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Pharmacology > module 12-14 > Flashcards

module 12-14 Flashcards

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
Q

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

A

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.

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26
Q

what are the symptoms of alzheimers disease?

A

memory loss, problems with language, judgment, behaviour, intelligence
early symptoms: confusion, memory loss, problems conducting routine tasks

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27
Q

pathophysiology of AD

A

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

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28
Q

neurofibrillary tangles

A

form inside neurons when micotubule arrangement is disrupted

abnormal production of protein tau

29
Q

risk factors AD

A

genetics
2 copies of apolipoprotein E4 (ApoE4)
mutations in amyloid precursor protein gene
head injury

30
Q

General info about schizophrenia

A

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
Q

positive symptoms of schizophrenia

A 
positive symptoms exaggerate or distort normal neurological function
delusions
hallucinations
agitation
paranoia
combativeness
disorganized speech
disorganized thinking
32
Q

negative symptoms of schizophrenia

A 
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
Q

risk factors schizophrenia

A

genetics
drug abuse (crystal meth, PCP, LSD)
LBW
low IQ

34
Q

brain regions affected by schizophrenia

A 
basal ganglia
frontal lobe
limbic system
auditory system
occipitak lobe
hippocampus
35
Q

pathophysiology schizophrenia

A

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
Q

what is epilepsy?

A

produces brief disturbances in the normal electrical activity in the brain
sudden, brief seizures

37
Q

epileptic seizure

A

caused by primary CNS dysfunction
excess depolarization and hypersynchronization of neurons
*epilepsy means these recur

38
Q

focal/partial seizures

A

arise in one area of the brain

2 types: simple partial and complex partial

39
Q

simple partial seizure

A

type of focal/partial seizure
no loss of consciousness
symptoms contralateral to where it happened

40
Q

complex partial seizure

A

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
Q

generalized seizure

A 
have a bilateral, diffuse onset seeming to arise from all brain areas at once
5 types (absence, tonic/clonic, myoclonic, tonic, atonic)
42
Q

Absence seizures

A

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
Q

tonic/clonic seizures

A

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
Q

myoclonic seizures

A

type of generalized seizure
sudden, brief muscle contractions
no loss of consciousness

45
Q

tonic seizures

A

type of generalized seizure
rigidity
impaired consciousness

46
Q

atonic seizures

A

type of generalized seizure

sudden loss of muscle tone

47
Q

describe seizure threshold

A

everyone has one
affects how susceptible one is to having a seizure
balance between excitable and inhibitory forces in brain

48
Q

factors that affect seizure threshold

A 
Stroke
head injury
drug/alcohol withdrawal
infection
tumour
severe fever
visual stimuli
49
Q

what needs to be present for depression to be diagnosed

A

5 symptoms occurring for at least 2 weeks

50
Q

two types of depression

A

exogenous and endogenous

51
Q

pathological grief

A

type of exogenous depression
prolonged grieving with excessive guilt
psychotherapy best tx

52
Q

adjustment disorder

A

type of exogenous depression
prolonged depression following failure or rejection
hypersomnia, hyperphagia
psychotherapy best tx

53
Q

Major depression

A

type of endogenous depression
loss of interest/no response to + stimuli
insomnia, weight loss

54
Q

severe depression

A

type of endogenous depression

same as major depression + severe suicidal ideation and psychoses

55
Q

atypical depression

A

similar to major except with hypersomnia, hyperphagia

usually obese

56
Q

dysthymia

A

mood is regularly low but symptoms not as severe as major depression
psychotherapy best tx

57
Q

SAD

A

mild or moderate symptoms of depression r/t lack of sunlight in winter mths

58
Q

postpartum depression

A

moderate to severe depression after birth

usually within 3 mths and up to a year

59
Q

bipolar

A

alternating periods of elevated or irritable mood with periods of depression

60
Q

what is the monoamine hypothesis?

A

the biochemical basis for depression is altered monoamine release, receptor sensitivity, or post-synaptic function leading to the symptoms

61
Q

what is anxiety?

A

normal physiological response to stress
it’s a disorder when the symptoms create functional impairment
*anxiety and depression are closely linked

62
Q

General anxiety disorder

A

uncontrollable worrying

unrealistic or excessive worry abotu several activities within last 6 mths or longer

63
Q

panic disorder

A

sense of impending doom unrelated to stressors

experience panic attacks

64
Q

Agoraphobia

A

anxiety where pt feels judged or situational anxiety where escaping would be difficult or embarassing

65
Q

OCD

A

persistent obession and compulsions that interfere with daily life

66
Q

social anxiety disorder

A

anxiety in social situations

67
Q

PTSD

A

anxiety that occurs after experiencing trauma

symptoms: re-experiencing the event and severe insomnia

68
Q

simple phobia

A

symptoms r/t specific fear

Pharmacology (7 decks)

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