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Flashcards in Chris Bailey Lecture Flash Cards Deck (109):

What three sub classes can memory be divided into?



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

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


What is a priming cue?

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


What is declarative memory?

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


What is procedural memory?

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


What is emotional memory?

To do with preferences and aversions
Eg having a strong like or dislike to something


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



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



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

Brain stem and spinal motor output


What are the areas called collectively that control memory?

The cortical association areas of the brain


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?

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.


What is the engram- Hebbs law?

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.


How do we study synaptic strengthening?

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


What is the increase in strength after repeated stimulation called?

Long term potentiation ( LTP)
This strengthened action potential stays around for months and is the basis of long term memory


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

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


What two things can prevent LTP?

Pharmacological blockade of NMDA receptor

Reducing extracellular Calcium levels

These result in EPSP not potentiated


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

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


What Is Mg-dependent gating very important in?

Synaptic plasticity, learning and memory


What relieves the Mg2+ block of the NMDAr receptor?

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


How can we increase LTP postsynaptically?

More AMPAr's
More sensitive AMPAr
More synapses


How can we increase LTP presynaptically?

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


What is classical conditioning to do with?

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


What is the unconditioned stimulus in fear conditioning?

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.


What drug addiction can pavlovian classical conditioning be linked to?

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.


___________ a memory will strengthen it..?



Stimulants are cognition (memory) enhancers. Examples?

Methyl phenidate


AMPAkines are cognition enhancers. Examples?

Positive AMPA-r modulators


Difference between retrograde and anterograde amnesia?

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.


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



Which artist drew pictures to show his descent into Alzeihmers?

William Utermohlen


Is Alzeihmers cortical or sub cortical?

(Parkinson's is cortical)


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

Early damage in entohinal cortex


What are Neuritic plaques made of?

They're extracellular


What are neurofibrillary tangles made of? (Alzeihmers)

Made of abnormal cytoskeleton protein: Tau
They're intracellular


What do plaques and tangles effect? (Alzeihmers)

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


Abnormal ___ processing results in formation of _____plaques

Abnormal APP processing,
Results in formation of amyloid plaques


What causes the formation of an amyloid plaque?

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


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

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


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



What enzyme cleaves APP to cause formation of amyloid plaques?

Beta secretase


What enzyme cleaves APP in a normal healthy brain?

Alpha secretase


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

Gamma- secretase (y-secretase)


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

ApoE4 mutations: leading to increased aggregation


What genetic mutation is identified in early onset Alzeihmers?

Mutation in presenillin genes leading to excess gamma secretase activity


How do tangles form?

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


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

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


What is the triad of general anaesthesia?

Muscle relaxation


Why do we want an anaesthetic to be reasonably selective?

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.


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

Plane 3 of stage 3.


What stage of anaesthesia needs to be avoided?

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


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

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


What does the patient experience in stage 2 of anaesthesia?

Lack of consciousness
Gagging, vomiting
Irregular cardio-respiration


What are the two main routes used for anaesthesia?

Inhalation of gases
IV injection


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

Halogenated ethers/ halogenated hydrocarbons


What analgesic could you supplement throughout the operation?

IV fentanyl, it's an opioid


Which gas is used by vets for anaesthesia?



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

Rapid, pain relief, low potency


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

Has rapid on off, no grogginess, low toxicity, but can be epileptogenic

Rapid on off (lecture states this is good for day surgery)


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

Very rapid metabolism, induction and maintenance
Used for day surgery


Tell me about thiopental?

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


What patients is ketamine used as an anethestetic in?

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


What are midozalam and benzodiazepines used for?

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


What's the difference between narcosis and necrosis?

Necrosis- death 


What is the lipid theory of anaesthetic mechanism?

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.


What's the protein theory of anathestics?

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.


Are general anaesthetics specific?

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


What is a stroke a result of?

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


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

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


What are the four risk factors of stroke?

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


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

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


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

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


How does an ischaemic stroke occur?

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.


How does a hemorrhagic stroke occur?

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


What are the symptoms of stroke?

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


The first __ hours are critical for stroke treatment?

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


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

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.


What is the primary cause of cell death in stroke?


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


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

Blue mussel poisoning
Guam disease


What is tissue plasminogen activator?

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.


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

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


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

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


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

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


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

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


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

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


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

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


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

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


Definition of pain

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


What is Nociception?

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


What are Nociception?

Structures which detect noxious stimuli


What is algesia?

The induction of a condition leading to Nociception and pain


What is analgesia?

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


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

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


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

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


Which are stronger thermal receptors? Mechanical or polymodal nociceptors?

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


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

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


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

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


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.

First sensation: alpha delta fibres
Second sensation: C fibres


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

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


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

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


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

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


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

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


Is Nociception just exaggerated sensory transmission? Why?

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


What is hyperalgesia?

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


What is allodynia?

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.


hyperalgesia and allodynia ....

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


What is neuropathic pain?

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.


Examples of neuropathic pain?

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)


What is phantom leg syndrome?

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. 


What is an itch?

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

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