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99 Cards in this Set
- Front
- Back
6th leading cause of death among adults |
Alzheimer's |
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4 characteristic s/sx of Alzheimer's |
-progressive memory loss -impaired thinking -neuropsychiatric problems -inability perform ADL |
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How many americans have alzheimer's? |
4.5 million, or 5 to 10% of populations |
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7 aspects of the pathophysiology of alzheimer's disease |
-degenerative -vascular -infectious -metabolic -psychiatric -development of senile plaques -development of neurofibrillary tangles |
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Progression of neuronal degeneration in Alzheimer's starts at what part of the brain? |
Hippocampus (memory) |
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What part of the brain is effected in alzheimer's that controls speech, perception, reasoning, and executive thinking? |
Cerebral cortex- decreased cerebral volume |
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What are advancing sx of Alzheimer's with advanced cortical degeneration? |
-complete loss of speech -loss of bladder -loss of bowel -complete inability for self care |
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What neurotransmitter declines in advanced Alzheimer's? |
Acetylcholine levels are 90% below normal |
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This neurotransmitter is critical for forming memories. |
Acetylcholine |
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spherical bodies composed of a central core of _________ (a protein fragment) surrounded by neuron remnants |
beta-amyloid |
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neuritic plaque in Alzheimer's |
beta-amyloid |
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when does beta-amyloid accumulation start to occur? |
perhaps 10 to 20 years before first symptoms of AD appear. |
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What is tau & what does it do in healthy person? What does it do in alzheimer's? |
Tau is a protein that normally forms cross bridges between microtubules. In alzheimer's tau twists into paired helical filaments that form tangles. |
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what is the major risk factor of alzheimer's? |
age. 90% of patients age of onset is 65 years or older. |
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What are the risk factors of alzheimer's? |
-advanced age over 65 -family hx of AD -female? -nicotine? -head injury? |
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4 mild sx of alzheimer's |
-confusion and memory loss -disorientation in familiar surroundings -problems with routine tasks -changes in personality & judgement |
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6 moderate sx of alzheimer's |
-difficulty with ADL -anxiety, agitation, paranoia -sleep disturbances -wandering -sundowning -difficulty recognizing family & friends |
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4 severe sx of alzheimer's |
-loss of speech -loss of appetite -loss of bladder & bowels -total dependance on caregiver |
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how to diagnose alzheimer's -definitive & 2 ballpark while alive. |
-autopsy -mini mental exam -clock drawing |
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2 goals of tx for Alzheimer's |
-improve symptoms -reverse cognitive decline |
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Four drugs for alzheimer's treatment |
1. DONEPIZIL- cholinesterase inhibitor 2. Galantine- cholinesterase inhibitor 3. Rivastigmine- cholinesterase inhibitor 4. Nemantine- blocks neuronal receptors for N-methyl-D-aspartate (MNDA) |
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how do cholinesterase inhibitors work? |
They prevent the breakdown of AcH by acetylcholinesterase and increase the availability of AcH at cholinergic synapses. |
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what are general side effects of the cholinesterase inhibitors? |
(TYPICAL CHOLINERGIC SIDE EFFECTS) -GI symptoms-nausea, vomiting, dyspepsia, diarrhea -Headache -dizziness -bronchoconstriction -CV |
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how does cholinesterase inhibitor dosing generally work? |
-highest does produce best result, but also produce biggest side effects. |
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Only cholinesterase inhibitor used for MILD, MODERATE, & SEVERE Alzheimer's disease. |
Donepezil (Aricept) |
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Cholinesterase inhibitor drug interactions: |
-Benedryl/dihydremine -Tricyclic antidepressants -Antipsychotics |
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Must be careful when treating Alzheimer's Patients with cholinesterase inhibitors when they have these 2 diseases |
-asthma -COPD |
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Donepezil (Aricept) is more selective for which form of AChE |
more selective for AChE found in the brain than for AChE found in periphery |
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What are pharmakinetics for Donepezil? |
-PO -metabolized by hepatic cytochrome P450 enzymes -elimination mainly in urine (some in bile) |
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what is the half life of Donepezil (Aricept) |
prolonged half life of 60 hours |
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dosing for Donepezil (Aricept) |
-carefully titrated doses -standard tablets 5-10 mg or 23 mg -ODT oral disintegrating tablets 5 and 10 mg |
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When & how to take Doneprizil (Aricept) |
Late in evening, with or without food |
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What is the new class of drugs for Alzheimer's |
NMDA receptor antagonists |
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What drug is in the class of NMDA receptor antagonists? |
Memantine (Named, Named XR, Ebixa) |
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What is the mechanism of action for NMDA receptor agonists |
modulates the effects of glutamate (major excitatory transmitter in CNS) at the NMDA receptors |
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What is the major excitatory transmitter of CNS that Memantine (Namenda) modulates? |
Glutamate |
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Which alzheimer's patients is Memantine (Namenda) indicated for? |
-moderate and severe NOT MILD. |
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How does Memantine help in Alzheimer's |
-it blocks calcium influx when extracellular glutamate is low, but permits calcium influx when extracellular glutamate is high. |
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What drug may be able to slow or even reverse decline in function? |
Memantine |
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What are the pharmacokinetics for Memantine? |
PO -well absorbed in presence and absence of food -plasma levels eat in 3 to 7 hrs -undergoes little metabolism -excreted largely unchanged in urine -long half life 60 to 80 hours -clearance reduced with renal impairment |
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Side effects of Memantine (Named) |
(Well tolerated) -dizzyness -headache -confusion -constipation |
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how many people in US have epilepsy? |
2.3 million |
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what percentage of epilepsy patients are seizure free with drugs? |
60 -70% |
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difference between seizures and epilepsy |
epilepsy- chronic condition seizure- isolated event |
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How are seizures initiated? |
by high frequency discharge from a group of hyper excitable neurons called a focus |
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What is a focus in terms of seizures? |
a group of hyper excitable neurons that initiate a high frequency discharge. May result from congenital defects, hypoxia, head trauma or cancer. |
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2 broad categories of seizures |
1. Partial (focal ) seizures 2. Generalized Seizures |
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True or false: As a rule, partial seizures and generalized seizures are treated with different drugs |
true |
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Duration of simple partial seizures |
20 to 60 seconds |
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This distinguishes a simple partial seizure from a complex partial seizure. |
There is no loss of consciousness. |
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These seizures are discrete, motor, sensory auditory, or visual. THERE IS NO LOSS OF CONSCIOUSNESS. Duration is 20 - 60 seconds. |
Simple partial seizure |
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These seizures have impaired consciousness. The patient is motionless with fixed gaze. Duration is 45 to 90 seconds. Often followed by automatism- repetitive, purposeless movements. |
Complex Partial Seizures |
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What is automatism? |
Repetetive, purposeless movements following a complex partial seizure. |
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These partial seizures begin as simple or complex and evolve into tonic clonic activity. Duration of 1 -2 minutes. LOSS OF CONSCIOUSNESS. |
Secondarily Generalized Seizures. |
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3 types of partial seizure |
-Simple Partial -Complex Partial -Secondarily Generalized Seizures |
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Tonis |
Stiffen |
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Clonis |
Thrashing |
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What is postictal period |
period of CNS depression following generalized seizure in which patient is slow to respond, sleepy. |
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2 categories of Generalized seizures |
-convulsive -nonconvulsive |
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6 major types of generalized seizures |
-Tonic Clonic (grand mal) -Absence Seizures (petit mal) -Atonic Seizures -Myoclonic Seizures -Status Epilepticus -Febrile Seizures |
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These seizures last 90 seconds or less and include periods of major convulsions and muscle rigidity, cause urination, and are followed by postictal state |
Tonic Clonic generalized seizures |
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These seizures are characterized by a loss of consciousness for a brief time (10 to 30 seconds) and may involve mild, symmetric motor activity or no motor activity at all. |
Absence Seizures (petit mal) |
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These seizures occur primarily in children and are characterized by sudden loss of muscle tone- head drops may occur, or patient may collapse. |
Atonic Seizures |
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These seizures consist of sudden muscle contraction that lasts for just 1 second, may be limited to one limb or may involve entire body. |
Myoclonic seizures |
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This is defined as a seizure that persists for 15 to 30 minutes or longer or as a series where patient does not regain consciousness |
Status Epilepticus |
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These seizures occur with fever, often manifest as generalized tonic-clonic, and are common among children ages 6 mo to 5 years. |
Febrile Seizures |
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5 basic mechanisms of AED's |
-suppression of sodium influx -suppression of calcium influx -promotion of potassium efflux -blockade of receptors for glutamate -potentiation of gamma-aminobutyric acid (GABA) |
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These 4 AED's prevent seizures by reversibly binding to sodium channels while they are in the inactivated state, and thereby prolong channel inactivation. |
-Phentoin (Dilantin) (traditional) -Carbamazepine (Tegretol) (traditional) -Valproic Acid (Depakote) (Traditional) -Lamotrigine (Lamictal) (newer) Phil Collins Values Love |
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these 2 drugs suppress calcium influx in axon terminals, blocking transmitter release. |
-Valproic Acid (Depakote)- traditional -Ethosuximide (traditional) |
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This drug suppresses both calcium influx and sodium influx |
Valproic Acid (Depakote) -traditional |
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This is the only drug that promotes potassium efflux by acting on voltage gated potassium channels to facilitate potassium efflux. |
Ezogabine |
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These 2 AEDs block the action of glutamate |
-Felbamate -Topirimate (Topomax)- new |
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-mate |
drugs that block the action of glutamate to prevent seizures |
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2 receptors for Glutamate |
-NMDA -AMPA |
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5 drugs that decrease neuronal excitability by potentiating the activity of GABA. |
-Gabapentine (Neurontin) -Benzodiazepines (Valium, diazepam) -Barbituates -Tiagabine -Vigabatrin |
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Inhibitory neurotransmitter widely distributed throughout brain |
GABA |
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This was the first medication to suppress seizures w/out depressing the entire CNS |
Phenytoin (Dilantin) |
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This AED suppresses high frequency neuronal discharge and is also used in bipolar disorder |
Carbamazepine (Tegretol) |
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This AED is widely used for all major types of seizures, and also treats bipolar disorder and migraines |
Valproic Acid (Depakote) |
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Phenytoin (Dilantin) mechanism for action |
at clinical concentrations phenytoin causes selective inhibition of sodium channels |
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Pharmacokinetics of Phenytoin (Dilantin) |
-unusual pharmacokinetics -PO/XR PO absorbtion varies substantially among patients -liver has limited ability to metabolize - |
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Phenytoin (Dilantin) can be used to treat all major forms of epilepsy EXCEPT |
Absence Seizures |
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This AED easily overwhelms the liver, leading to: |
Hepatotoxicity |
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You will need to have plasma levels drawn to make sure this drug is within a safe Therapeutic range of 10 - 20 mcg/mL |
Phenytoin (Dilantin) |
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Side effects of Phenytoin (Dilantin) |
-Nystagmus -Gingival Hyperplasia -Dermatologic -Teratogenic |
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What can you mix Phenytoin (Dilantin) with when giving as IV? |
ONLY NORMAL SALINE |
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What rate can you give IV Phenytoin (Dilantin)? |
50mg/minute |
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What category teratogenic drug is Phenytoin (Dilantin) |
Category D, give only if necessary and no other seizure drug will work. |
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What AED drug must you cardiac monitor during entire infusion when giving as IV |
Phenytoin (Dilantin) |
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What are four newer AED's |
-Oxcarbazepine (Trileptal) -Lamotrigine (Lamictal) -Gabapentin (Neurontin) -Topiramate (Topamax) (T LOG) |
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This AED blockades the voltage-sensitive sodium channels and its most common adverse effect is dizziness (up to 49%) |
Oxcarbazepine (Trileptal) |
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This AED was introduced in 1994. It can blockade sodium and calcium channels. It is also used in bipolar disorder |
Lamotrigine (Lamictal) |
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This AED was introduced in 1993. Only FDA approved for seizures. However, widely used for neuralgia and neuropathic pain. |
Gabapentin (Neurontin) |
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This AED was introduced in 1996 and has wide off label usage including: weight loss, bipolar disorder, cluster headaches and neuropathic pain. |
Topiramate (Topamax) |
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How does the AED Levetiracetam (Keppra) work? |
It is chemically and pharmacologically different from all other AEDs and it is unknown how it its. |
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This is the one AED that does not interact with other drugs |
Levetiracetam (Keppra) |
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Levetiracetam (Keppra) side effects |
Drowsiness and lack of strength |
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Pharmacokinetics of Levetiracetam (Keppra) |
-PO, oral solution, IV -rapid and complete absorption w/ or w/out food -metabolism is minimal, not mediated by liver cytochrome P450 enzymes -excreted in urine, largely unchanged |
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Monitor all seizure disorder patients for_____ |
suicide risk |