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33 Cards in this Set

  • Front
  • Back
Partial seizures

Bilateral or unilateral neuronal involvement?

Local onset?

Originate where?

Generally caused by?
Involves neurons unilaterally

Often have local onset

Usually originates from cortical brain tissue

Often caused by tumor or underlying problem
Generalized seizures

Bilateral or unilateral neuronal involvement?

Local onset?

Originate where?

Is consciousness maintained?

Name 2 types?
Bilateral neuronal involvement

Usually do NOT have local onset

Usually originate from a subcortical (thalamus, limbic system, not cortex) or deeper brain focus

Consciousness is always impaired or lost

Absence, tonic clonic, myoclonic, atonic
Define status epilipticus.
Is it an emergency? Why or why not?
Seizures lasting > 30 min or subsequent seizure prior to full recovery of previous (In postical state).

Yes, it is a medical emergency b/c the brain can become hypoxic, resulting in death or extreme brain damage.
Seizure provoking factors. (7)
Alcohol (> 2 drinks triples likelihood of seizure)
Nutritional deficiencies (hypoglycemia, low B6, Na+, Ca2+, Mg2+)
Drug abuse (cocaine, amphetamines)
OTC drugs (beadryl)
Menstrual period (catamenial seizures)
Sleep deprivation
Stress
Describe the pathophysiology of Alzheimer's Diease
Neurofibrillary tangles and neuritic plaques in the cerebral cortex & hippocampus.

Tangles destroy microtubles; decreased Tau protein associated.
Plauqe forms from protein pieces of beta amyloid that clump together
Loss of neurons in hippocampus and area of cortex that plays key role in new memory formation is seen.
Describe some of the clinical presentation of Alzheimer's Disease.

When are you likely to see Parkinson type symptoms with AD?
Progressive forgetfulness
Decreased ability to concentrate
Progressive decline in abstract thinking, problem solving, judgment, mathematical ability.
Agitation and irritability are common, esp in early stages.
If frontal lobe of cortex is involved motor changes and Parkinson's type problems may be seen (rigidity and flexion posturing)
Parkinson Disease

What part of brain is affected?
Which neurotransmitter is associated?
Degenerative disorder of the basal ganglia.
DA secreting neurons in substania nigra are progressively lost
Multiple Sclerosis

What happens to nerves in MS?
Is there a genetic component to the disease?
What are some of the immune responses seen/involved?
Demyelination and plaque formation on nerves slows impulses in CNS.

Yes, there is a specific haplotype for MS susceptibility genes that alter body's immune response in some types of MS.

CD8 & T-cells attack myelin
Increase in pro-inflammatory cytokines
Integrins facilitate passage of immune cells into CNS
Chemokines increase, promoting migrateion of immune cells
Antibodies contribute to inflammatory response
Amyotrophic lateral sclerosis (ALS)

Involves which motor neurons?

Is remission common?

Give clinical manifestations
Upper and lower motor neurons degenerate, reulting in progressive muscle wasting and scarring of corticospinal tract.

Usually no remission, progressive to paralysis.

Muscle weakness, starting in single groups and progressing; no associated mental, sensory or autonomic symptoms; deep tendon reflexes absent
Guillain-Barre Syndrome

Normally affects which nerves?

What often triggers?

Clinical manifestations?
Acquired inflammatory disease that results in demyelination of peripheral nerves.

Often preceded by viral infection

Paralysis, respiratory insufficiency, ANS instability
Myesthenia Gravis

What neurotrasmitter is involved?

Characterized by?
Antibodies are produced against ACh receptors @ neuromuscular junctions.

Characterized by muscle weakness and fatigability. Some may have local symptoms, some may have systemic effect.
Migraines

What nerve involved?

What neurotransmitter is thought to be involved?

Common prodromal symptoms?
Trigeminal nerve is involved, releases neuro-inflammatory peptides. Trigeminal nerve becomes sensitized.

Serotonin 5HT initially causes vasoconstriction, eventually leading to vasodilation, causes pain and further irritating nerves in the area

Visual and sensory deficits are common. May also have scalp tenderness, photophobia, auras.
Thrombotic stroke

Caused by?

Risk factors?
Arterial occulsions caused by thrombi in arteries supplying brain or intracranial vessels.

Risk factors artherosclerosis (most common), diabetes mellitus, elevated cholesterol, sedentary lifestyle
Embolic stroke

Caused by?

What is arrhythmia commonly associated with emobolic stroke?

Risk factors?
Involves fragments that break off from a thrombus formed outside brain.

Atrial fibrillation

a-fib, MI, endocarditis, rheumatic heart disease, valvular prostheses
Hemorrhagic stroke

What differentiates this from thrombotic or embolic stroke?
Caused by intracranial hemorrhage from HTN, ruptured aneurysms, arteriovenus malformation, bleeding into a tumor
What are the 4 main ways AEDs prevent or suppress seizure activity.
Block Na+ channels
Block Ca2+ channels
Potentiates GABA (neurotransmitter that prolongs channel openings)
Inhibit glutamate (excitatory)
Describe 3 types of Extrapyramidal effects?

Are older or newer antipsychotics associated with EPS? Any specifically?

Which neurotransmitter receptor is involved?
Parkinsonian symptoms (altered gain, rigid movement)
Neuroleptic malignant syndrome (hyperthemia, muscle rigidity-life threatening)
Tardive dyskinesia-results from prolonged use, repetitive involuntary movements

Older antipyschotics with high potency are more likely to cause EPS, esp trifluoperazine and haloperidol.

D2 receptors are blocked to decrease dopamine, but can cause EPS
Name 2 enzymes required for synthesis of dopamine?

Name 4 involved in the breakdown of dopamine?
Synthesis:
Tyrosine hydroxylase (tyrosine to DOPA) and DOPA decarboxylase (DOPA to dopamine)

Breakdown:
DA-B hydroxylase (dopamine to NE)
Phenylethanolamine-N-methyltransferase (NE to epineph)
MAO (dopamine to DOPAC)
COMT (dopamine to 3-metho/DOPAC to HVA)
Parkinson's drugs

Which are dopamine agonists? (3)
Anticholinergics? (2)
Dopamine precursors? (2)
MAO-B inhibitors?
COMT inhibitors?
Dopamine agonists: pramiperxole (Mirapex), ropinirole (Requip), bromocriptine (Parlodel)

Anticholinergics- benztropine (Cogentin), trihexyphenidyl (Artane)

Dopamine precursors-levodopa and levodopa + carbadopa

MAO-B inhibitors: selgiline (Eldepryl) and rasagiline (Azilect)

COMT inhibitors-tolcapone (Tasmar), entacapone (Comtan)
Why are BZDs safer than barbiturates?
BZDs have weaker effects on respiratory depression than barbiturates
Contraindications & Caution for Beta Blockers?
ABCDE
ABCDE:
Asthma
Block (heart block)
COPD
Diabetes mellitus
Electrolyte (hyperkalemia)
Calcium Channel Blocker usage
Think of C2 MASH:
or CHASM
Cerebral vasospasm & CHF
Angina
Migranes
Atrial flutter, fibrillation
Supraventricular tachycardia
Hypertension

"CHASM":
Cererbral vasospasm / CHF
Hypertension
Angina
Suprventricular tachyarrhythmia
Migranes
Warfarin (Coumadin): metabolism

Think SLOW
SLOW:
· Has a slow onset of action.
· But is quicK Vitamin K antagonist

Small lipid-soluble molecule
Liver: site of action
Oral route of administration.
Warfarin
Amiodarone: action, side effects

6Ps
6 P's:
Prolongs action potential duration
Photosensitivity
Pigmentation of skin
Peripheral neuropathy
Pulmonary alveolitis and fibrosis
Peripheral conversion of T4 to T3 is inhibited -> hypothyroidism
Nonselective beta-blockers

"Tim Pinches His Nasal Problem" (because he has a runny nose...):
"Tim Pinches His Nasal Problem" (because he has a runny nose...):
Timolol
Pindolol
Hismolol
Naldolol
Propranolol
Hyperthyroidism: signs and symptoms

THYROIDISM
THYROIDISM:
Tremor
Heart rate up
Yawning [fatigability]
Restlessness
Oligomenorrhea & amenorrhea
Intolerance to heat
Diarrhea
Irritability
Sweating
Musle wasting & weight loss
Alkalosis vs. acidosis: directions of pH and HCO3

ROME
ROME:
Respiratory= Opposite:
· pH is high, PCO2 is down (Alkalosis).
· pH is low, PCO2 is up (Acidosis).
Metabolic= Equal:
· pH is high, HCO3 is high (Alkalosis).
· pH is low, HCO3 is low (Acidosis).
Cardioselective betablockers

"Betablockers Acting Exclusively At Myocardium"
"Betablockers Acting Exclusively At Myocardium"
· Cardioselective betablockers are:
Betaxolol
Acebutelol
Esmolol
Atenolol
Metoprolol
Class IB Antiarrhythmics
"Medical Lab Technician"

Class IC Antiarrhythmics
FEP

Class III Antiarrhythmics
SIBA

Beta 1 Selective Blockers
A-BEAM
Class 1B Antiarrhythmics
Medical Lab Technician
M exilietine
L idocaine
T ocainide

Class IC Antiarrhythmics FEP
F lecainide
E ncainide
P ropafenone

Class III Antiarrhythmics SIBA
S otalol
I butilide
B retylium
A miodarone

Beta 1 Selective Blockers A-BEAM
A cebutalol
B etaxolol
E smolol
A tenolol
M etoprolol
Drugs Causing Agranulocytosis
The 3Cs
C lozapine

C olchicine

C arbamazepine
Short Acting Benzodiazepines
TOM thumb
TOM thumb

T riazolam

O xazepam
Beta receptor activity
Remember you have 1 heart & 2 lungs
1 heart, 2 lungs

Beta-1 receptors are primarily on the heart, and the airway is Beta-2 receptors
Anti-arrythmics: for AV nodes

"Do Block AV"
Do Block AV

D igoxin
B -blockers
A denosine
V erapamil