module 9 Neurology Flashcards
1
Q
- Define dementia:
- What 5 functions are lost in dementia?
- What does dementia do to the brain (4)?
- Is dementia genetic?
- What are the top two causes of dementia?
A
- Progressive failure of many cerebral functions including impairment of intellectual processes
- Orientation, Memory, Language, Judgment, Decision making
- Neuron degeneration, Brain tissue compression, Atherosclerosis, Brain trauma
- yes but not limited to genetics.
- Alzheimer’s disease and vascular insufficiency
2
Q
- Name the well known disease that is a type of dementia:
- Why do some people get early onset vs late onset Alzheimer’s, and which is more common?
- Which chromosome is involved in early onset? What does this mean?
- 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
- Alzheimers
- early onset is genetic, late onset is sporadic. Sporadic is much more common
- Often people w/ downs syndrome get early onset Alzheimer’s
- 19, apolipoprotein E. People w/ high cholesterol would be at greater risk
3
Q
- Name the 2 causes of Alzheimer’s disease:
- How does the beta-amyloid protein deposition cause Alzheimer’s?
- In what part of the brain does this happen and why does that contribute to memory loss?
- How does the intracellular accumulation of tau protein cause Alzheimer’s?
A
- an extra cellular deposition of Beta-amyloid: Senile plaques. Intracellular accumulation of tau protein: neurofibrillary tangles.
- 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.
- Happens in hippocampus, the area responsible for memory.
- 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.
4
Q
- What are signs of Alzheumer’s?
- how to diagnose Alzheimer’s?
- How do we treat Alzheimer’s?
A
- extended development of signs and symptoms: behavioral (hostility, irritability,, mood swings), forgetfulness, imapired learning and poor judgement, decline of intellectual function
- no diagnostic tests, just elimination of other disorders leaving Alzheimer’s.
- no specific treatment. Anticholinesterase drugs provide temp improvement, occupational therapy, speech therapy. Team approach
5
Q
- which disorder causes severe degeneration of the basal ganglia involving the dopaminergic nigrostriatal pathway.
- What is the name of the pathway that produces and releases dopamine?
- What are the 2 types of Parkinson’s and which is more common?
- This is a …….kinetic disorder which means that there is a loss/ decrease of which neurotransmitter?
- The pathophysiology of Parkinson’s involves the loss of which type of neurons and which part of the brain?
- The presence of ……. bodies and Lewy neurites, and an accumulation of ………… .
A
- Parkinson’s disease
- the dopaminergic nigrostriatal pathway.
- idopathic (or primary) and secondary from multiple head traumas (muhammad ali). There can be some cases coming from genetic/environmental. Majority is idiopathic/primary
- hypokinetic, dopamine
- pigmented dopaminergic neurons of the substantia nigra pars compacta (basically it is a destruction of the superhighway between the
- Lewy, α-synuclein
6
Q
- What are the signs and symptoms of Parkinson’s disease?
- How do we diagnose Parkinson’s?
- How do we treat Parkinson’s?
A
- Resting tremors, shuffling steps, stooped posture, cogwill rigidity, masked facies
- Clinical diagnosis. Symptoms and signs are classic
- Removal of cause, if known, Dopamine (levodopa), MAO-B inhibitor, Anticholinergic drugs, Speech pathologist, Physical therapy, Occupational therapy
7
Q
- What kind of disease is Huntington’s?
- How is Huntington’s similar to Parkinson’s
- What chromosome is Huntington’s on? At what age does it manifest?
- Huntington’s is marked by a depletion of what?
- Levels of …………. in brain appear to be reduced
- This is a ………kinetic disorder
A
- autosomal dominant
- Both lead to degeneration of basal ganglia
- chromosome 4, manifests at 40-50 years old
- GABA
- acetylcholine
- hyperkinetic
8
Q
- What are the signs and symptoms of Huntington’s Disease?
- How do we diagnose Huntington’s
- How do we treat Huntington’s? How long do they live?
A
- Mood swings, personality changes, Restlessness, choreiform movements in arms and face
- DNA analysis
- No treatment. Disease is progressive. Live maybe 3-5 years.
9
Q
- What is ALS?
- What causes it?
- Does it impair cognition like Alzheimer’s, Parkinson’s, and Huntington’s?
- What is the pathogenesis of this disease?
- How does patient die and how long do they live?
- The initial part of the disease (upper motor neuron degeneration) what are the symptoms? When it progresses to lower motor neurons?
A
- Amyotrophic Lateral Sclerosis (Lou Gehrig’s)
- No known cause, but genes on various chromosomes have been linked.
- No
- 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
- Die from respiratory failure, usually live 5-7 years.
- Hyperreflexia and spastic paralysis. Flaccid paralysis
10
Q
- What are the signs and symptoms of ALS?
2. What is the treatment?
A
- stumbling and falling and loss of coordination.
- No treatment, but stem cell therapy is being investigated. Drugs (Riluzolen) to slow neuronal damage, respiratory therapy, exercise, and rest
11
Q
- What vascular disorders can affect the brain?
- In what 3 ways do vascular disorders happen?
- What are the 3 types of strokes?
A
- TIA’s (transient ischemic attacks) and Strokes (CVA)
- interference with blood supply, hemorrhage, and vascular malformations
- thrombotic, embolic, and hemorrhagic strokes.
12
Q
- in TIA does brain tissue die? How long do these episodes last?
- What are signs/symptoms of TIA?
- What do repeated TIAs indicate?
A
- no. < 1 hour
- difficlut to diagnose after event, short episodes of impaired function (like weakness in limb), visual disturbances, numbness in face, confusion
- a warning sign for obstruction related to atherosclerosis.
13
Q
- Describe a thrombolytic stroke and its main cause:
- Describe an embolic stroke and its main cause:
- Describe a hemorrhagic stroke and its main cause:
- What are the signs and symptoms of strokes?
- How do we diagnose?
- Name some treatments for strokes:
- How do we prevent strokes?
A
- thrombi formed in arteries supplying the brain or in the intracranial vessels. Gradual onset. May be preceded by TIAs. Atherosclerosis
- Fragments that break from a thrombus formed outside the brain. Sudden onset. Atherosclerosis of carotid or systemic source.
- Aneurysm that bleeds into brain causing intracranial pressure. Sudden onset. Hypertension. Third most common type of stroke
- lack of voluntary movement or sensation on opposite side, flaccid paralysis,
- NIHSS (National Institute of Health Stroke Scale)
- Restore perfusion to prevent necrosis, fibrinolytics, surgery, control BP, glucocorticoids, supportive treatments (OT, PT, speech therapy etc). Treat underlying problems.
- Platelet antiaggregant - aspirin
Statins – lower cholesterol, BP meds, Exercise, Lifestyle
14
Q
- What type of microbes can cause meningitis? Which is most common and what is its name?
- What are 2 physical tests for meningitis?
- Describe what areas are infected in meningitis:
A
- bacterial, viral, and fungal. Bacterial is most common: streptococcus and neisseria meningitidis
- Kernig test (hurts to straighten knee) and Brudzinski sign (unable to flex neck w/o flexing knees and hips)
- infection crosses blood brain barrier and infects meninges, ventricular system and CSF
15
Q
- How do we diagnose meningitis?
- What are the indicators we look for in the CSF of the lumbar puncture? What types of wbc’s address different infections?
- How do we treat meningitis?
A
- lumbar puncture
- 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.
- aggressive antimicrobial therapy, glucocorticoids, reduce cerebral inflammation and edema. Vaccines are available.