module 9 Neurology Flashcards

1
Q
  1. Define dementia:
  2. What 5 functions are lost in dementia?
  3. What does dementia do to the brain (4)?
  4. Is dementia genetic?
  5. What are the top two causes of dementia?
A
  1. Progressive failure of many cerebral functions including impairment of intellectual processes
  2. Orientation, Memory, Language, Judgment, Decision making
  3. Neuron degeneration, Brain tissue compression, Atherosclerosis, Brain trauma
  4. yes but not limited to genetics.
  5. Alzheimer’s disease and vascular insufficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q
  1. Name the well known disease that is a type of dementia:
  2. Why do some people get early onset vs late onset Alzheimer’s, and which is more common?
  3. Which chromosome is involved in early onset? What does this mean?
  4. An alteration on which chromosome is linked to late onset Alzheimer’s? What is the name of the protein that is affected? What patient would be at greater risk?
A
  1. Alzheimers
  2. early onset is genetic, late onset is sporadic. Sporadic is much more common
    1. Often people w/ downs syndrome get early onset Alzheimer’s
  3. 19, apolipoprotein E. People w/ high cholesterol would be at greater risk
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q
  1. Name the 2 causes of Alzheimer’s disease:
  2. How does the beta-amyloid protein deposition cause Alzheimer’s?
  3. In what part of the brain does this happen and why does that contribute to memory loss?
  4. How does the intracellular accumulation of tau protein cause Alzheimer’s?
A
  1. an extra cellular deposition of Beta-amyloid: Senile plaques. Intracellular accumulation of tau protein: neurofibrillary tangles.
  2. Dysfunctional beta and gamma secretase (enzymes responsible for cleaving and metabolizing beta-amyloid) allow beta-amyloid to persist extracellularly. Accumulations of it (plaques) are toxic to neuron and it dies.
  3. Happens in hippocampus, the area responsible for memory.
  4. Tau proteins act as stabilizers to the structure of a neuron. Dysfunctional tau protein causes neurotubule to fall apart. Tau proteins clump together and form a toxic environment killing more neurons.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q
  1. What are signs of Alzheumer’s?
  2. how to diagnose Alzheimer’s?
  3. How do we treat Alzheimer’s?
A
  1. extended development of signs and symptoms: behavioral (hostility, irritability,, mood swings), forgetfulness, imapired learning and poor judgement, decline of intellectual function
  2. no diagnostic tests, just elimination of other disorders leaving Alzheimer’s.
  3. no specific treatment. Anticholinesterase drugs provide temp improvement, occupational therapy, speech therapy. Team approach
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q
  1. which disorder causes severe degeneration of the basal ganglia involving the dopaminergic nigrostriatal pathway.
  2. What is the name of the pathway that produces and releases dopamine?
  3. What are the 2 types of Parkinson’s and which is more common?
  4. This is a …….kinetic disorder which means that there is a loss/ decrease of which neurotransmitter?
  5. The pathophysiology of Parkinson’s involves the loss of which type of neurons and which part of the brain?
  6. The presence of ……. bodies and Lewy neurites, and an accumulation of ………… .
A
  1. Parkinson’s disease
  2. the dopaminergic nigrostriatal pathway.
  3. idopathic (or primary) and secondary from multiple head traumas (muhammad ali). There can be some cases coming from genetic/environmental. Majority is idiopathic/primary
  4. hypokinetic, dopamine
  5. pigmented dopaminergic neurons of the substantia nigra pars compacta (basically it is a destruction of the superhighway between the
  6. Lewy, α-synuclein
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q
  1. What are the signs and symptoms of Parkinson’s disease?
  2. How do we diagnose Parkinson’s?
  3. How do we treat Parkinson’s?
A
  1. Resting tremors, shuffling steps, stooped posture, cogwill rigidity, masked facies
  2. Clinical diagnosis. Symptoms and signs are classic
  3. Removal of cause, if known, Dopamine (levodopa), MAO-B inhibitor, Anticholinergic drugs, Speech pathologist, Physical therapy, Occupational therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q
  1. What kind of disease is Huntington’s?
  2. How is Huntington’s similar to Parkinson’s
  3. What chromosome is Huntington’s on? At what age does it manifest?
  4. Huntington’s is marked by a depletion of what?
  5. Levels of …………. in brain appear to be reduced
  6. This is a ………kinetic disorder
A
  1. autosomal dominant
  2. Both lead to degeneration of basal ganglia
  3. chromosome 4, manifests at 40-50 years old
  4. GABA
  5. acetylcholine
  6. hyperkinetic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q
  1. What are the signs and symptoms of Huntington’s Disease?
  2. How do we diagnose Huntington’s
  3. How do we treat Huntington’s? How long do they live?
A
  1. Mood swings, personality changes, Restlessness, choreiform movements in arms and face
  2. DNA analysis
  3. No treatment. Disease is progressive. Live maybe 3-5 years.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q
  1. What is ALS?
  2. What causes it?
  3. Does it impair cognition like Alzheimer’s, Parkinson’s, and Huntington’s?
  4. What is the pathogenesis of this disease?
  5. How does patient die and how long do they live?
  6. The initial part of the disease (upper motor neuron degeneration) what are the symptoms? When it progresses to lower motor neurons?
A
  1. Amyotrophic Lateral Sclerosis (Lou Gehrig’s)
  2. No known cause, but genes on various chromosomes have been linked.
  3. No
  4. Usually starts with head trauma (or SOD-1 gene dysfunction) causing a loss of upper motor neurons in cerebral cortex which damages lower motor neurons causing flaccid paralysis and progressive loss of muscle control
  5. Die from respiratory failure, usually live 5-7 years.
  6. Hyperreflexia and spastic paralysis. Flaccid paralysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q
  1. What are the signs and symptoms of ALS?

2. What is the treatment?

A
  1. stumbling and falling and loss of coordination.
  2. No treatment, but stem cell therapy is being investigated. Drugs (Riluzolen) to slow neuronal damage, respiratory therapy, exercise, and rest
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q
  1. What vascular disorders can affect the brain?
  2. In what 3 ways do vascular disorders happen?
  3. What are the 3 types of strokes?
A
  1. TIA’s (transient ischemic attacks) and Strokes (CVA)
  2. interference with blood supply, hemorrhage, and vascular malformations
  3. thrombotic, embolic, and hemorrhagic strokes.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q
  1. in TIA does brain tissue die? How long do these episodes last?
  2. What are signs/symptoms of TIA?
  3. What do repeated TIAs indicate?
A
  1. no. < 1 hour
  2. difficlut to diagnose after event, short episodes of impaired function (like weakness in limb), visual disturbances, numbness in face, confusion
  3. a warning sign for obstruction related to atherosclerosis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q
  1. Describe a thrombolytic stroke and its main cause:
  2. Describe an embolic stroke and its main cause:
  3. Describe a hemorrhagic stroke and its main cause:
  4. What are the signs and symptoms of strokes?
  5. How do we diagnose?
  6. Name some treatments for strokes:
  7. How do we prevent strokes?
A
  1. thrombi formed in arteries supplying the brain or in the intracranial vessels. Gradual onset. May be preceded by TIAs. Atherosclerosis
  2. Fragments that break from a thrombus formed outside the brain. Sudden onset. Atherosclerosis of carotid or systemic source.
  3. Aneurysm that bleeds into brain causing intracranial pressure. Sudden onset. Hypertension. Third most common type of stroke
  4. lack of voluntary movement or sensation on opposite side, flaccid paralysis,
  5. NIHSS (National Institute of Health Stroke Scale)
  6. Restore perfusion to prevent necrosis, fibrinolytics, surgery, control BP, glucocorticoids, supportive treatments (OT, PT, speech therapy etc). Treat underlying problems.
  7. Platelet antiaggregant - aspirin
    Statins – lower cholesterol, BP meds, Exercise, Lifestyle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q
  1. What type of microbes can cause meningitis? Which is most common and what is its name?
  2. What are 2 physical tests for meningitis?
  3. Describe what areas are infected in meningitis:
A
  1. bacterial, viral, and fungal. Bacterial is most common: streptococcus and neisseria meningitidis
  2. Kernig test (hurts to straighten knee) and Brudzinski sign (unable to flex neck w/o flexing knees and hips)
  3. infection crosses blood brain barrier and infects meninges, ventricular system and CSF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q
  1. How do we diagnose meningitis?
  2. What are the indicators we look for in the CSF of the lumbar puncture? What types of wbc’s address different infections?
  3. How do we treat meningitis?
A
  1. lumbar puncture
  2. color of fluid (should be clear), protein ( >45mg/dL indicates infection), glucose (<45 indicates infection), and number of wbcs (>5 indicates infection). Lymphocytes are high for virus.
  3. aggressive antimicrobial therapy, glucocorticoids, reduce cerebral inflammation and edema. Vaccines are available.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q
  1. Describe what is encephalitis?
  2. What usually causes it?
  3. What are the early signs?
A
  1. Infection of the parenchymal or connective tissue in the brain and spinal cord. Necrosis and inflammation develop in brain tissue. Result in some permanent damage
  2. usually virus - herpes family
  3. Severe headache, stiff
    neck, lethargy, vomiting, seizures, fever
17
Q
  1. Describe MS:
  2. At what age do people get it?
  3. What are the signs and symptoms?
  4. Are there periods between episodes when symptoms subside? What does this indicate?
  5. How do we diagnose MS.
  6. how do we treat MS?
A
  1. Loss of myelin disrupts nerve conduction. Results in death of neurons and brain atrophy.
  2. 20-40
  3. Paresthesia, Weakness, impaired gait, Visual disturbances (diplopia- double vision and scotoma - spot in vision), Urinary incontinence, dysarthria
  4. yes. neural function returns for a time. Severity of disease depends on how often there are recurrences.
  5. neuro exam and MRI (test of choice)
  6. No treatment yet. Supportive treatment (PT, OT,), trials are in process for possible meds.
18
Q
  1. What is myasthenia gravis?
  2. Which parts of the body are affected first?
  3. What are the signs and symptoms?
  4. How do we treat myasthenia gravis (5)?
  5. What is test of choice? Name a few other tests:
A
  1. an autoimmune disorder that attacks acetylcholine (ACh) receptors. Destruction of receptors prevents muscle stimulation
  2. Areas that move a lot (think blinking of eyes). Face and ocular muscles.
  3. facial/eye muscle weakness, impaired chewing, swallowing, vision, speech, head droop, upper respiratory infections
  4. Anticholinesterase agents (stops breakdown of ACh), Glucocorticoids (suppress immune system), Plasmapheresis
    (Removal of antibodies) Thymectomy, immunosuppressants
  5. serum antibody test. tensilon test, ice test, CT and MRI of thymus gland
19
Q
  1. Name the only 2 neurotransmitters that are inhibitory:
  2. What part of the brain controls motor function?
  3. Is dopamine inhibitory or excitatory?
A
  1. glycine and GABA
  2. basal ganglia
  3. excitatory