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PA30324 > Pharmacology and Therapeutics - C Bailey > Flashcards

Pharmacology and Therapeutics - C Bailey Flashcards

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1
Q

At rest, which part of the cell is the most positively charged….

The inside or outside?

A

The outside!

As the K+ channel is open allowing the high K+ concentration inside to move to the outside

Also due to the high sodium content outside

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2
Q

What is an ionotropic receptor?

What is a metabotropic receptor?

A

Ionotropic –> A ligand gated ion-receptor

Metabotropic –> A GPCR

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3
Q

Explain Glutamate and GABA synapses and how they work

A

Glutamate –> Activate Na+ channels which cause an excitatory response (EPSP)

GABA –> Activate Cl- channels which make an inhibitory response (IPSP)

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4
Q

If a synapse causes a Gi response or Gs response, what will occur?

A

Gi –> Make action potentials less likely

Gs –> Make action potentials more likely

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5
Q

Will Myelin Shieth speed up or slow down transmission?

A

Speed up

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6
Q

What is CSF?

A

Cerebrospinal Fluid

Produced in the choroid plexus

A solution of NaCl and glucose (with low levels of K+ and Ca2+) that gives protection to the brain

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7
Q

Define Noiciception

A

The physical process of detection and transmission of damaging or potentially damaging (noxious) stimuli

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8
Q

What is the main cause of depolarisation in free nerve endings?

A

An influx of Na+ ions via various transporters that are activated due to different reasons

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9
Q

Why does referred pain occur?

A

When 2nd order neurones are shared. So signals are sent to more than just the one place

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10
Q

What’s the different between hyperalgesia and allodynia?

A

Hyperalgesia –> Increased response to a noxious stimulus

Allodynia –> Painful responses to a non-noxious stimulus

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11
Q

How does Noiciceptor Sensitization occur?

A

After an injury or autoimmune response, H+/ATP/K+ will directly depolarise the noiciceptors

Substance P (from the noiciceptor) makes the blood vessels contract/leaky and causing more mast cell degranulation

These make noicieptors more sensitive due to tissue damage, causing action potentials to occur more often.

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12
Q

What are the 2 types of receptor that glutamate will bind to?

A

AMPA –> Rapid depolarisation

NMDA –> Slow but sustained depolarisation

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13
Q

What is ‘Wind-Up’ in terms of nociception?

A

Stimulation of the same magnitude will cause more action potentials as the number of stimulations increase

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14
Q

Why will holding injuries in sport actually decrease the pain that is felt? (Gate Control)

A

As touch receptors (mechanoreceptors) in the skin stimulate the inhibition of the the dorsal horn projection pathway, which tells us of pain.

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15
Q

Why do Enkephalins help reduce our pain levels?

A

The 4 enkephelins we have will bind to all opiate receptors via Gi coupled GPCRs, increased K+ efflux and minimising Ca2+ influx. This has an inhibitory effect on action potentials, meaning that they are less likely

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16
Q

How do opioids work in the Periaqueductal Grey (PAG)?

A

GABA is inhibited by opioids, which means the neurone towards the raphe magnus is stimulated. This is good as 5-HT is produced in the raphe magnus, which reduces pain

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17
Q

What is the main opioid receptor?

And why?

A

Mu

This is because it is the most widespread in the body and gives the most analgesic effect

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18
Q

What is the main effect/outcome of opioids and NSAIDs?

A

Opioids –> Boost the decending inhibiton of noiciception

NSAIDs –> Inhibit peripheral sensitisation

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19
Q

How do NSAIDs work?

A

Block the COX1/2 enzymes, hence preventing the conversion of Arachiadonic Acid to Prostaglandin H2

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20
Q

How is neuropathic pain treated?

A

Due to it being unrelated to noiciception, it cant be treated with NSAIDs or opioids.

Treated with TCAs and antiepileptic drugs mainly

Also: Capsacin cream/CGRP receptor blockers/Na+ receptor blockers/Cannabinoid receptor agonists

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21
Q

What’s the difference between psychological and physcial dependence?

A

Psychological - ‘Addicition’ such as craving and loss of control

Physcial - When stopping a drug will cause withdrawal effects

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22
Q

What is known as the ‘Reward Pathway’?

Study These Flashcards
A

The Mesolimbic Pathway

From the Ventral Tegmental Area (VTA) to the Nucelus Accumbens

23
Q

What are 2 ways of preventing the reward pathway being successfully stimulated?

Study These Flashcards
A

Use 6-OHDA –> Destroys the dopaminergic neurone that completes the pathway

D1/2 Antagonists –> Act on the nucleus accumbens

24
Q

How do opioids increase dopamine levels in the body?

Study These Flashcards
A

They inhibit GABA neurones, increasing the stimulation of dopaminergic neurones (and so dopamine)

25
How does **Ethanol increase dopamine levels**?
They stimulate dopamine neurones directly, by keeping K+ channels open for longer...which **speeds up repolarisation (decrease after-hyperpolarisation) and so more action potentials fire** (quicker)
26
Why does **ethanol** cause the characteristic **memory and movement problems**?
**An NMDA Antagonist** --\> causes memory loss **A Calcium Channel Antagonist** --\> Causes movement problems
27
How does **Cannabis** and **Nicotine** **affect the mesolimbic pathway**?
**THC (Cannabis)** --\> Same as opioids...inhibit GABA which in term stimulates dopamine production **Nicotine** --\> Acts on ACh receptors on dopaminergic neurones in the VTA
28
What are the **2 types of Stroke**? And which is the **most common**?
**Ischaemic** --\> Occurs from blocked arteries This is the most common **Haemorrhagic** --\> Blood vessels leak out/rupture
29
What is the **main mechanism of action of strokes**?
**Excitotoxicity** Glutamate is excessively released, which stimulates Ca2+ influx...causing a positive membrane potential (due to lack of O2/glucose meaning the Na+/K+ pump to not function!!)
30
How can increased **calcium levels cause more calcium to enter the cell during a stroke**
The elevated **calcium activates proteases and lipases which causes structual damage**. This damage allows more calcium to enter the neurones
31
What is **Peri-Infarct Depolarisation**?
Where **neurones are damaged in the penumbra when blood returns**. This causes the ATP/O2 to run out and cause the depolarisation cycle to occur again. This **cannot occur for neurones in the core**
32
What is the **only licenced treatment for ischaemic stoke**?
**Tissue Plasminogen Activator (tPA)** Must be **used** within **3 hours of the stroke occuring** for it to be effective
33
What type of drugs can cause **food-induced excitotoxicity**?
**Glutamate receptor agonists**
34
What are the **4 main types of drugs** used for secondary **prevention of strokes**?
**Antihypertensives** **Antiplatelets** (ischaemic only) **Statins** (ischaemic only) **Anticoagulants** (ischaemic only)
35
What are the **4 key components of psychosis**?
Hallucinations Delusions Confused and disturbed thoughts Lack of insight and self-awarness (not aware that the hallucinations aren't real)
36
What is **Schizophrenia**? And what are the **3 components that the effects** are categorized into?
A divided mind.....A division between interal thought and external reality **Positive** --\> Increase in abnormal active behaviours **Negative** --\> Absense of normal active behaviours **Cognitive** --\> Disturbances of normal thought processes
37
Who are most likely to develop **schizophrenia**?
Those with **strong genetic connections** Young men and post-menopausal women
38
What **pathways cause schizophrenic effects**? And why?
**Mesocortical** --\> Decreased levels of D1 receptors cause negative and cognitive symptoms **Mesolimbic** --\> Increased levels of D2 receptors which cause positive symptoms
39
What are the differences between **typical and atypical antipsychotics**?
**Typical** - High affinity D2 antagonists that have lots of extrapyrimidal side effects like parkinsonism (due to their work in the nigrostriatal pathway) and increased pro-lactin level (due to work in the tuberoinfundibular pathway) Effective only against positive symptoms **Atypical** - D2 and 5HT3 antagonists, so effective against the positive and negative effects (negative as 5HT3 activates D1 receptors). Also less motor side effects Side effects include weight gain and diabetes
40
# Define **Engram** And what is **Hebb's Law?**
A physical representation or location of memory **Hebb's Law** states that if a neurone is releasing a neurotransmitter at the same time as another (connected neurone) is firing APs then the synapse becomes stronger This over time produces **a long term memory that can be activated with only part of the memory being shown** (as the brain can fill in the gaps)
41
What are the **3 subdivisions of memory**?
**Declarative** --\> The consious part of memory **Emotional** **Procedual**
42
Why is the **amygdala** useful?
It allows us to **remember fearful experiences**....so we're less likely to get into that same situation again!
43
What does **removing the temporal lobe** do?
Lose the ability to make new short term memories, but long term was okay
44
What is **Long Term Potentiation (LTP)**?
Consistant stimulation of glutamate-mediated EPSPs through AMPA receptors will cause an increased signal strength once the threshold has been reached **High levels of Ca2+ (to act on NMDA receptors) is vital** for LTP...along with the NMDA receptors
45
Why is **Magnesium** so important in the brain?
**As it blocks NMDA receptors** at the resting membrane potential (-70mV) and will only be removed at -40mV, which occurs when AMPA receptors are consitatnly activated Glutamate is also required to activate this receptor...hence the name 'dual gating'
46
How can we make **LTPs more likely**?
47
What are the **3 mechanisms of LTP generation**?
PKC can cause phosphorylation of AMPA receptors, stimulating more AMPA receptors being made. This is stimulated by calcium **(1)** CaMKII can cause the insertion and synthesis of new AMPA receptors **(2)** Nitric Oxide can move rapidly across the synapse (due to being a gas) which stimulates glutamate release from the pre-synaptic membrane **(3)**
48
What is **consolidation** and **re-consilidation** in terms of memory?
**Consolidation** - Going over already known knowledge **Re-consolidation** - Using the memory over and over again
49
Where is the **most damage done in Alzheimers disease**?
**The entorhinal cortex** Hence the memory and speech problems
50
How are **Plaques and Tangles formed in Alzheimer's**?
**Plaques** --\> B-secretase cleaves APP and then so does Y-secretase, forming AB40/42 Enzyme ApoE4 then causes these to aggregate into a plaque **Tangles** --\> The plaque aggregate then active kinases, causing hyperphosphorylation of Tau...which forms the tangles that can cause neuronal death
51
What are the **2 main treatments for the symptoms of Alzheimer's**?
**Cholinesterase inhibitors** --\> Due to cholinegic neurones being damaged early on **Memantine** --\> Can improve congnition via its non-competitive NMDA receptor blocking
52
What are **2 diagnostic hallmarks of Alzheimer's disease**?
**Neuritic Plaques (NP)** --\> Extracellular, non-soluble amyloid B protein **Neurofribrillary Tangles (NFT)** --\> Intracellular, abnormal cytoskeletal protein tau
53
What are the **main negatives of stimulating each of the opioid receptors**?
**Mu** --\> Respiratory depression **Kappa** --\> Dysphoria **Gamma** --\> Pro-convulsant

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