Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
55 Cards in this Set
- Front
- Back
- 3rd side (hint)
a. Name each group and it's components.
b. Which group has high capacity and moderate flow? c. Which group has a negligible flow and capacity? d. Which group has high capacity and low flow? e. Which group has low capacity and high flow? |
a. VRG: brain, liver, kidneys
MG: muscle, skin FG: fat VPG: bone, cartilage, ligaments b. MG -muscle group c. VPG-vessel poor group d. FG- fat group e. VRG-vessel rich group |
Tissues can be divided into four groups based on their level of perfusion and capacity to take up anesthetic. The high perfusion and low capacity allow Pvrg to equilibrate rapidly with Part.Also, the VRG makes the largest contribution to the mixed venous return partial Pressure Pmvr.
|
|
What degenerates in MS?
|
OLIGODENDROCYTES
|
|
|
What are the function of Astrocytes?
|
Help form BBB and other functions(glutamate sink).
|
|
|
What is the function of the Oligodendrocyte Glial cells?
|
Form nyelin sheath around axons
|
|
|
Explain ion activity at Na+ and K+ channels during an action potential.
|
-At the voltage threshold, Na+ channel opens and Na+ rushes in. Action Potential. K+ channels are also triggered but are slower to react.
-At Vmax, voltage-gated Na+ channels turn off. and potassium channels are still on and stay on until the potassium potential Vk(hyperpolarized) is reached. As Vk is approached, potassium channels increasingly shut off but some remain active to keep neuron at Vr. -Sodium channels recover and can be triggered again by voltage changes across the membrane. |
|
|
What is the driving force at synapse and what physical property can affect it?
|
Diffusion. Can be affected by temperature.
|
|
|
Which of the two main classes of neurotransmitters AFFECT ION CHANNELS such as sodium, potassium, calcium, and chloride; faster action.
|
Ionotropic
|
|
|
Which of the two main classes of neurotransmitters AFFECT GPCR causing conformational changes; SLOWER action.
|
METABOTROPIC. Most drugs used to treat psychosis and depression affect metabatropic neurotransmitter receptors.
|
|
|
Explain what occurs @ each step.
|
1. Xmitter synthesis & storage
2. Arrival of action potential 3. Depolarization of terminal and triggering of voltage-dependent Calcium channel; Ca influx 4. Ca mediated vesicle fusion and xmitter release 5. Xmitter diffussion&binding; 5a affects ionotropic receptors, excitaroty or inhibitory; 5b affects metabatropic receptors evoking second messengers; 5c autoreceptor binding (ellipse) 6. Signal termination: 6a. enzyme-meditated degradation; 6b. reuptake by xmitter transporter; 6c. uptake by glia 7. For G-protein coupled metabatropic receptors the transmission process may continue inside the neuron and outlast the xmitter-receptor coupling process 8. Xmitter events at the neuronal membrane can be transmitted all the way to the nucleus and can affect transcription 9. Multiplicity of G-protein coupled receptors |
|
|
breakdown in this neuroxmitter leads to seizures.
|
GABA
|
|
|
What are three drug targets of synaptic transmission.
|
• POSTSYNAPTIC RECEPTORS
– GABAa drugs (agonist properties) such as antianxiety drugs like diazepam. – Dopamine receptor blockers like haloperidol (antagonists or inverse agonists) •NEUROTRANSMITTER METABOLISM – Acetylcholinesterase inhibitors such as donezepil • NEUROTRANSMITTER REUPTAKE – Selective serotonin reuptake inhibitors such as fluoxetine |
|
|
|
|
|
|
|
|
|
|
Where do these parts of the CNS originate?
a. Sensory neurons b. Somatic motor neurons c. Sympathetic preganglionic neurons |
a. sensory-have cell bodies nad nuclei in the dorsal root ganglia, and project onto neurons located in the dorsal horn of the spinal cord.
b. somatic motor neurons- arise in the ventral horn of the spinal cord c. Sympathetic preganglionic neurons-arise in the ventral horn of the thoracic and lumbar segments of the spinal cord. Project onto postganglionic neurons in the paravertebral and prevertebral ganglia. |
|
|
What innervates the pineal gland in the brain?
|
Superior cervical ganglion
|
|
|
Sympathetic or Parasympathetic:
1. Flight or fight 2. Crainiosacral 3. Thoracolumbar 4. Neuroeffector xmitter-NE 5. Neuroeffector xmitter: ACh, muscarinic 6. Rest and digest 7. Long preganglionic fibers, short postgang. 8. Ganglionic xmitter 9. Turns on Epinephrine release from adrenal gland. |
1. Sympathetic
2. Parasympathetic 3. Sympathetic 4. Sympathetic 5. Parasympathetic 6. Parasympathetic 7. Parasympathetic 8. Sympathetic and Parasympathetic 9. Sympathetic |
|
|
Which two nerutransmitters are required to mediate neurotransmission in the PNS?
|
Acetylcholine and Norepinephrine
|
|
|
integration of information from other lobes; planning, problem solving, behavioral inhibition, social behavior; voluntary motor control
|
Frontal Lobe
|
|
|
language(more left than right), auditory sensation; inferior part of this: recognition of faces.
|
Temporal lobe
|
|
|
sense of location in space, somatic sensation(somatosensory)
|
Parietal lobe
|
|
|
emotion, pain
|
Cingulate gyrus
|
|
|
(bundle of Axons): unites the 2 hemispheres
|
Corpus Callosum
|
|
|
(basal ganglia): movement, Parkinson's disease
|
Caudate/Putamen
|
|
|
Sensory radiations to cortex
|
Thalamus
|
|
|
motor outflow to spinal cord
|
Internal capsule
|
|
|
deep within thalamus and heavily involved in normal memory processing
|
Hippocampus
|
|
|
timing of short duration intervals, coordination of movements, has a role in cognition and emotion, receives massive imputs from cerebral cortex
|
Cerebellum
|
|
|
Essential tremor is associated with disfunction of this.
|
Cerebellar dysfunctions
|
|
|
Ethanol ataxia mediated by this
|
Cerebellum
|
|
|
Which part of spinal cord is responsible for sensory relays to the brain
|
Dorsal horn
|
|
|
Which part of the brain is responsible for motor relays to the brain?
|
Ventral horn
|
|
|
Where do single-source divergent neurons typically originate? Where does it normally have axonal terminals that innervate thousand of Neurons?
|
Originate in a nucleus in the brainstem and axonal terminals usually innervate in the cerebral cortex.
|
|
|
Where do Dopaminergic neurons arise? What are they associated with?
|
Arise in the substantia nigra and the ventral tegmental area and are associated with te initiation of movement and the brain reward pathways.
|
|
|
What neurons are responsible for maintaining sleep-wake cycles and regulating sensory transmission
|
Cholinergic neurons
|
|
|
What neurons are responsible for maintaining alertness?
|
Noradrenergic neurons
|
|
|
Believed to have a role in modulating affect and pain
|
Serotonergic neurons
|
|
|
Which amino acids are excitatory and inbibitory in CNS.
|
Excitatory(glutamate and aspartate)
Inhibitory(glycine and GABA) |
|
|
|
|
|
|
Which molecule is precursor for synthesis of Tryptophan?
|
Serotonin
*Tryptophan is first oxidized by tryptophan hydroxylase(TPH) adn then decarboxylated by aromatic L-amino acid decarboxylase to yield SEROTONIN. |
|
|
Name some differing features between capillaries in CNS and PNS.
|
In the periphery, capillary endothelial cells have gaps(termed fenestrae) b/w them and use intracellular pinocytotic vesicles to facilitate the transcapillary transport of fluid and soluble molecules. In contrast, CNS vessels are sealed by tight junctions b/w the endothelial cells. The cells have fewer pinocytotic vesicles and are surrounded by pericytes and astroglial processes. In addition, capillary endothelial cells in the CNS have more mitochondria than tose in systemic vessels; these mitochondria may reflect the energy requirements necessary for CNS endothelial cells to transport certain molecules into the CNS and transport other molecules out of the CNS.
|
|
|
Name some differing features between capillaries in CNS and PNS.
|
In the periphery, capillary endothelial cells have gaps(termed fenestrae) b/w them and use intracellular pinocytotic vesicles to facilitate the transcapillary transport of fluid and soluble molecules. In contrast, CNS vessels are sealed by tight junctions b/w the endothelial cells. The cells have fewer pinocytotic vesicles and are surrounded by pericytes and astroglial processes. In addition, capillary endothelial cells in the CNS have more mitochondria than tose in systemic vessels; these mitochondria may reflect the energy requirements necessary for CNS endothelial cells to transport certain molecules into the CNS and transport other molecules out of the CNS.
|
|
|
What would absence of GAD enzyme cause?
|
Absence of GAD(glutamic acid decarboxylase) would stop conversion of Glutamate to GABA and lead to lowered inhibition and heightened excitation.
|
|
|
Are glutamate receptors found mostly on pre or postsynaptic membranes?
|
Postsynaptic
|
|
|
Which type of Glutamate receptors are fast, excitatory receptors?
Name the three subtypes of glutamate-gated ion channels, classified according to their activation by the selective agonists. |
Ionotropic.
-NMDA- Increases Ca++ influx, increase K+ efflux. -Kainate - Increases Na+ influx, increase K+ efflux -AMPA - Increase Na+ and Ca++ influx, increase K+ efflux |
|
|
Which type of Glutamate receptors are slower, mixed actions?
|
Metabotropic glutamate receptors
|
|
|
Name two ways Ionotropic NMDA receptors differ from the other ionotropic glutamate receptors.
Protein structure? |
1. dual binding of of inhibitory glycine and glutamate.
2. membrane depolarization that removes Mg+ block of the channel pore. -Tetrameric |
|
|
These conditions can all be related to defects in which receptor?
Stroke and CNS trauma, Hyperalgesia, Epilepsy, Neurodegerative diseases |
Glutamate receptors
|
|
|
What is the main GABA receptor
|
GABAa receptors.
*Picrotoxin used to reduce seizures and Flumazenil is a strong antagonist of Benzodiazepine |
|
|
What are the relative potency and efficacy of benzodiazepines and barbiturates.
|
Benzodiazepines such as Midazolam are high-potency, low-efficacy modulators of GABAa receptor activity.
-Barbiturates such as phenobarbital are low-potency, high efficacy modulators. |
|
|
Name some sedative-hypnotics classes
|
•Ethanol (later)
•Barbiturates •Chloral hydrate, trichloroethanol (mostly of historical interest) •Benzodiazepines (widely used) [emphasis here] •Zolpidem, Zaleplon (modern hypnotics) •Buspirone (unique mechanism) |
|
|
Give some uses of sedative-hypnotics
|
•Sleep-induction
•Anti-anxiety •Anti-convulsants •Some have muscle relaxant effects •Some have amnestic effects |
|
|
Which benzo has the longest half life and active metabolites?
|
Flurazepam
|
|
|
What are some of the main uses of benzodiazepines?
|
•Reduce or eliminate anxiety
•Induce sleep –Importance of sleep physiology –REM and NREM, relation to memory •Treat epilepsy •Adjunct to anesthesia (midazolam) and pre- anesthesia •Amnestic effects for painful procedures (midazolam) |
|
|
This could possibly caused experience-induced over-activity of the amygdala in the emotional circuits of the brain.(amygdala also associated with epileptic seizures.
|
Anxiety
|
|
|
This antianxiety drug is in a class all it's own with a therapeutic lag of 2 weeks or more, and is indicated for generalized anxiety.
|
Buspirone: acts as 5HT1a agonist
|
|