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61 Cards in this Set

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  • Back
What's the danger in taking COX inhibitors? Why?
They can increase risk of GI bleeding because mucus production is decreased.
What do prostaglandins do? What inhibits this activity?
Prostaglandins sensitize pain receptors and cause inflammation. NSAIDs inhibit this activity.
What's the nature of degradation in HD?
There are two pathways involved.
What part of the brain is implicated in both Parkinson's and HD?
The basal ganglia.
Compare Parkinson's vs. HD
HD has too much firing in the thalamus, whereas Parkinson's doesn't have enough firing. HD = dance, Parkinson = akinetic.
What results from Complex 1 poisoning? What is a known poison?
-Calcium overload
-Free radicals
3-NPA is a known poison.
What are two treatments for Parkinson's?
Sinemet, which works by increasing dopamine release. Another treatment called Mirapex works by mimicking dopamine.
Why is olfaction susceptible to damage?
-Inhaling things in the environment
-Prime location for physical injury
Where does olfactory damage typically occur?
At the olfactory bulb.
What causes loss of smell?
-Nasal obstruction like a cold or allergies
-Nasal polyps, which are growths in the nose and sinus
-Blow to the head
-Exposure to chemicals
How do you test for olfaction problems?
Scratch and sniff tests and nasal examinations normally. If there's a nerve problem, then use X-ray or CAT scan.
What are the symptoms of a loss of taste and smell?
-Foods may have a metallic taste
-Weight loss from skipping meals
What's important about the origin of the sense of taste?
Our sensation of taste comes from smell receptors combined with taste receptors.
What are the risks associated with losing taste/smell?
-Too much salt > hypertension
-Too much sugar > diabetes
-Malnutrition in general
-Spoiled foods
-Environmental risk factors
-Depression about not enjoying eating
What's the prostaglandin pathway?
Damaged tissues > prostaglandins > sensitize the whole pain pathway
What's another name for pain receptors?
What are the hallmarks of the 2 types of pain receptors?
C-fibers stimulate chronic pain and are slow because they don't have myelin.

Aδ (A-delta) fibers are rapid and associated with acute pain.
What's the counterpoint of nociceptive pain? Where should pain treatment start?
The counterpoint is neuropathy. Always start treatment with nociceptive pain.
What are the easy treatments for nociceptive pain?
Over-the-counter drugs like NSAIDs.
What do NSAIDs do to reduce pain?
NSAIDs inhibit COX production, which is crucial for production of prostaglandins.
What are neuropathic pain treatments? How do they work?
Anti-depressants work because they increase serotonin, which is secreted in descending fibers during pain to reduce irritation.
What's the CNS pathology of MS?
Demyelination of nerve cell axons.
What causes CNS pathology of MS?
Autoimmune dysfunction from a breakdown in the blood-brain barrier, which leads to inflammation
What causes MS?
It could be genetic predisposition, but not always. Otherwise:
-Environmental factors
-Virus infections
-Bacteria and parasite infections
What reduces the risk of MS?
Sunlight and vitamin D.
How do you diagnose MS?
Neurological exam and patient history. MRI is the next step, where you look for focal lesions using contrast agents. EEG also is abnormal in 50% of patients.
What's the most common form of MS?
Relapsing-remitting, consisting of 85% of patients.
Compare inflammation in MS vs. other autoimmune diseases. What mechanisms are involved with each?
MS is extrinsic to the brain, involving macrophages, lymphocytes (*especially T-cells), and neutrophils. Other diseases like PD and AD are intrinsic and involve microglia and astrocytosis.
What genes, in general and in particular, are associated with MS?
Generally genes associated with immune response, specifically a breakdown of ch6p21.
What are the classes of drugs for treating MS? What are some specific ones? How do they work?
Anti-inflammatories and immunomodulators like Avonex and Rebif. They work by blocking hormones released by T-cells, like interferons, which activate macrophages that chew up myelin.
Compare incidents of MS in men and women. What's special about MS in women? What's the implication?
Women have 2x more incidents than men. It seems likely that estrogen reduces the fierceness of the immune system. Possible treatments may include synthetic estrogens.
What controls MS relapses? How?
Corticosteroids, which suppress the immune system.
What part of the motor neuron system is affected by ALS?
Both upper and lower motor neuron systems.
What are the symptoms of ALS?
-Muscle weakness
-Impaired arm and leg use
-Speech "thickness"
Compare incidents of ALS in men and women.
Much more common in men than women.
What neurons does ALS affect?
Only motor neurons and other neurons anterior to them.
What are the classes of ALS?
-Sporadic, 90% of cases
-Familial, less than 10%
-Guamanian from ingesting excitotoxic foods that stimulate glutamate
How do you treat ALS?
With drugs that block glutamate.
What causes Huntington's disease?
It's 100% autosomal dominant genetic.
Describe the HD neuropathology pathway.
Chromosome 4 > too many CAG repeats > caudate and putamin damage (cortex later) > globus pallidus inhibition, so thalamus goes crazy firing
What's the treatment for Huntington's disease?
Dopamine receptor blockers like haldol for early treatment. Then Tetrabenazine to block transport of dopamine into vessicles. Lastly tranquilizers act as GABA allosteric agonists.
What part of the brain is most susceptible to damage from HD?
The striatum, followed by the cerebral cortex.
What kind of disease does HD appear to by, and why?
It may be a mitochondrial disease. This is illustrated by the case where spoiled sugarcane in China got people sick.
Compare Parkinson's in men and women and explain why there's a difference.
Men have it more than women because of lifestyle choices, namely working in industrial places and taking more risks.
What specific lifestyle choice can increase odds of getting Parkinson's? Why?
Living in rural areas because it increases the odds of consuming pesticides.
What's the neuropathology of Parkinson's?
MPP+ inhibits Complex 1 in mitochondria in substantia nigra > mitochondria makes superoxide and stops ATP production
How do you diagnose Parkinson's?
PET scan
How do treatments for Parkinson's work?
They increase dopamine to facilitate pathway leading to the thalamus and motor cortex. The basal ganglia inhibits movement, so dopamine serves to free up movement. Specifically use sinemet, which is L-dopa and carvidopa, a precursor to dopamine. We don’t just use dopamine because it doesn’t cross the blood-brain barrier. We use carvidopa to prevent L-dopa from doing anything outside the blood-brain barrier. Also, putting an electrode into the basal ganglia to excite it can be effective.
What's the most common cause of dementia? What's the biggest risk factor for that cause?
Alzheimer's disease - 40%. CVD is the biggest risk factor.
What are the warning signs of infectious dementias? What are 3 examples? How do you diagnose them? Treatment?
History of systemic infections, unexplained fever, meningeal symptoms. Examples: AIDS, bacterial meningitis, and systemic infections. Diagnose with CT, MRI, and lumbar puncture. Treat with antibiotics.
What are the warning signs of viral dementias? What's an example? How do you diagnose? How do you treat?
Signs are meningitis, encephalitis, and demyelenation due to infectious agents or immunological responses. Example is Herpes Simplex type 1. Diagnose with brain biopsy. Treat with antiviral agent like acyclovir.
What are the 2 ways that people can be infected by prion disease?
1. Acquired through diet or following medical procedures like growth hormone injection or corneal transplants.
2. Hereditary transmission via autosomal dominant trait.
What's the diagnosis for Alzheimer's?
Postportem diagnosis looking for plaques and tangles.
What causes plaques in Alzheimer's? What's the implication?
APP on chromosome 21 gets disrupted, meaning that everyone with Alzheimer's gets down syndrome.
What causes tangles in Alzheimer's?
Hyper-phosphorylation leads to disintegrating microtubules.
Compare autosomal dominant Alzheimer's to other cases.
Autosomal dominant is less than 1% of cases and involves abnormal gamma secretase clipping. Other forms involve cleavage at Abeta 42 (instead of 40) that result in toxic beta-amyloid plaques.
What % of AD cases results from ApoE phenotype? What mechanisms are involved? How do you treat it?
40% of cases. Lipid and cholesterol delivery is involved because ApoE is associated with LDL. Treat with lower cholesterol diet and/or statins.
Name 3 risks for AD.
1. Autoimmune disorder
2. Head injury
3. Low eduction - "use it or lose it" idea for neurons
Name 3 treatments for AD and 1 possible future treatment.
1. Increase cholinergic projections for focusing attention - increase acetylcholine levels w/ Cognex or Exelon
2. Memantine to increase signal:noise ratio
3. Statins to reduce cholesterol

Future drugs are gamma- and beta-secretase inhibitors.
What are the two forms of genetic AD and what chromosomes are implicated? Which is most common?
Presenilin 1 (most common) with chromosome 14 and presenilin 2 with chromosome 2.
How do drugs that treat AD work? Name two.
They block the activity of acetylcholine esterase to make ACh stay around longer. Eg. Cognex and Exelon.