front 61

note on rising phase and conduction

Back 61

cells with less negative (more positive ) Vm conduct more slowly

Front 62

is hyperkalemia a de-polarizing factor or hyperpolarizing factor ?

causes of ?

Back 62

de-polarizing

more positive charge

Drugs, kidney failure, severe trauma or burns