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30 Cards in this Set

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Functions of CSF

1. Mechanical protection


2. ICP buffering


3. Source of glucose/O2 and for removal of metabolites/CO2


4. Acid-base - low protein so small CO2 changes = larger pH changes


5. Transport of hormones/neuropeptides to other parts of brain


6. Interstitial fluid absorption as no lymph in brain


7. Maintains constant ionic environment conducive to neuronal function.

Describe CSF production

- 150mL total with 3-4x turnover/day ie 500mls/day


- produced in choroid plexus (67%) and directly via ependymal cells of lateral ventricles (33%)


- decreased formation only when CPP<70mmHg. NOT affected by ICP unless ICP reduces CPP.


- plasma ultrafiltrate via fenestrated capillary endothelium.


- promoted by bulk flow and hydrostatic pressure


- active transport of Na, glucose and K out


- passive transport in of Cl, HCO3


- H2O down osmotic gradient

Differences between plasma and CSF

- higher pCO2 and lower pH


- decreased protein ++


- decreased K, glucose


- identical osmolality 295, Na, HCO3


- Increased Cl

Path of CSF

1.Choroid plexus/lateral ventricles down foramen of Monro


2. 3rd ventricle


3. Sylvian aqueduct


4. 4th ventricle


5. Foramen of Luschka/ Magendie


6. Cisterna magna


7. Subarachnoid of brain/SC


8. Arachnoid villi into venous system

Describe CSF absorption

Occurs in arachnoid villi or directly via cerebral venules via a pressure gradient


- ICP 15mmHg - venous 9mmHg



Therefore increased CSF pressure favours absorption.



Normally production = absorption

What is structure of BBB

- formed primarily by endothelial layer of capillaries


Physical - tight junctions w/o fenestrations + increased mitochondria to allow increased active transport.


Chemical - enzymes such as MAO/DA decarboxylase degrade toxic substances crossing BBB



- Astrocytes not part of BBB but apply foot processes W/I perivascular areas to form clefts and channels

Permeability of BBB

- generally permeable to small (<30kDA), non-polar,lipophilic substances including resp gases, H2O


- active transport of other substances such as glucose, aas, electrolytes, some drugs

What are the circumventricular organs of brain

- Small areas surrounding 3rd/4th ventricles outside the BBB


E.g.


- choroid plexus


- area postrema


- median eminence of hypothalamus

Functions of the blood-CSF barrier

- regulate contents of newly-formed CSF


- release of hormones into CSF


- sensory analysis of CSF ie with CTZ

Monro-Kellie doctrine

In adults, rigid/closed cranial vault forms a fixed brain volume that contains:


- parenchyma 1500g (80%)


- CSF 75mLs (10%)


- cerebral blood/vessels 75ml (10%)



Therefore any change in any of these components will alter one or both of the other components.

Cerebral blood flow

CBF = MAP - ICPor CVP/CVR

Features of REM sleep

1. CNS


- Rapid, low voltage irregular EEG similar to awake state


- Active dreaming - remembered


- CMRO2 matches awake


- Difficult to rouse


2. Resp\\


- Irregular RR


- ↓ TV/MV - much more than non-REM


- ↓ response to hypercarbia/hypoxia


- Profound loss of upper airway tone + ↑ resistance - OSA


- ↓ FRC


3. CVS


- BP/HR irregular


4. Muscle


- Marked ↓ muscle tone


5. Other


- Decreased temperature, metabolic rate


- Release GCs

Neurological features of Non-REM sleep

EEG - 4 stages that gradually generate more synchronised, lower frequency and higher amplitude waveform.



1. α waves (8-13Hz) replaced by low amplitude/frequency θ (theta) wave (4-6Hz)




2. Bursts of high frequency α-like waves called "sleep spindles"




3. High amplitude but lower frequency δ waves



(1-2Hz) with bursts of rapid waves superimposed (K complexes)




4. δ waves become higher amplitude, lower frequency and synchronised.




- Decreased CMRO2

Non-neuro features of Non-REM sleep

1. CVS


- Decreased HR and BP




2. Resp


- ↓ RR/TV/MV (less than REM)


- ↓ FRC secondary to ↓muscle tone


- ↓ hypoxic, hypercarbic response (less than REM)


- ↓ upper airway tone and ↑AWR causes OSA (less than REM)




3. Muscle


- ↓ muscle tone (less than REM)




4. Other


- ↓ temp


- ↓ metabolic rate

Cycling of sleep phases

- Usual sleep cycle approx 90 minutes




1. Phases 1-4 of Non-REM


2. REM sleep (5-30mins)


3. Phases 4 to 1 of Non-REM sleep




REM sleep apart 15 minutes >50yrs


In babies 45-65% spent in REM sleep

Basis of EEG

- Measures the spontaneous electrical activity of superficial layer of pyramidal cells perpendicular to electrodes


- Processed by low and high frequency filters to remove muscle artefact


- Analysed for frequency/amplitude and recognition of wave patterns

Clinical use of EEG

- Can only detect abnormalities in cortical tissue as this is where electrical potentials originate


- 3 types of abnormalities


- Generalised excess of slow wave activity i.e. infective or metabolic encephalopathy


- Focal excess of slow wave activity i.e. focal abnormality


- Abnormal high voltage electrical discharge i.e. epileptiform disturbance.

Effect of CO2 on cerebral blood flow

- ↑PaCO2 causes cerebral vasodilation


- 4% per mmHg CO2 increase between 20-80mmHg




- PaO2 has no effects unless <50mmHg



Nernst equation

Veq = equilibrium potential of the ion
R = universal gas constant
T = absolute temp
z = Elementary charge of ion
F = Faraday's constant

Veq = equilibrium potential of the ion


R = universal gas constant


T = absolute temp


z = Elementary charge of ion


F = Faraday's constant















What is the Nernst potential?

- The voltage that exists across a membrane for an ion which is fully permeable when the electrical and concentration gradients are equal

Resting membrane potential?

Is the potential difference across the cell membrane when electrical and concentration gradients are at equilibrium.




Different in tissues due to differing permeabilities to certain ions


Ie


Excitable cell = -70mV


Cardiac myocyte = -90mV


Cardiac pacemaker cell = -60mV


Skeletal muscle cell = -80mV

How to calculate the resting membrane potential















Goldman-Katz equation:





Goldman-Katz equation




P=relative permeability




















Goldman-Katz equation:



Factors that generate RMP

K+ equilibrium potential


= Main factor


- 3Na-2K ATPase pumps Na EC and K IC to establish a large concentration gradient.


- membrane very permeable to K+ due to non-gated K channels


- Therefore more K lost from cell than Na in and creates a -ve membrane potential.




Na+ influx


- Membrane impermeable to Na at rest however small leak of Na into the cell causes RMP to be more positive than K+ equilibrium potential.




Gibbs-Donnan effect


- Large non-diffusible anions (proteins) inside cells affects the distribution of permeable ions.

Steps for a nerve action potential

1. RMP = -70mV


2. Impulse increases the RMP to threshold of -55mV upon which VG-gated Na channels open and depolarise the membrane to 35mV. Open only 1msec before closing.


3. Delayed opening of VG-gated K channels repolarise the membrane. Slowed closing causes hyperpolarisation and then back to RMP

Steps for a nerve action potential

1. RMP = -70mV


2. Impulse increases the RMP to threshold of -55mV upon which VG-gated Na channels open and depolarise the membrane to 35mV. Open only 1msec before closing.


3. Delayed opening of VG-gated K channels repolarise the membrane. Slowed closing causes hyperpolarisation and then back to RMP

Refractory periods of AP

Absolute RP


- 1msec of AP when all Na channels are open and an AP cannot occur regardless of intensity



Relative RP


- 10-15msecs when supramaximal stimulus needed


- only when all Na channels reset and membrane is not hyperpolarised by increased K permeability



- RPs allow flow to be unidirectional and limits frequency of nerve conduction.

Steps for a nerve action potential

1. RMP = -70mV


2. Impulse increases the RMP to threshold of -55mV upon which VG-gated Na channels open and depolarise the membrane to 35mV. Open only 1msec before closing.


3. Delayed opening of VG-gated K channels repolarise the membrane. Slowed closing causes hyperpolarisation and then back to RMP

Refractory periods of AP

Absolute RP


- 1msec of AP when all Na channels are open and an AP cannot occur regardless of intensity



Relative RP


- 10-15msecs when supramaximal stimulus needed


- only when all Na channels reset and membrane is not hyperpolarised by increased K permeability



- RPs allow flow to be unidirectional and limits frequency of nerve conduction.

Factors affecting speed of nerve propagation

1. Axon diameter


- larger area produces lower resistance to current flow



2. Myelination


- myelin sheath around the nerve between nodes of ranvier has high resistance and low capacitance such that flow can pass undisturbed though the myelin to the next node


- causes AP to jump from node to node

Front (Term)t

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