Exam 4 ADHD Flashcards
(76 cards)
When the body first receives sensory or internal milieu input, where does it go?
Brainstem Reticular Formation
Ultimately, where does all sensory input end up going? (This place mediates conscience)
Cerebral Cortex
What are two possible causes of ADHD in early life?
-Low birth weight
-Fetal alcohol syndrome
What is the main implicated system in ADHD?
Dopamine transporters
What is the main physiological goal of ADHD treatment?
Increase brain activity by causing more action potentials to fire
What classifications must someone meet to be diagnosed with ADHD?
6 or more symptoms present
(for adults 17 and older, 5 symptoms are required)
Several inattentive or hyperactive symptoms must be present prior to age 12
Significant impairment in two or more settings
*Interferes with functioning and development
What is a possible circuity mechanism of ADHD?
Medial Prefrontal Cortex (mPFC) may not be fully developed
*this brain region is important for inhibition of impulsive thoughts
*not fully formed during childhood and suppressed with alcohol
What are methylxanthines and how do they work?
Indirect-Acting Sympathomimetics
-stimulants that mimic the effect of endogenous agonists of the sympathetic nervous system (fight or flight)
*stimulate the brain and make it more active
What substance is considered a stimulant and has a similar structure to the stimulant meds?
Caffeine
What are the 3 actions of methylxanthines?
-Antagonize Adenosine Receptors
(naturally produced by brain, quiets body down and slows heart rate, block this to increase alertness)
-Inhibit Phosphodiesterases
(increase cAMP)
-Increase Activity of Ryanodine Receptors
(Increase intracellular Ca)
How does Adenosine work?
-Enhances exocytosis of glutamate so there is less, this quiets the system down
-Opens the K channels so it exits the cell, this hyperpolarizes the cell and quiets it down
want to block this
Which G protein is the adenosine receptor A1 linked to?
Gi/o
(i=inhibitory)
*Inhibits modulation of many neurotransmitters
*Causes sedation/quieting down
Activation of adenosine receptor A1 causes what?
CNS: Sedation, Anxiolysis, Anticonvulsant Activity
Peripheral: Decreased heart rate
Adenosine A2A receptors are linked to which G protein?
Gs
(s=stimulatory)
Activation of Adenosine A2A receptors leads to what?
Vasodilation
Adenosine A2B receptors are linked to which G-protein and where are they found*?
Gs-linked
*Glial cells
(unknown function)
When are Adenosine A3 receptors activated?
Excessive catabolism
(seizures, hypoglycemic stroke)
*Not antagonized by methylxanthines
What are the two main functions of methylxanthines?
Increase alertness
Decrease fatigue
How does Cocaine affect norepinephrine?
Directly blocks the norepinephrine transporter (NET)
-this blocks NE reuptake
-there is an excessive amount of NE in the extracellular space, makes person feel very energized
How do amphetamines affect norepinephrine?
-Can be up taken by norepinephrine transporters (NET)
*Bind VMAT
-This confuses the transporters and they start pumping out more dopamine and NE
-Higher levels of these extracellularly increase alertness and reduce fatigue
Amphetamines act as mimics of NE and reverse transport to outside of the cell
NO DIRECT BLOCKING
What does VMAT stand for?
Vesicular Monoamine Transporter
*note: these package NE and dopamine into transport vesicles
What is a downside of using stimulants?
Target many reward pathways, potential for abuse
What is the primary monoamine affected by stimulants?
Dopamine
*also NE
What is the pharmacology of stimulants?
Monoamine transporters
