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61 Cards in this Set
- Front
- Back
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What's the danger in taking COX inhibitors? Why?
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They can increase risk of GI bleeding because mucus production is decreased.
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What do prostaglandins do? What inhibits this activity?
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Prostaglandins sensitize pain receptors and cause inflammation. NSAIDs inhibit this activity.
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What's the nature of degradation in HD?
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There are two pathways involved.
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What part of the brain is implicated in both Parkinson's and HD?
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The basal ganglia.
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Compare Parkinson's vs. HD
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HD has too much firing in the thalamus, whereas Parkinson's doesn't have enough firing. HD = dance, Parkinson = akinetic.
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What results from Complex 1 poisoning? What is a known poison?
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-Calcium overload
-Free radicals -No ATP 3-NPA is a known poison. |
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What are two treatments for Parkinson's?
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Sinemet, which works by increasing dopamine release. Another treatment called Mirapex works by mimicking dopamine.
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Why is olfaction susceptible to damage?
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-Inhaling things in the environment
-Prime location for physical injury |
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Where does olfactory damage typically occur?
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At the olfactory bulb.
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What causes loss of smell?
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-Nasal obstruction like a cold or allergies
-Nasal polyps, which are growths in the nose and sinus -Surgery -Blow to the head -Exposure to chemicals |
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How do you test for olfaction problems?
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Scratch and sniff tests and nasal examinations normally. If there's a nerve problem, then use X-ray or CAT scan.
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What are the symptoms of a loss of taste and smell?
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-Foods may have a metallic taste
-Weight loss from skipping meals |
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What's important about the origin of the sense of taste?
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Our sensation of taste comes from smell receptors combined with taste receptors.
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What are the risks associated with losing taste/smell?
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-Too much salt > hypertension
-Too much sugar > diabetes -Malnutrition in general -Spoiled foods -Environmental risk factors -Depression about not enjoying eating |
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What's the prostaglandin pathway?
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Damaged tissues > prostaglandins > sensitize the whole pain pathway
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What's another name for pain receptors?
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Nociceptors
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What are the hallmarks of the 2 types of pain receptors?
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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. |
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What's the counterpoint of nociceptive pain? Where should pain treatment start?
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The counterpoint is neuropathy. Always start treatment with nociceptive pain.
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What are the easy treatments for nociceptive pain?
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Over-the-counter drugs like NSAIDs.
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What do NSAIDs do to reduce pain?
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NSAIDs inhibit COX production, which is crucial for production of prostaglandins.
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What are neuropathic pain treatments? How do they work?
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Anti-depressants work because they increase serotonin, which is secreted in descending fibers during pain to reduce irritation.
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What's the CNS pathology of MS?
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Demyelination of nerve cell axons.
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What causes CNS pathology of MS?
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Autoimmune dysfunction from a breakdown in the blood-brain barrier, which leads to inflammation
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What causes MS?
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It could be genetic predisposition, but not always. Otherwise:
-Environmental factors -Virus infections -Bacteria and parasite infections |
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What reduces the risk of MS?
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Sunlight and vitamin D.
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How do you diagnose MS?
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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.
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What's the most common form of MS?
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Relapsing-remitting, consisting of 85% of patients.
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Compare inflammation in MS vs. other autoimmune diseases. What mechanisms are involved with each?
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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.
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What genes, in general and in particular, are associated with MS?
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Generally genes associated with immune response, specifically a breakdown of ch6p21.
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What are the classes of drugs for treating MS? What are some specific ones? How do they work?
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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.
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Compare incidents of MS in men and women. What's special about MS in women? What's the implication?
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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.
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What controls MS relapses? How?
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Corticosteroids, which suppress the immune system.
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What part of the motor neuron system is affected by ALS?
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Both upper and lower motor neuron systems.
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What are the symptoms of ALS?
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-Muscle weakness
-Twitching -Impaired arm and leg use -Speech "thickness" |
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Compare incidents of ALS in men and women.
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Much more common in men than women.
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What neurons does ALS affect?
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Only motor neurons and other neurons anterior to them.
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What are the classes of ALS?
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-Sporadic, 90% of cases
-Familial, less than 10% -Guamanian from ingesting excitotoxic foods that stimulate glutamate |
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How do you treat ALS?
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With drugs that block glutamate.
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What causes Huntington's disease?
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It's 100% autosomal dominant genetic.
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Describe the HD neuropathology pathway.
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Chromosome 4 > too many CAG repeats > caudate and putamin damage (cortex later) > globus pallidus inhibition, so thalamus goes crazy firing
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What's the treatment for Huntington's disease?
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Dopamine receptor blockers like haldol for early treatment. Then Tetrabenazine to block transport of dopamine into vessicles. Lastly tranquilizers act as GABA allosteric agonists.
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What part of the brain is most susceptible to damage from HD?
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The striatum, followed by the cerebral cortex.
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What kind of disease does HD appear to by, and why?
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It may be a mitochondrial disease. This is illustrated by the case where spoiled sugarcane in China got people sick.
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Compare Parkinson's in men and women and explain why there's a difference.
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Men have it more than women because of lifestyle choices, namely working in industrial places and taking more risks.
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What specific lifestyle choice can increase odds of getting Parkinson's? Why?
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Living in rural areas because it increases the odds of consuming pesticides.
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What's the neuropathology of Parkinson's?
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MPP+ inhibits Complex 1 in mitochondria in substantia nigra > mitochondria makes superoxide and stops ATP production
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How do you diagnose Parkinson's?
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PET scan
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How do treatments for Parkinson's work?
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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.
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What's the most common cause of dementia? What's the biggest risk factor for that cause?
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Alzheimer's disease - 40%. CVD is the biggest risk factor.
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What are the warning signs of infectious dementias? What are 3 examples? How do you diagnose them? Treatment?
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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.
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What are the warning signs of viral dementias? What's an example? How do you diagnose? How do you treat?
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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.
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What are the 2 ways that people can be infected by prion disease?
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1. Acquired through diet or following medical procedures like growth hormone injection or corneal transplants.
2. Hereditary transmission via autosomal dominant trait. |
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What's the diagnosis for Alzheimer's?
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Postportem diagnosis looking for plaques and tangles.
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What causes plaques in Alzheimer's? What's the implication?
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APP on chromosome 21 gets disrupted, meaning that everyone with Alzheimer's gets down syndrome.
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What causes tangles in Alzheimer's?
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Hyper-phosphorylation leads to disintegrating microtubules.
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Compare autosomal dominant Alzheimer's to other cases.
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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.
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What % of AD cases results from ApoE phenotype? What mechanisms are involved? How do you treat it?
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40% of cases. Lipid and cholesterol delivery is involved because ApoE is associated with LDL. Treat with lower cholesterol diet and/or statins.
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Name 3 risks for AD.
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1. Autoimmune disorder
2. Head injury 3. Low eduction - "use it or lose it" idea for neurons |
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Name 3 treatments for AD and 1 possible future treatment.
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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. |
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What are the two forms of genetic AD and what chromosomes are implicated? Which is most common?
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Presenilin 1 (most common) with chromosome 14 and presenilin 2 with chromosome 2.
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How do drugs that treat AD work? Name two.
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They block the activity of acetylcholine esterase to make ACh stay around longer. Eg. Cognex and Exelon.
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