Pharmacology CNS Flashcards
What are the 5 different types of synapses
1) Excitatory ion channel synapses: Increase the likelihood of action potentia;
2) Inhbitory ion channel synapses: Decrease the likelihood of action potential
3) Non channel synapses: Non-Channel Synapses work by using special receptors on the cell membrane that activate enzymes inside the cell instead of opening ion channels. These enzymes then send signals inside the cell to create a response. Think of it like a doorbell—instead of opening a door directly (like ion channels), it rings a bell inside to trigger an action.
4)Neuromuscular Junctions → Synapses between motor neurons and muscle cells using acetylcholine (ACh); always excitatory.
5)Electrical synaspses:Direct connection between cells through shared proteins, allowing fast action potential transmission
Explain Excitatory synapses
makes the next neuron more likely to fire by depolarizing it (making it more positive).Neurotransmitters (like acetylcholine or glutamate) are released from the presynaptic neuron into the synaptic cleft.
They bind to sodium (Na⁺) channels on the postsynaptic membrane.
This opens sodium channels, allowing Na⁺ ions to flow in, making the inside of the neuron more positive.
This depolarization makes an action potential (nerve signal) more likely.
List typical excitatory neurotransmitters
acetylcholine, glutamate, aspartate, or catecholamines.
Explain how inhabitory synapses work
The neurotransmitter at inhibitory synapses hyperpolarizes the postsynaptic membrane.
These synapses have neuroreceptors that are chloride channels. When the channels open, negative ions flow in causing a local hyperpolarisation and making an action potential less likely.
Give neurotransmitter examples of inhibitory synapses
GABA and Glycine
How do drugs work on the nervous system
1)Synthesis: increase/block neurotransmitters
2)Packaging: affect how neurotransmitters are stored in vesicles
3)Release: Heteroreceptors meaning influence other neurotransmitters to increase or decrease release and Autoreceptors: Drugs can inhibit or enhance release by affecting feedback receptors on the same neuron
4)Actions at Receptor
5)Reuptak
6) breakdown: Some drugs inhibit enzymes that break down neurotransmitters, prolonging their effects
List the different types of receptors and their functions
adrenergic,Dopaminergic
GABAergic,Glutaminergic Histaminergic, Cholinergic
Opioid,Serotonergic,Glycinergic
Adrenergic receptor function
Responds to epinephrine & norepinephrine (fight-or-flight response).
Dopaminergic receptor function
Binds dopamine, regulating mood, movement, and reward.
GABAergic receptor function
Responds to GABA, the main inhibitory neurotransmitter (calming effect).
Glutaminergic receptor function
Binds glutamate, the main excitatory neurotransmitter (learning & memory).
Histaminergic receptor function
Uses histamine, involved in wakefulness and immune response
Cholinergic receptor function
Binds acetylcholine (ACh), important for muscle movement & memory.
Opioid receptor function
Responds to endorphins & opioids, regulating pain and pleasure.
Serotonergic receptor function
Uses serotonin, controlling mood, sleep, and appetite.
Glycinergic receptor function
Uses glycine, an inhibitory neurotransmitter that helps with motor control & reflexes.
Mechanism of ADHD
Excess dopamine reuptake, decreased dopamine availability
Reduced norepinephrine levels
Lower serotonin levels may contribute as well.
refrontal cortex dysfunction
The prefrontal cortex which controls executive functions like attention, planning and impulse control is less active in the ADHD brain.
Increased cortisol and stress sensitivity
Many ADHD brains show higher cortisol responses to stress, making emotional regulation more difficult
May contribute to higher anxiety and emotional reactivity
What do CNS stimulants do and what are they used for
medicines that speed up physical and mental processes
-used to treat ADHD
-narcolepsy
Good and bad side of CNS stimulants
increased alertness, improved concentration, and enhanced energy. However, their therapeutic use is restricted because of potential side effects like insomnia, increased heart rate, high blood pressure, anxiety, and the risk of dependence or abus
How do CNS stimulants work
The exact mechanism of action is not clear, but it may involve stimulating the cerebral cortex and increasing the activity of norepinephrine, dopamine, and other catecholamines in the prefrontal cortex, which control attention and impulse regulation.
list 3 CNS stimulants
-Caffiene=blocks adenosine receptor
-Amphetamine
-Methylphenidate
How does amphetamine
1) forces neruons to release dopamin into the synapse
2)makes the vesicles dump out more dopamine
3)Blocks MAO enzyme from destroying it
4)Reverses the dopamine transporter, making it push dopamine out instead of taking it back i
CNS stimulants side effects
palpitations, cardiac dysrhythmias, hypertension, nervousness, nausea
Highly addictive and widely abused outside therapeutic therapy (especially methamphetamine)
Why might doctor recommend a nonstimulant medication forADHD.
Stimulant medications didn’t work.
Stimulant medications had intolerable side effects.
A child withADHDmight have another disorder as well.
Stimulants could be risky for a teenager with substance-use problems or a history of drug use.
What are the two catagories for Non stimulant medication for ADHD
Norepinephrine modulators and Alpha agonists
mnemonic to help you memorize non-stimulant ADHD medications:
“A Cool Guide for ADHD”
A=Atomoxetine → Attention booste
C=Clonidine → Calms hyperactivity
G=Guanfacine → Gentle impulse control
What is Obsessive compulsive disorder (OCD)
-recurrent intrusive thoughts or repetitive behaviors that interfere with normal activities or relationships.
Mechanism behind anxiety disorders
-Overactive amygdala
-Weakened prefrontal cortex
-Dysregulated neurotransmitters
-low GABA levels (which normally calms the brain) or overactive excitatory signals, leading to excessive fear and stress responses.
Seratonin
involved in mood and worry – lower levels in people with anxiety disorders
Dopamine
– involved in fear and motivation
-people with anxiety have it dysregulated – typically lower
difference between sedatives and hypnotics
Sedatives calm the central nervous system and reduce anxiety without causing sleep.
Hypnotics induce drowsiness and sleep.
The difference is mainly dosage—low dose = sedative, high dose = hypnotic.
What are the main uses of benzodiazepines
Treat anxiety disorders, panic disorders, insomnia, seizures, and muscle relaxation.
Specifically anxiolytic (reduces anxiety).
Fast-acting but addictive.
Does not cause coma or death unless combined with other respiratory depressants.
What are the two main types of GABA receptors and how do they function?
GABA_A → Ionotropic receptor (ligand-gated ion channel) that allows Cl⁻ ions to enter the neuron, causing hyperpolarization and inhibition of neurotransmission.
GABA_B → Metabotropic receptor (G-protein-coupled) that works indirectly to inhibit neuron activity.
Serious side effect of Benzodiazepines
CNS and respiratory depression, hypotension, coma
Contraindications of benzodiazepines
Interact with alcohol, omeprazole to cause increased CNS depression
Barbiturates use
Classified as CNS agents, used as anxiolytics, hypnotics and as anticonvulsants.
May work by inhibiting reticular-activating system, thereby interfering with impulse transmission of cerebral cortex
Used to treat insomnia and for some types of seizures.
Barbiturates are still widely used in surgical anesthesia.
diffrenece between mechanism of barbituates and benzoodiazepines
Benzodiazepines → Make GABA work better by opening the chloride channel more often (but only when GABA is there). Safer.
Barbiturates → Force the chloride channel to stay open longer, even without GABA. More dangerous.
💡 Think of it like a door:
Benzos = Tap the door to open & close quickly (needs GABA).
Barbs = Hold the door open for a long time (can work without GABA → overdose risk).
Serious side effects of barbituates
Serious: respiratory depression, circulatory shock, renal or hepatic damage
Common side effect of barbituates
sedation, nausea, vomiting, constipation, diarrhea, bradycardia
Do not use barbituates if..
patients with familial history of porphyria or with severe respiratory or kidney disease; and in pregnancy or lactation.
Interact with alcohol, oral anticoagulants, corticosteroids, oral contraceptives.
Explain the diffrent types of sezirues
Tonic-Clonic (Grand Mal) → Full-body shaking, loss of consciousness.
Absence (Petit Mal) → Brief staring spells, no shaking.
Myoclonic → Quick muscle jerks, no loss of consciousness.
Partial (Focal) → Affects one part of the brain, may or may not cause confusion.
What are the main classes of medications for anxiety
SSRIs → Increase serotonin, used for general anxiety, panic, OCD, PTSD
SNRIs → Increase serotonin + norepinephrine, also helps with chronic pain
Beta Blockers → Block adrenaline, used for performance anxiety, panic
Non-Benzodiazepines → Partial serotonin agonists, treat general anxiety
Alpha-2 Agonists → Lower stress response, used for ADHD + anxiety, PTSD
How do antiepileptic medcations work
1) Sodium (Na⁺) Channel Blockers → Stop neurons from firing too much
2)Calcium (Ca²⁺) Channel Blockers → Regulate neurotransmitter release
3)GABA Enhancers → Increase brain’s calming effect
4) Glutamate Inhibitors → Reduce brain excitability
5)Mixed Mechanism AEDs → Work through multiple pathways
6)Potassium (K⁺) Channel Openers → Calm neurons by enhancing potassium flow
trick to remmeber how antiepileptic medcations
sodium Blockers = Stop rapid neuron firing → ⚡ (Phenytoin, Carbamazepine)
Calcium Blockers = Slow neurotransmitter release → 🚚 (Gabapentin, Pregabalin)
GABA Enhancers = Boost brain’s brakes → 💤 (Benzos, Vigabatrin, Tiagabine)
Glutamate Blockers = Reduce brain overexcitement → 🔕 (Perampanel, Felbamate)
Potassium Openers = Keep neurons stable → 💨 (Potassium cha
Phenytoin: Adverse Effects
Common: blurred vision, dizziness, drowsiness, fatigue, thrombocytopenia, aplastic anemias
AND
All antiepileptic drugs can increase the risks of suicidal thoughts and behavior.
How does Ethosuximide (Zarontin) work
blocking calcium channels, which helps stabilize neuronal excitability and raises the threshold for seizures. Additionally, it inhibits the sodium-potassium ATPase system, reducing the burst firing of thalamocortical neurons, which are involved in seizure generation. Ethosuximide also decreases non-inactivating sodium currents and blocks calcium-dependent potassium channels, further preventing excessive neuronal excitability. Unlike some other anti-seizure drugs, it does not alter GABA levels in the brain. Overall, ethosuximide helps prevent seizures by reducing neuron excitability and stabilizing electrical activity in the nervous system.
