Chris Bailey Lecture Flash Cards

Question 0

What are motor skills and what sub class are they part of?

Answer 0

Skills like riding a bike and walking, skills we have learnt but have become subconscious of 
Part of procedural subclass of memory

Question 1

What three sub classes can memory be divided into?

Answer 1

Declarative
Emotional
Procedural

Question 2

What is a priming cue?

Answer 2

If something happened in the past, a past memory makes you hate for example the smell of something, a past memory triggers/ cues an emotional feeling.
It's in the subclass of procedural memory

Question 3

What is declarative memory?

Answer 3

A type of long term memory involved in recalling facts and knowledge, words and meaning, history and episodic memory which stores specific daily experiences.

Question 4

What is procedural memory?

Answer 4

Another type of long term memory (declarative the other type)
It’s involved with unconscious memory such as skills, eg riding a bike, puzzle solving, walking

Question 5

What is emotional memory?

Answer 5

To do with preferences and aversions

Eg having a strong like or dislike to something

Question 6

What Part of the brain is mostly involved with emotional memory?

Answer 6

Amygdala

Hypothalamus

Question 7

What part of our brain is mostly involved with declarative memory?

Answer 7

Hippocampus

Question 8

Which part of our brain is mostly involved with procedural memory?

Answer 8

Cerebellum
Striatum
Brain stem and spinal motor output

Question 9

What are the areas called collectively that control memory?

Answer 9

The cortical association areas of the brain

Question 10

What was the name of the man who had epilepsy, who had his entorhinal cortex, hippocampus and amygdala removed to try and cure his epilepsy? What did this result in? What are these parts of the brain all a part of?

Answer 10

Henry Molaison (H.M)
Had his whole temporal lobe removed
This resulted in memory loss.
Indicated that the entorhinal cortex, hippocampus and amygdala are all involved with memory.
His short term memory was still in tact, and working memory too, but he couldn’t form new long term memories.
Therefore we knew the hippocampus was important in making long term memories stick.

Question 11

What is the engram- Hebbs law?

Answer 11

When two neurones are active, so that one repeatedly releases neurotransmitter at the same time as its post synaptic partner is firing action potentials, then that synapse will become STRONGER. The synapse is strengthened by this intense activity.
Memory depends on populations of interacting neurones
The pattern of strengthened synapses defines memory.

Question 12

How do we study synaptic strengthening?

Answer 12

We use a rat temporal lobe slice 
We stimulate glutamate excitatory axons
And then record membrane potential of neurones

Question 13

What is the increase in strength after repeated stimulation called?

Answer 13

Long term potentiation ( LTP)

This strengthened action potential stays around for months and is the basis of long term memory

Question 14

What needs to be reached for long term potentiation of memory to be achieved?

Answer 14

A threshold,
EPSPs produced by a High rate of stimulation summary together and reach the threshold, ie a synapse stimulated repeatedly

Question 15

What two things can prevent LTP?

Answer 15

Pharmacological blockade of NMDA receptor

Reducing extracellular Calcium levels

These result in EPSP not potentiated

Question 16

What does removal of Mg2+ from the NMDA receptor channel allow?

Answer 16

Allows both calcium and Na+ to flow through the channel

Calcium entry into the cell results in cellular changes, which leads to increased AMPAr responses and therefore LTP

Question 17

What Is Mg-dependent gating very important in?

Answer 17

Synaptic plasticity, learning and memory

Question 18

What relieves the Mg2+ block of the NMDAr receptor?

Answer 18

Repetitive activation of AMPA r results in increased extracellular calcium levels. This causes depolarisation and therefore relieves the Mg2+ block of the NMDA receptor.

Question 19

How can we increase LTP postsynaptically?

Answer 19

More AMPAr’s
More sensitive AMPAr
More synapses

Question 20

How can we increase LTP presynaptically?

Answer 20

Increase release of glutamate from releasing synaptic vesicles
Increased release sites
More vesicles

Question 21

What is classical conditioning to do with?

Answer 21

Animals
If you ring a bell- no salivation
If you give food and ring a bell - salivation (classical conditioning)
Then if you ring the bell again with no food- salivation
Food is the unconditioned stimulus, the sound of the bell is the conditioned stimulus.
It is the learning in which the conditioned stimulus (bell) comes to signal the occurrence of a second stimulus, the unconditioned stimulus (food).
Salivation is the unconditioned response

Question 22

What is the unconditioned stimulus in fear conditioning?

Answer 22

Pain (electric shock)
Again a bell is the conditioned stimulus.
The animal learns that when it hears the bell it will get an electric shock, therefore it freezes.
Conditioning is usually done by pairing the two stimuli, as in Pavlov’s classic experiments.

Question 23

What drug addiction can pavlovian classical conditioning be linked to?

Answer 23

Cocaine
People get off it, then something, a memory trace, eg seeing somebody else have it, may trigger them to start it again.
We’re looking to erase this memory trace with drug treatment to cure drug addicts, need to block these cues.

Question 24

___________ a memory will strengthen it..?

Answer 24

Reactivating!

Question 25

Stimulants are cognition (memory) enhancers. Examples?

Answer 25

Amphetamine Caffeine Methyl phenidate

Question 26

AMPAkines are cognition enhancers. Examples?

Answer 26

Positive AMPA-r modulators Piracetam IDRA-21

Question 27

Difference between retrograde and anterograde amnesia?

Answer 27

Retrograde amnesia: where most memories created prior to the event that caused amnesia are lost while new memories can still be created. Anterograde: loss of the ability to create new memories after the event that caused the amnesia, but not lost memories that were created prior to the event that caused the amnesia.

Question 28

What's the percentage chance of developing Alzeihmers if you're over 95?

Answer 28

53%

Question 29

Which artist drew pictures to show his descent into Alzeihmers?

Answer 29

William Utermohlen

Question 30

Is Alzeihmers cortical or sub cortical?

Answer 30

Cortical | Parkinson's is cortical

Question 31

Which part of the brain deteriorates in early stages to cause memory and speech defects?

Answer 31

Early damage in entohinal cortex

Question 32

What are Neuritic plaques made of?

Answer 32

Amyloid-B-protein | They're extracellular

Question 33

What are neurofibrillary tangles made of? (Alzeihmers)

Answer 33

Made of abnormal cytoskeleton protein: Tau | They're intracellular

Question 34

What do plaques and tangles effect? (Alzeihmers)

Answer 34

Primarily Affect glutamate and acetylcholine neurones and terminals This results in synapse loss and neuronal death, which leads to brain shrinkage 

Question 35

Abnormal ___ processing results in formation of _____plaques

Answer 35

Abnormal APP processing, | Results in formation of amyloid plaques

Question 36

What causes the formation of an amyloid plaque?

Answer 36

Abnormal cleavage of APP (amyloid precursor protein) by the enzyme BETA-secretase Cleavage products are AB40-42 and soluble APPbeta AB40-42 levels build up and aggregate Aggregation enhanced by ApoE4 Forms amyloid plaque

Question 37

Are low or high levels of Abeta40/42 found in the brain of a healthy person?

Answer 37

Low levels! | Normal cleavage of APP does not result in Abeta40/42 normally, only with abnormal cleavage leading to plaques.

Question 38

What is aggregation of AB40/42 enhanced by to form a plaque?

Answer 38

ApoE4

Question 39

What enzyme cleaves APP to cause formation of amyloid plaques?

Answer 39

Beta secretase

Question 40

What enzyme cleaves APP in a normal healthy brain?

Answer 40

Alpha secretase

Question 41

What enzyme cleaves off the extra chain (AICD) on the AB40/42 molecule to form AB40/42 alone?

Answer 41

Gamma- secretase (y-secretase)

Question 42

What's a Genetic risk factor in late onset Alzeihmers?

Answer 42

ApoE4 mutations: leading to increased aggregation

Question 43

What genetic mutation is identified in early onset Alzeihmers?

Answer 43

Mutation in presenillin genes leading to excess gamma secretase activity

Question 44

How do tangles form?

Answer 44

Lots of fibrillar amyloid deposition (beta amyloid) at nerve terminals, forms plaques. Plaques destruct terminals Plaques get caught up together forming tangles Tangles cause neurone death

Question 45

What could we treat alzheimers patients with at the moment? Will this stop progression?

Answer 45

Cholinesterase inhibitors, to increase levels of acetylcholine Cholinergic neurones get damaged early, and a lot of the cortex receives Cholinergic innervation

Question 46

What is the triad of general anaesthesia?

Answer 46

Unconsciousness Analgesia Muscle relaxation

Question 47

Why do we want an anaesthetic to be reasonably selective?

Answer 47

We want it to suppress brain function so that we become unconscious, but we don't want it to suppress the respiratory system or the heart too much.

Question 48

What stage of anaesthesia do anaesthetists aim get the patient to and keep them at during surgery?

Answer 48

Plane 3 of stage 3.

Question 49

What stage of anaesthesia needs to be avoided?

Answer 49

Stage 4, medullary paralysis | This stage is overdose stage, and can lead to cardio respiration depression and therefore death. 

Question 50

What are the warning signs that show the anaesthetists the patient is close to stage 4 and they should ease off the gas?

Answer 50

Decreased respiratory rate Dilation of pupils  No light reflex in eye- happens in plane 4 of stage 3 so definite warning sign. Zero muscle tone

Question 51

What does the patient experience in stage 2 of anaesthesia?

Answer 51

``` Excitement Lack of consciousness Delirium Spasticity Gagging, vomiting Irregular cardio-respiration ```

Question 52

What are the two main routes used for anaesthesia?

Answer 52

Inhalation of gases | IV injection

Question 53

What are the gases called that are usually used for anaesthesia?

Answer 53

Halogenated ethers/ halogenated hydrocarbons

Question 54

What analgesic could you supplement throughout the operation?

Answer 54

IV fentanyl, it's an opioid

Question 55

Which gas is used by vets for anaesthesia?

Answer 55

Halothane

Question 56

Which gas is used for anaesthesia for obstetrics (pregnancy) ?

Answer 56

N2O | Rapid, pain relief, low potency

Question 57

Which gases are good for short procedures/ day surgery? Why?

Answer 57

Enflurane Has rapid on off, no grogginess, low toxicity, but can be epileptogenic Desflurane Rapid on off (lecture states this is good for day surgery)

Question 58

What's the most commonly used IV anaesthetic used these days?

Answer 58

Propofol Very rapid metabolism, induction and maintenance Used for day surgery

Question 59

Tell me about thiopental?

Answer 59

``` Commonly used intravenous aesthetic It's a barbiturate Very fast on (20 secs) off (15 mins) Non analgesic Can cause respiratory depression Hangover effects ```

Question 60

What patients is ketamine used as an anethestetic in?

Answer 60

``` Used in children  Hallucinogenic- not sure if children experience these Slow onset Dissociative- dissociate from real world Analgesic and Bradycardic ```

Question 61

What are midozalam and benzodiazepines used for?

Answer 61

They're given to lower peoples anxiety before operations | They're not anaesthetics

Question 62

What's the difference between narcosis and necrosis?

Answer 62

Narcosis-unconsciousness | Necrosis- death 

Question 63

What is the lipid theory of anaesthetic mechanism?

Answer 63

Lipid theory suggests potency is proportional to lipid solubility Suggests anaesthetic physically sits between the lipids on the membrane and on sodium channels, expands the membrane, effects fluidity so that sodium channels can't undergo a conformational change and therefore can't open.

Question 64

What's the protein theory of anathestics?

Answer 64

Suggests membrane proteins such as receptors and ion channels interact with the anaesthetic, and suggests the anaesthetic alters their function. This was seen through a close correlation between anaesthetic potency and the potency of luciferase inhibition of anaesthetics.

Question 65

Are general anaesthetics specific?

Answer 65

No They're pretty much non specific They don't target a specific receptor They target many different proteins: ion channels, sodium channels, glutamate, potassium channels, GABA... All of the, inhibit the Nicotinic acetylcholine receptor

Question 66

What is a stroke a result of?

Answer 66

Transient or permanent interruption in cerebral blood supply, leads to ischemia, which is the lack of oxygen/ glucose needed for cellular metabolism

Question 67

What are seen as signs that a stoke may occur within 5 years of these starting?

Answer 67

Transient ischaemic attacks (TIAs) Referred to as mini strokes They're short lived (transient) episodes of neurological function, caused by lack of blood supply They're neurological signs that a stroke may occur in the next 5 years

Question 68

What are the four risk factors of stroke?

Answer 68

Hypertension Obesity (high cholesterol levels, increased risk of ischemia) Smoking Alcohol 

Question 69

What's the incidence and mortality levels of ischaemic stroke?

Answer 69

``` Incidence = 80% (most common form of stroke) Mortality = 40% ```

Question 70

What's the incidence and mortality levels of haemorrhaging stroke?

Answer 70

Incidence=20% (a lot less common than ischemic!) | Mortality= 50% (more fatal than ischemic strokes)

Question 71

How does an ischaemic stroke occur?

Answer 71

Thrombotic-caused by narrowing of lumen of large or small blood vessels, by a blood clot forming inside these vessels. Can also be embolic- lodging of an embolus, which may be a blood clot, a fatty lump or a gas/air bubble in the bloodstream, which can cause a blockage. Remember ischemic stroke= BLOCKED VESSELS These both result in restricted blood supply in brain, leading to stroke.

Question 72

How does a hemorrhagic stroke occur?

Answer 72

occurs when a blood vessel in the brain breaks leaking blood into the brain intracerebral hemorrhage stroke is most common type, occurs when a blood vessel inside the brain ruptures and leaks blood into surrounding brain tissue. subarachnoid hemorrhage occurs when blood spills into the space surrounding the brain, ie not into the brain tissue itself like intracerebral

Question 73

What are the symptoms of stroke?

Answer 73

Difficulty talking and understanding words Loss of feeling and strange feeling on one side Weakness of the face arm or leg on one side Severe headache Blurry vision Dizziness, loss of balance

Question 74

The first __ hours are critical for stroke treatment?

Answer 74

First 3 hours If they haven't had treatment in the first 3 hours then prognosis is very bad Good recovery within first 3 hours

Question 75

The longer the stroke is left without treatment, the more ___ damage occurs

Answer 75

Structural damage occurs This spreads from the core as time progresses At first, in a matter of minutes, only reduced function spreads, then within hours, structural damage starts to spread further and further across the brain.

Question 76

What is the primary cause of cell death in stroke?

Answer 76

Excitotoxcity! This is where neurons get excited to death. The neurotransmitter glutamate is actually highly toxic to neurones Calcium overload is an essential factor in excitotoxicity

Question 77

Dietary intake of amino acid agonists (eg glutamate) can also lead to cell death and stroke... What three ways is this through?

Answer 77

Blue mussel poisoning Guam disease Neurolathyrism

Question 78

What is tissue plasminogen activator?

Answer 78

tPA is the ONLY LICENSED treatment for ischeamic Strokes Is restores blood flow and gets rid of the thrombus (blockage) It only works within 3 hours of stroke onset, need to act FAST Only works for ischeamic (thrombotic) stroke.

Question 79

What possible "blockers" could you use to treat stroke?

Answer 79

AMPA/NMDA receptor blockers Glutamate release blockers Na+/Ca+ (exchange pumps) blockers Free radical scavengers (break down free radicals) NO synthase blockers (stops hydroxyl free radicals being produced) Protease inhibitors

Question 80

What pharmacological treatment could you use to decrease the risk of stroke?

Answer 80

ACE inhibitors; these decrease blood pressure Statins for cholesterol reduction Aspirin Stockings?possibly stop blood clots in legs! Lowering blood pressure is key in decreasing the risk of stroke.

Question 81

Treating a patient with ___ within __ hours of stroke onset really works!!

Answer 81

Treat them with tPA, (tissue plasminogen activator), within 3 hours of stroke onset gives a good prognosis

Question 82

What do long term symptoms and recovery of the brain after a stroke depend on?

Answer 82

Depends on the region of the brain effected | Could be the motor cortex, Brocas area, or Wernickes area

Question 83

Eating something that is a ____receptor agonist can trigger excitotoxicity. examples?

Answer 83

A glutamate receptor agonist, so NMDA or AMPA receptor or KAINATE receptor agonist Eg DOMOIC ACID (produced by diatom, a type of algea) KAINIC ACID Results in damage to hippocampus, amygdala and entorhinal cortex, by triggering excitotoxicity to occur. This both stimulate KAINATE receptors

Question 84

What does Beta-N-oxalylamino-L-alanine (BOAA) cause?

Answer 84

Neurolathyrism, a neurological disease caused by eating Legumes It's an AMPAreceptor agonist Targets spinal chord Results in muscle rigidity and paralysis of lower limbs resulting in spasticity Damages thoracic and lumber motoneurones

Question 85

What does Beta-N-Methyl-amino-L-alanine cause (BMAA)?

Answer 85

Guam disease BMAA present in certain seeds It's an AMPA and NMDA receptor agonist Results in symptoms of Alzeihmers, Parkinson's, and amyotrophic lateral sclerosis.... Leads to muscle weakness, paralysis, dementia

Question 86

Definition of pain

Answer 86

The subjective conscious appreciation of a stimulus this is causing, or threatening to cause tissue damage

Question 87

What is Nociception?

Answer 87

The physical process of detection and transmission of a damaging or potentially damaging (noxious) stimulus.

Question 88

What are Nociception?

Answer 88

Structures which detect noxious stimuli

Question 89

What is algesia?

Answer 89

The induction of a condition leading to Nociception and pain

Question 90

What is analgesia?

Answer 90

Simply: pain relief Reduction or prevention of either Nociception or pain without loss of consciousness (loss of consciousness is by anaesthesia)

Question 91

What are the nociceptive (pain) fibres in our periphery?

Answer 91

Free nerve endings These contain mechanical nociceptors and polymodal nociceptors These free nerve endings will only respond to potentially harmful stimuli

Question 92

Mechanical Nociceptors and poly modal nociceptors are both ____ ______ ______ receptors.

Answer 92

Both High intensity Mechanical receptors | Note: they're both mechanical receptors, just the mechanical nociceptors are mechanical only!

Question 93

Which are stronger thermal receptors? Mechanical or polymodal nociceptors?

Answer 93

Mechanical are strong thermal receptors, detect when something's over 60 degrees

Question 94

What fibres are associated with fast pain, sharp pricking, well tolerated pain?

Answer 94

Alpha- delta fibers These are myelinated and thicker than other fibres, so transmit action potential very fast Pain intensity will be great.

Question 95

What fibres are associated with slow pain; burning, aching, throbbing pain that's poorly tolerated?

Answer 95

C fibres These aren't myelinated so APs go down these fibres slowly This pain is poorly tolerated, and lasts longer than pain from alpha delta fibres

Question 96

First sensation of pain is always activated by ____ fibres. Second phase of pain (after first initial sharp pain) is activated by ____ fibres. This is more throbbing pain.

Answer 96

First sensation: alpha delta fibres | Second sensation: C fibres

Question 97

What are the thickest, most myelinated afferent fibres from skin? From muscle? What sensory receptors are associated with these?

Answer 97

Thickest axons from skin: A alpha Thickest Axons from muscle: group I Sensory receptors: proprioceptors of skeletal muscle

Question 98

What are the second thickest, myelinated afferent fibres from skin? From muscle? What sensory receptors are associated with these?

Answer 98

From skin: A beta From muscle: group II Receptors? Skin mechanoceptors

Question 99

What are the third thickest, myelinated afferent fibres from skin? From muscle? What do the sensory receptors detect ?

Answer 99

Axons from skin: A delta axons from Muscle: group III Receptors: pain and temperature

Question 100

What are the thinnest, un-myelinated afferent fibres from skin? From muscle? What do their sensory receptors detect?

Answer 100

Axons from skin: C Axons from muscle: IV Detect pain, temperature and itch

Question 101

Is Nociception just exaggerated sensory transmission? Why?

Answer 101

No Nociception axons conduct at slower velocities Nociceptors have different thresholds of activation Nociceptors have different SITES of projection into the spinal chord They induce different physiological responses Information ascends in different pathways

Question 102

What is hyperalgesia?

Answer 102

Increased response to a noxious stimulus | Eg if you pinch you hand when it's already burnt; you get much more pain

Question 103

What is allodynia?

Answer 103

Painful response to a non-noxious stimuli This is where something that isn't usually harmful causes pain. This is due to you touching an area of skin that is already damaged, eg touching a swollen part of the skin will cause pain, when touching skin normally wont.

Question 104

hyperalgesia and allodynia ....

Answer 104

Are a result of Increased sensitivity of peripheral nociceptors (peripheral sensitisation) Increased transmission in the spinal chord (central sensitisation)

Question 105

What is neuropathic pain?

Answer 105

Pain unrelated to peripheral Nociception, ie it serves no purpose, not from an outside stimulus causing harm, sometimes called pathological pain. Neuropathic pain is usually due to damage of the nerves themselves.

Question 106

Examples of neuropathic pain?

Answer 106

Thalamic Stroke (destroys some nociceptor input in the thalamus, causes you to feel pain all the time rather than non at all ) Peripheral nerve damage Peripheral nerve terminal damage/ infection Spinal damage (eg slipped disc)

Question 107

What is phantom leg syndrome?

Answer 107

A type of neuropathic pain Leg gets amputated, but people get chronic pain from a leg that doesn't exist. This is because you've cut nerve terminals, which then fire all the time, pain is coming from something that isn't there, but these nerve terminals firing lead to chronic pain. 

Question 108

What is an itch?

Answer 108

We know it's affront input via A delta and C fibres We know inflammation, particularly histamine, can cause it But we don't know much about it Analgesics won't inhibit it much To cure, you scratch