Week 1 Flashcards
Neuronal cell body
Perikaryon (controls cells)
Excitatory neurotransmitter
Glutamate
Inhibitory neurotransmitter
GABA (gamma aminobutyric acid)
How does direct action work?
Neurotransmitter binds to and opens ion channels
Rapid response by altering membrane potential
How does indirect action work?
Binds to G protein and caused and indirect response through secondary messengers
Broader actions with longer lasting effects
What is another name for a ligand gated ion channel?
ionotropic
What is a metabotropic receptor?
Usually a G protein and have long term effects. There are membrane-delimited (all reaction occur in membrane) and Second messenger ones that require intracellular second messengers
What is an autoreceptor?
It is when there is a receptor on the never terminal that binds the neurotransmitter that is released (usually a negative feedback)
What is a heteroreceptor?
Receptor on other axon terminals through which neurotransmitters from other neuronal types can influence their function
What make the nerve terminal for acetylcholine unique?
There is not acetylcholine transporter (has to return as choline) and uses acetylcholine esterases
What do endorphins bind to?
m-opioid receptors that inhibit GABA release causing more excitation
In the autonomic nervous system, how many nerves are used?
2, a pre-ganglionic and post-ganglionic
All pre-ganglionic nerves use this neurotransmitter and bind to this type of receptor?
ACh and nicotinic
Where do sympathetic nerves originate?
Thoracolumbar spine
Where do parasympathetic nerves originate?
craniosacral
What is unique about the adrenal medulla?
It is directly innervated by the pre-ganglionic nerve and causes release of NE and Epi
Where do parasympathetic pre-ganglionic nerves go?
To the ganglia that is closest to the effector organs/tissues
Motor neurons use what neurotransmitter and bind to what type of receptor?
ACh and Nicotinic
DA activates what receptors?
D1-D5 and alpha and beta adrenergic
What is a seizure?
a finite clinical manifestation of abnormal & excessive excitation of a population of cortical neurons
What is epilepsy?
syndrome characterized by chronic, recurrent seizures unprovoked by systemic or neurologic insults
3 unprovoked seizures=epilepsy
What is epileptogenesis?
sequence of events that converts a normal
neuronal network into a hyperexcitable network
Life time prevalence of seizures?
9-10% of the population
Prevalence of epilepsy?
1%
What is the biggest inherited cause of epilepsy?
Ion channel issues
What is the fastest growing cause of acquired reasons for epilepsy?
Trauma
What are common seizure precipitants?
Metabolic and/or Electrolyte Imbalance Stimulant or other pro-convulsant intoxication Sedative or ethanol withdrawal Sleep deprivation Reduction or inadequate ASD treatment Hormonal variations Stress Fever or systemic infection Concussion and/or closed head injury
Who is at most risk of getting epilepsy?
The young and the old
What is the common cause of epilepsy among all ages?
status epilepticus, a seizure lasting longer than 3 minutes
Simple partial seizure
Localized
Minimal spread
Normal awareness, memory and consciousness
Short duration
Could be different areas of the cortex that are involved
Complex partial seizure
Localized onset but spreads
awareness, memory, and/or consciousness are lost during seizure
short duration
Secondarily generalized seizure
begin as partial but end as generalized. tonic (stiffening) and clonic (jerking) phases and postictal phase
Another name for tonic-clonic seizure?
grand-mal
Another name for absence seizure?
petit-mal
What is characteristic of an absence seizure?
spike wave pattern
Are grand-mals synchronized or asynchronized?
Synchronized
Ideal ASD?
Effective for the Seizure Type Wide therapeutic index
No organ toxicity
No teratogenicity
No drug-drug interactions Long half-life (t1/2)
No protein binding
Water soluble (easily absorbed) No active metabolites
What is the biggest difference between old and new ASDs?
newer drugs have fewer drug enzyme interactions
What are the three main mechanisms for ASDs?
1-increase inhibition
2-reduce excitation
3-modulate inhibition and/or excitation
Carbamazepine
Used for all types of seizures
May cause steven-johnson’s syndrome
May cause increased absence seizures
Block use-dependent voltage gated ion channels Na+ to stop re-firing of neurons
What are the dietary concerns with grapefruit?
They causes an increase in carbamazepine levels because they block the enzyme that metabolizes it
Ethosuximide
only drug that focuses on absence seizures
reduces t-type Ca 2+ channel currents
Phenobarbitol
All types of seizures cheap long term cognitive, memory, and behavior effects Big time INDUCER may cause absence seizures
Phenytoin
all types
gingival hyperplasia
zero order kinetics at high doses
Block use-dependent voltage gated ion channels Na+ to stop re-firing of neurons
Topiramate
all types
Weight loss
inc. metabolism of estrogen
word-finding difficulty
Valproic acid
all types weight gain reye-like syndrome, hepatic failure don't give if pt has liver issues neural tube defects (spina bifida)
What are the two types of parasympathetic receptors?
Nicotinic and muscarinic
Muscarinic agonists, functions, antagonists?
Agonists-ACh, bethanechol, pilocarpine
Function-rest and digest
Antagonists-atropine, scopolamine
What are the 2 nicotinic receptors?
Muscle and Neuronal
Nicotinic (muscle) agonist, function, and antagonist?
Agonist-ACh
Function-neuromuscular junction
Antagonist-succinylcholine
Nicotinic (neuronal) agonist, function, and antagonist?
Agonist-ACh
Function-autonomic ganglia, adrenal medulla, CNS
Antagonist-mecamylamine
What are the two classes of neuromuscular blockers?
Depolarizing-succinylcholine, depolarized neuron making it so it cannot react to further signals
Non-depolarizing-competes with ACh
3 cholinesterase inhibitors
physostigmine-short duration, used for glaucoma antidote for atropine
Donepezil-used for Alzheimer’s
Sarin-nerve gas
What does botulinum toxin do?
Prevent release of ACh
What cholinergic drugs are used in dentistry?
Cevimeline-xerostomia in Sjogren’s
Pilocarpine-xerostomia in radiotherapy
Alpha 1 receptors
Agonist-Epi>NE, phenylephrine Tissues and actions -radial muscle of iris/dilates pupil -GU and GI sphincters/contract -Vasculature/Contracts Antagonist-prazosin
Alpha 2 receptors
Agonist-Epi>NE, clonidine, guanfacine Tissues and actions -Vasculature/Contracts -NE terminals/decrease NE release -Brainstem/decrease NE release
If a drug ends in -olol what is it?
Beta blocker
Beta 1 receptors?
Agonist-Epi=NE, isoproterenol
Tissue and action
-Heart/everything increases
Antagonists-propranolol
Beta 2 receptors?
Agonists-Epi»»NE, isproterenol, albuterol, and terbutaline
Tissue and actions
-Ciliary muscle of eye/ relaxation for far vision
-vasculature/relaxation/dilation of skeletal muscle vasculature
-lung smooth muscle/relaxation
-bladder and uterine wall/relaxation
Antagonists-propranolol
What happen in the liver under adrenergic stimulation of Beta 2 and Alpha receptors?
Gluconeogenesis and glycogenolysis
D1 receptors?
Agonist-DA and fenoldapam
Tissue and action
-Kidney/increase blood flow, increase GFR, and sodium excretion
-vasculature and heart/vasodilation
D2 receptors?
Agonist-DA
Tissues and actions
-DA nerve terminals/negative feeback
-chemoreceptor trigger zone/nausea and vomiting
Barorecetors do what?
Maintain BP
Depending on the speed that Epi is given and the dose what happens?
Slow dose not much, increase HR and decrease TPR
High dose-more alphas get involved so increased HR and increased TPR
What does Epi do to the eye?
dilates pupil (mydriasis)
How can pilocarpine be used to treat glaucoma?
acts on muscarinic receptors on iris sphincter muscle causing them to contract, also causes ciliary muscles to contract opening the trabecular meshwork through increased tension. This facilitates fluid flow decreasing the pressure.
What are the mixed adrenergic drugs?
ephedrine, ephedra, and pseudoephedrine
uses as decongestants and dietary supplements
How do indirect adrenergic drugs (Amphetamines, cocaine, methylphenidate, SSRIs, TCA,s) work?
Block re-uptake of DA
What can food with tyramine do if taking an MAO inhibitor?
if taking an MAO inhibitor it gets into the blood stream and gets into nerve terminals and displaces NE
Non-selective alpha antagonists?
phenoxybenzamine, phentolamine
Orthostatic hypotension
What is tamsulosin?
Flomax, benign prostatic hypertrophy
alpha 1 antagonist
