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Pharmacology > module 12-14 > Flashcards

module 12-14 Flashcards

(68 cards)

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1
Q

what is neuropharmacology? what is its intention?

A

study of how drugs affect the function of the central nervous system
attempt to treat SYMPTOMS of disease by treating biochemical imbalances with drugs

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2
Q

what is the resting membrane potential of cells?

A

-70 mV

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3
Q

what happens during depolarization?

A

Na+ enters cell through voltage-gated ion channels, making the cell more + charged

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4
Q

what happends during repolarization?

A

once Na+ channles close, K+ channels open which efflux K+ out of cell bringing the charge back to - (first overshooting then returning to the baseline of -70 mV)`

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5
Q

what are the monoamine neurotransmitters?

A

norepinephrine (depression & anxiety)
epinephrine - anxiety
dopamine - parkinson’s & schizophrenia
serotonin - depression & anxiety

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6
Q

what are the amino acid neurotransmitters?

A

excitatory - glutamate (alzheimers) & apartate (alzheimers)

inhibitory - GABA (anxiety) & glycine (anxiety)

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7
Q

what’s another neurotransmitter thats not a monoamine or amino acid?

A

acetylcholine - alzheimers & parkinsons

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8
Q

what are the basic mechanisms of CNS drug action?

A 
replacement
agonists/antagonists
inhibiting enzymatic breakdown 
blocking reuptake
nerve stimulation
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9
Q

what are some general facts about parkinsons?

A

-progressive loss of dopaminergic neurons in substantia nigra of brain

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10
Q

what are symptoms of parkinsons?

A

chronic movement disorder

  • temor
  • rigidity
  • bradykinesia
  • masklike face
  • postural instability
  • dementia (later in disease)
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11
Q

Pathophysiology of parkinsons

A

imbalance between acetylcholine & dopamine

  • dopamine release is decreased, resulting in not enough GABA inhibition
  • relative excess of acetylcholine, increases GABA release
  • excess GABA causes movement disorders in PD
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12
Q

what is the etiology of PD?

A

largely unknown but there are factors assoc with it

drugs, genetics, environ toxins, brain trauma, oxidative stress

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13
Q

what is the association between drugs & parkinsons?

A

A by-product of illicit street drug synthesis produces the compound MPTP. MPTP causes irreversible death of dopaminergic neurons.

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14
Q

what is the association between Genetics & parkinsons?

A

Mutation in 4 genes (alpha synuclein, parkin, UCHL1, and DJ-1) is known to predispose patients to PD

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15
Q

what is the association between environmental toxins & parkinsons?

A

Certain pesticides have been associated with PD.

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16
Q

what is the association between brain trauma & parkinsons?

A

Direct brain trauma from injury (i.e. boxing, accidents) is linked with increased risk for developing PD.

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17
Q

what is the association between oxidative stress & parkinsons?

A

Reactive oxygen species are known to cause degeneration of dopaminergic neurons. There is a link between diabetes induced oxidative damage and PD

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18
Q

what is the goal of drug treament of parkinsons?

A

The ideal treatment for PD would be to reverse the degeneration of dopaminergic neurons. Unfortunately, no such treatment exists.

  • we treat the symptoms of PD by trying to improve the balance between dopamine and acetylcholine.
  • Drug treatment of PD improves the dopamine acetylcholine balance by either:
    1. Increasing dopamine
    2. Decreasing acetylcholine
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19
Q

explain details of Levodopa

A

A.K.A. L-Dopa

  • it’s dopamine replacement
  • most effective treatment
  • effects decrease over time
  • crosses BBB by active transport protein
  • inactive on its own but is converted to dopamine in dopaminergic nerve terminals.
  • conversion mediated by decarboxylase enzymes in the brain.
  • cofactor pyridoxine (vitamin B6) speeds up this reaction
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20
Q

why can’t dopamine just be given as a drug for PD?

A
  • doesn’t cross BBB

- very short half-life in bloodq

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21
Q

what are the adverse effects of L-Dopa?

A
  • nausea & vomiting
  • dyskinesias - abnormal involuntary movements
  • cardiac dysrhythmias - conversion of L-DOPA to dopamine in the periphery can result in activation of cardiac beta 1 receptors
  • orthostatic hypotension
  • Psychosis
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22
Q

what percentage of L-dopa goes to brain? how is this resolved?

A

1%

  • resolved by giving carbidopa, a decarboxylase inhibitor that inhibits the peripheral metabolism of L-DOPA.
  • this ups it to 10% reaching brain
  • using carbidopa allows lower does to be given & decreases incidence of cardiac dysrhythmias & N/V
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23
Q

what are two types of “loss of effect” that may be experiences by pt.s taking L-Dopa?

A

wearing off - gradual loss of effect of the drug

on-off - abrupt loss of effect

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24
Q

how is the wearing off loss of effect combatted with L-dopa?

A

Usually occurs at the end of the dosing interval and indicates that drug levels might be low.
can be minimized by:
-shortening dosing interval
-give drug inhibits metabolism of the drug (eg. COMT inhibitor)
-add dopamine agonist to the therapy

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25
how is the on-off loss of effect combatted with L-dopa?
Can occur even when drug levels are high. can be minimized by: -Dividing the medication into 3-6 doses per day. -Using a controlled release formulation. -Moving protein-containing meals to the evening.
26
what are the symptoms of alzheimers disease?
memory loss, problems with language, judgment, behaviour, intelligence early symptoms: confusion, memory loss, problems conducting routine tasks
27
pathophysiology of AD
degeneration of cholinergic neurons in the hippocampus early in the disease followed by degeneration of neurons in the cerebral cortex *significant decrease in cholinergic function compared to healthy people
28
neurofibrillary tangles
form inside neurons when micotubule arrangement is disrupted | abnormal production of protein tau
29
risk factors AD
genetics 2 copies of apolipoprotein E4 (ApoE4) mutations in amyloid precursor protein gene head injury
30
General info about schizophrenia
hard to... tell diff between real and unreal experiences think logically have normal emotional response behave normally in social situations *usually begins in adolescence or early adulthood
31
positive symptoms of schizophrenia
``` positive symptoms exaggerate or distort normal neurological function delusions hallucinations agitation paranoia combativeness disorganized speech disorganized thinking ```
32
negative symptoms of schizophrenia
``` there is a loss of normal neurological function social withdrawal poverty of speech poor self-care poor insight poor judgment emotional withdrawal blunted affect lack of motivation ```
33
risk factors schizophrenia
genetics drug abuse (crystal meth, PCP, LSD) LBW low IQ
34
brain regions affected by schizophrenia
``` basal ganglia frontal lobe limbic system auditory system occipitak lobe hippocampus ```
35
pathophysiology schizophrenia
increased dopaminergic nerve transmission ie. excess dopamine although mainly dopamine, also serotonin (5-HT) and glutamate involved schizophrenics have less 5-HT2A and more 5-HT1A receptors int he frontal cortex glutamate binds to and activates NMDA receptor - PCP is an antagonist of NMDA receptor -schizophrenics have decreased number of NMDA receptors in some regions of the brain
36
what is epilepsy?
produces brief disturbances in the normal electrical activity in the brain sudden, brief seizures
37
epileptic seizure
caused by primary CNS dysfunction excess depolarization and hypersynchronization of neurons *epilepsy means these recur
38
focal/partial seizures
arise in one area of the brain | 2 types: simple partial and complex partial
39
simple partial seizure
type of focal/partial seizure no loss of consciousness symptoms contralateral to where it happened
40
complex partial seizure
type of focal/partial seizure involves loss of consciousness may appear awake but not aware of surroundings no memory of events the symptoms are seen contralateral to where it is in the brain
41
generalized seizure
``` have a bilateral, diffuse onset seeming to arise from all brain areas at once 5 types (absence, tonic/clonic, myoclonic, tonic, atonic) ```
42
Absence seizures
type of generalized seizure loss of consciousness, behavioural arrest, staring usually brief but may occurs in clusters and multiple x/day more common in childhood
43
tonic/clonic seizures
type of generalized seizure abrupt loss of consciousness tonic period (rigid) clonic period (invol muscle contractions) incontinent and tongue biting after the seizure may be drowsy, confused and freq complain of headaches
44
myoclonic seizures
type of generalized seizure sudden, brief muscle contractions no loss of consciousness
45
tonic seizures
type of generalized seizure rigidity impaired consciousness
46
atonic seizures
type of generalized seizure | sudden loss of muscle tone
47
describe seizure threshold
everyone has one affects how susceptible one is to having a seizure balance between excitable and inhibitory forces in brain
48
factors that affect seizure threshold
``` Stroke head injury drug/alcohol withdrawal infection tumour severe fever visual stimuli ```
49
what needs to be present for depression to be diagnosed
5 symptoms occurring for at least 2 weeks
50
two types of depression
exogenous and endogenous
51
pathological grief
type of exogenous depression prolonged grieving with excessive guilt psychotherapy best tx
52
adjustment disorder
type of exogenous depression prolonged depression following failure or rejection hypersomnia, hyperphagia psychotherapy best tx
53
Major depression
type of endogenous depression loss of interest/no response to + stimuli insomnia, weight loss
54
severe depression
type of endogenous depression | same as major depression + severe suicidal ideation and psychoses
55
atypical depression
similar to major except with hypersomnia, hyperphagia | usually obese
56
dysthymia
mood is regularly low but symptoms not as severe as major depression psychotherapy best tx
57
SAD
mild or moderate symptoms of depression r/t lack of sunlight in winter mths
58
postpartum depression
moderate to severe depression after birth | usually within 3 mths and up to a year
59
bipolar
alternating periods of elevated or irritable mood with periods of depression
60
what is the monoamine hypothesis?
the biochemical basis for depression is altered monoamine release, receptor sensitivity, or post-synaptic function leading to the symptoms
61
what is anxiety?
normal physiological response to stress it's a disorder when the symptoms create functional impairment *anxiety and depression are closely linked
62
General anxiety disorder
uncontrollable worrying | unrealistic or excessive worry abotu several activities within last 6 mths or longer
63
panic disorder
sense of impending doom unrelated to stressors | experience panic attacks
64
Agoraphobia
anxiety where pt feels judged or situational anxiety where escaping would be difficult or embarassing
65
OCD
persistent obession and compulsions that interfere with daily life
66
social anxiety disorder
anxiety in social situations
67
PTSD
anxiety that occurs after experiencing trauma | symptoms: re-experiencing the event and severe insomnia
68
simple phobia
symptoms r/t specific fear

Pharmacology (7 decks)

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