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11 Cards in this Set

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  • Back
Name three important vitamins that pregnant mothers should name and briefly explain why they are important to normal development.
1) Folic Acid--> prevention of neural tube defects
2) Zinc--> important for CNS development
3) Choline --> important precursor for ACh, impt NT
4) Glutamate --> important NT, signaling and protein synthesis
Name two defects that may occur with neural tube development
1) Anancephaly--> the anterior neuropore usually closes around days 23-25 of development, however in these patients, it fails to close. Result is absence major parts of the brain, skull, and scalp. Death will result

2) Spina Bifida--> the caudal portion of the neural fails to close. There are several variations of these, with the myelomenigocele being the most common and most signficant. In this, the spinal cord may protrude through the unfused portion of the spinal cord
Name 3 CNS structures that are derived from neural crest cells
1) pia mater
2) arachnoid mater
3) Schwann cells
Why is increased cranial pressure dangerous?
increased ICP is dangerous because it may cause ischemia of brain tissue. According to the equation cerebral perfusion pressure = mean arterial pressure (MAP)-ICP, we can see that an increase in ICP will, after a certain level (>15mmHg) cause a decrease in cerebral perfusion pressure, which will lead to ischemic damage to the tissue
Explain the concept of the blood-brain barrier, and which structures form this in the human
The blood brain barrier is made up of the tight junction of the CNS capillaires (other capillaries in the body are fenestrated). Other stuctures that contribute to this barrier are the basal lamina and the foot processes of astrocytes, which are non-neuronal, glial cells. The purpose of the blood brain barrier is to protect the brain from toxins that my be in the blood and to regulate what substances that brain tissue is exposed to
What is valproic acid and what is its mechanism of action?
Valproic acid is as class of anticonvulsants that is used primarily to treat seizures and epilepsy. Its MOA in treating these things is that it inhibits GABA transaminase, which normally breaks down GABA. In this way, valproic acid potentiates the effects of GABA in the brain, allowing for an inhibitory or depressant effect on the CNS. In addition, valproic acid has some voltage gated Na+ channel blocking effects. This also aids in its function, as this would make neuronal cells less excitable.
Describe the course of diabetic peripheral neuropathy
Three main courses:
1) symmetric distal sensory and motor neuropathy, sensory moreso with paresthesias --> "glove and stocking" presentation, typically worse in the feet and lower extremities and can result in ulcers
2) autonomic neuropathy--> disturbances in bladder and bowel function, BP regulation, and sometimes sexual impotence
3) focal or multifocal asymmetric neuropathy--> may present as sudden wrist drop or ankle drop or isolated CN palsies
Discuss methods for helping patients with advanced (symptomatic) diabetes initiate and maintain life style changes aimed at limiting disease and disability progression.
DSME--> Diabetes self management education: Team of healthcare workers work closely with patient and educate on diabetes prevention and lifestyle changes
PCMH model --> at Carilion, there is the patient-centered medical home model which is also a multidisciplinary team that works with the patient to offer education and resources for diabetes management
Discuss approaches to addressing the problem of patient non-compliance with a therapeutic plan.
avoid conscending talk
make sure that patient is part of plan making process and understands plan
plan should include specifics
Empathize with patient and show understanding for a frustrating situation
Do not accuse the patient but rather phrase it so that your goals as a doctor are in line with their goals
Inquire into what is the specific concern so that those can be addressed
“What would it take to make you change your mind?”
Describe the neurological factors that support the most plausible explanation for spasticity and why this patient demonstrated hyperreflexia and clonus.
There are four proposed hypothesis that explain spasticity
1) Decrease inhibition to gamma MN
2) Decrease excitation to Renshaw cells
3) Decrease presynaptic inhibition to 1a fiber input
4) Decreased excitation to alpha motor neurons
#4 is currently considered the most plausible
Upper motor neuron injuries cause spasticity via decreased excitation in alpha motor neurons through loss of higher input. The result is 1a having the most “say” in the segmental muscle movements, and then intiating contracting when external alpha stimulus is applied by a physician. Clonus and hyperreflexia are also seen in these pts often and are causes by mechanisms of the same origin (loss of inhibitory input from higher center)
Distinguish between spasticity and rigidity. `
Spasticity is usually due to an upper corticospinal injury. Symptoms are usually velocity and amplitude dependent, and are more often than not unilateral. Usually you see symptoms in the antigravity muscles. Rigidity on the other hand tends to be bilateral and is not velocity or amplitude dependent. It usually is due to damage to an extrapyramidal tract and you see cog-wheeling or lead pipe rigidity.