Biom 2009 Flash Cards - Term 2

Front 1

How does a local anaesthetic work?

Back 1

prevents or relieves pain by interrupting nerve conduction. reversible. act on every type of nerve, cause sensory and motor paralysis. block sodium channels

Front 2

chemical structure of local anaesthetics

Back 2

aromatic region linked by ester or amide and basic side chain.
weak bases (pka8-9), partially ionized at physiological ph

Front 3

why are ester and amide bonds important in local anaesthetics

Back 3

metabolic hydrolysis in plasma and liver

Front 4

Examples of local anaesthetics

Back 4

procaine, cocaine, tetracaine, cinchocaine, LIDOCAINE, prilocaine, bupivacaine, benzocaine

Front 5

mode of action of local anaesthetic

Back 5

block initation and propagation of action potential. BLOCK NA+ channels by physically plugging the transmembrane pore

Front 6

Sodium concentration inside neurons

Back 6

less than outside.
open channel -> sodium rushes in causes depolarisation

Front 7

what triggers release of neurotransmitter

Back 7

action potential.
causes Ca++ influx which causes release of vesicles

Front 8

explain why pain sensation is blocked more readily than touch

Back 8

nociceptive impulses are carried by a(delta) and C fibers which are smaller in diameter and responsible for pain

Front 9

unwanted effects from local anaesthetic

Back 9

CNS and cardiovascular.

CNS (tremors, restlessness, confusion, agitation, CNS depression which can lead to respiratory depression)

Cardio (myocardial depression and vasodilation, decreased blood pressure)

Front 10

tissue penetration of anaesthetics

Back 10

varies and affects rate of onset and recovery

esters rapidly cleaved
amides metabolised in liver

Front 11

Autonomic nervous system

Back 11

only part of the nervous system where synpases occur outside the protection of the skull and vertebrae

sympathetic and parasympathetic

Front 12

CNS

Back 12

brain and spinal cord
more complex than ANS

Front 13

Blood brain barrier

Back 13

tight junctions between endothelial cells and surrounding astrocytes and capillaries

Front 14

White matter

Back 14

inner of brain contains bundles of axons with myelin

Front 15

grey matter

Back 15

outer of brain
contains cell bodies and dendrites

Front 16

Cerebrospinal fluid

Back 16

source: choroid plexi (lateral, 3rd, 4th ventricle of brain)
5 hour rate turnover
cushions brain, regulates extracellular fluid, nutrition, sink that collects waste.

Front 17

CNS blood supply

Back 17

brain = highly metabolically active
a constant flow of blood to the brain. flow rates vary depending on which part of the brain is active at any given time.

Front 18

Lumbar puncture

Back 18

test for infection
sample of CSF
needle inserted below end of spinal cord to prevent damage.
if increased pressure can NOT do lumbar puncture because will relieve pressure outflow of CSF in uncontrolled fashion

Front 19

Neurotransmission in CNS

Back 19

many neurons in close proximity so release of NT can lead to diffusion of NT into postsynaptic neuron, not intended postsynatpic neuron or glia cells.

Front 20

amino acid neurotransmitters in CNS

Back 20

glutamate, GABA, glycine, asparate

Front 21

synthesis of amino acids

Back 21

linked to each other.

e.g. glutamate undergoes GAD to become GABA

Front 22

Synthesis of glutamate

Back 22

from glucose of glutamine

Front 23

Glutamate link with BBB

Back 23

BBB becomes impermeable to Glu seven days after birth.

Normally 1uM but can increase to 20uM under pathological conditions characterised by defects in BBB or cellular damage such as ms, stroke

can lead to excitotoxicity

Front 24

Life cycle of glutamate

Back 24

glutamine -> via glutaminase -> glutamate ->Vglut (transporter) -> uptake into vesicles -> released into synapse -> 1/2

1 - uptake via EAAT (excitatory amino acid transporter) into astrocyte -> via glutamine synthase -> glutamine -> released via glutamine transporter and reupatked into original neuron.

2-> uptake via EAAT into original neuron and re enters cycle as glutamate

Front 25

four glutamate receptor subtypes

Back 25

NMDA [Na+, Ca+], AMPA[Na+, Ca+], Kainate[Na+, Ca+], Metabotropic receptor[GPCR -> similar to mACh]

Front 26

glutamate

Back 26

causes depolarisation

Front 27

GABA

Back 27

hyperpolarisation

Front 28

glycine

Back 28

hyperpolarisation

Front 29

GABA life cycle

Back 29

similar to glutamate but uses gabanergic neuron

GAD convert glutamate to GABA

little GABA found out of CNS

Front 30

GABA-a
GABA-b

Back 30

GABA-a = movement of Cl to hyperpolarise
GABA-b = movement of K+ out to hyperpolarise or reduce Ca++ in to hyperpolarize

Front 31

GABA subunits

Back 31

30 different combinations
common - (a1)2, (b2)2, (gamma1)

Front 32

Sites of GABAa

Back 32

GABA binding site
benzodiazepines - gamma subunit, conformational change to increase affinity of NT to GABA

Front 33

sites of gaba b

Back 33

two 7TMGPCR
K+ and Ca++

Front 34

Baclofen

Back 34

agonist for gabab
treat spasticity

Front 35

benzodiazepine

Back 35

agonist for gaba A - reduces affnity for gaba
axiolytic or sedative

Front 36

glycine life story

Back 36

similar to GABA and glutamate

Front 37

Glycine

Back 37

similar to gaba-a (rely on astrocytes, Cl- channel - inhibitory)

Front 38

are glycine receptors pharmacological targets

Back 38

no therapeutic drugs
strychnine is a convulsant (antagonist) which used to cause seizures

Front 39

tetanus

Back 39

acts on glycine receptors
blocks glycine release from interneurons resulting in hyperactivity and violent muscle spasms

Front 40

aim of anaethesia

Back 40

to render patient unconscious and unresponsive to painful stimuli

Front 41

anaesthetic state

Back 41

amnesia, immobility in response to noxious stimuli, analgesia, unconciousness

Front 42

Mechanism of action of anaesthetic drugs - lipid theory

Back 42

close correlation between anasthetic potency and lipid solubility
now largely discredited

Front 43

Mechanism of action of anaesthetic drugs

Back 43

bind to ion channels,

inhibit excitatory receptors (glutamate, ACh, 5-HT)
Exhancement of inhibitory receptors (GABAa, glycine)
activation of K+ channels

Front 44

Effect on the nervous system

Back 44

reduction of transmitter release
inhibition of NT action
reduction of excitability

brain regions -> thalamic sensory relay nuclei, hippocampus

stage 1: analgesia
stage 2:excitatory (want to delete this stage)
stage 3: surgical anaesthesia
stage 4; medullary paralysis

Front 45

anaesthetics reduce ____

Back 45

excitability

Front 46

effects of anaesthetics on cardiovascular and respiratory systems

Back 46

halogenated anaesthetics cause cardiac dysrhythmias

all anaesthetics (except NO2 and ketamine) depress respirations

Front 47

which drugs are lipophilic

n2o, cyclopropane, halothane, ether

Back 47

halothane and ether

slow curve on graph (slow induction into blood)
potent

Front 48

what does low blood solubility have to do with potency

Back 48

low blood solubility means lower potency

Front 49

blood:gas coefficient for anaesthetics

Back 49

solubility in blood (rate of induction and recovery)
lower = faster induction and recovery

Front 50

oil:gas coefficient for anaesthetics

Back 50

measure of lipophilicity
influences distribution, induction and recovery.
more lipophilic = slower recovery

Front 51

inhalation anaestetics

Back 51

halothane (non explosive = hepatotoxicity, malignant hyperthermia), N2O (childbirth), enflurane, isoflurane (MOST USED), desflurane and sevoflurane

Front 52

intravenous anaesthetics

Back 52

thiopental, ketamine, propoful, etomidate, midazolam.

GABAa agonist for most
ketamine -> glutamate nmda antagonist

Front 53

peripheral nervous system

Back 53

clusters of nerve cell bodies and processes

physical continuity with CNS

cranial nerves, spinal nerves and ganglia

Front 54

brain 5 regions

Back 54

telencephalon (cortex, basal ganglia), diencephalon (thalamus, hypothalamus), mesencephalon (cerebral peduncle, tectum), metencephalon (pons and cerebellum), myelencepaholon (medulla oblongata)

Front 55

cortex

Back 55

multilayers of neurons
planning and initiation of movement
learning and memory
50-100 billion cells
perception and integratino of sensory information

Front 56

cortex arrangment

Back 56

suli, gyri and fissures

made up of primary motor and sensory areas

Front 57

homunculus

Back 57

diagram of which part of the cortex is responsible for each body part

(more area = more sensitive)

Front 58

limbic system

Back 58

hippocampal formation (memory, emotion)
amygdala (fear)

Front 59

thalamus

Back 59

input from basal ganglia, cerebellum, limbic system and sensory system.
output to ipsilateral cortex

intergrates sensory information
regulates cortical activity
control movement

Front 60

hypothalamus

Back 60

controls appetite, fluid balance, metabolism, circadian cycle, body temperature.

integrates functions

Front 61

basal ganglia

Back 61

inputs from cortex and thalamus

outputs to thalamus and brainstem

motor planning and execution
important in mvmt disorders such as parkinsons

Front 62

cerebellum

Back 62

coordination of movement
speed, direction, precision and timing of muscle activity and maintenance of balance

Front 63

reticular formation

Back 63

central core of brainstem

functions like breathing

influences of autonomic nervous system, biological systems and endocrine functions

Front 64

cerebrospinal fluid

Back 64

choroid plexus

rich in sodium, potassium, chloride
protection and nutrition
free difusion to ECF

Front 65

blood brain barrier

Back 65

isolate brain from blood stream
tight junction between cells
active cellular transport
passive diffusion

Front 66

glia

Back 66

glue

astrocytes
ogliodendricites
microglia

Front 67

soma

Back 67

cell body

cytoplasm rich in RER (mitochondria)

Front 68

cytoskeleton

Back 68

shape and transport

Front 69

axons

Back 69

one per neuron

proper (can be myelinated)
terminal (arborization)

Front 70

dendrites

Back 70

transmit signal towards body

highly branched

receives input from different sources

Front 71

myelin

Back 71

layers of oligodendrocytes wrapped around short section of axon
nodes of ranvier

Front 72

water and ions

Back 72

more Na+ outside, K+ inside, Ca2+, Cl-

Front 73

membrane

Back 73

phospholipid bilayer
hydrophoblic core

Front 74

movement of ions via....

Back 74

passive diffusion

Front 75

sodium potassium pump

Back 75

maintains membrane potential by pumping 3 sodium out and 2 potassium in

Front 76

action potential

Back 76

depolarization of membrane by Na+ entering cell.

all or nothing

propagation and saltatory conduction

Front 77

chemical synapse

Back 77

normal

Front 78

electrical synapse/tight junction

Back 78

tight junction, small molecules and ions, electrical coupling

Front 79

information transmission

Back 79

one direction due to refractory period

Front 80

information processing

Back 80

single cell computation/integration

Front 81

location of primary somato-sensory cortex

Back 81

post central gyrus of parietal lobe

Front 82

three neuron synaptic chain

Back 82

central axons of sensory neurons enter dorsal root of spinal cord

synapse with 2nd order neurons in medial lemniscal tract and ascent to thalamus

synapse with 3rd order neurons at thalamus which transmit information to somato-sensory cortex

Front 83

spatial discrimination

Back 83

ability of cortex neurons to process sensory information and IDENTIFY THE PRECISE AREA OF THE BODY BEING STIMULATED

Front 84

left side of the body controlled by _____ side of brain

Back 84

right

Front 85

damage to somatosensory cortex

Back 85

destroys ability to feel and localize touch, pressure and vibration

ability to feel pain and temperature is lost but can still be felt vaguely (poorly localised)

Front 86

somatosensory association area

Back 86

posterior to primary somato sensory cortex

function: integrate and analyse different somatic sensory inputs (touch, pressure) relayed to it by primary somato sensory cortex

draws upon stored memories of past experiences to perceive the object allowing you to regonise familiar objects without looking

Front 87

perception of pain

Back 87

peripheral nociceptors detect pain --> pain pathways relay info via action potentials to spinal cord --> 1. & 2.

1 --> monosynapic withdrawal reflex

2--> sensory info submitted to brain via spinothalamic tract -> cortex localises brain and induces appropriate motoric behaviour

Front 88

limbic system and pain

Back 88

limbic system adds to pain (dysphoria)


amygdala hippocampus

Front 89

peripheral nociception

Back 89

nociceptors can detect mechanical, thermal or chemical change above a set threshold. once stimulated a nociceptor transmits a signal along the spinal cord to the brain.

Front 90

painful stimuli which directly activate nociceptors

Back 90

K+, ATP, 5-HT, Bradykinin, histamine.

Front 91

stimuli which sensitize nociceptors

Back 91

prostaglandins, leukotrienes, substance P.

Front 92

pain receptors transmit to which part of spine

Back 92

different
e.g. A may go to 1, 3, 5
C to 1, 2 or something

Front 93

central processing of pain

Back 93

ascending pathway (spinothalamic tract) takes information to brain past thalamus to somatosensory cortex where it is localised and processed (with help from motor cortex and associated cortex)

descending tract then takes info (plus input from thalamus) back to place of pain)

Front 94

gate control mechanism

Back 94

descending inhibitory pathway reduces response at synapse and + at SG neuron which - at synapse (decreases info processed to CNS).

makes pain less

mechanoreceptors (AB) also activate SG neurons which decrease info processed to CNS

activates opioid receptors (dynorphines at K)