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Pharmacology > Neurology Part 2 > Flashcards

Neurology Part 2 Flashcards

1
Q

Norepinephrine.

A
  • An excitatory neurotransmitter (a.k.a Adrenaline)
  • Increase Heart Rate
  • In High amounts can cause; paranoia, anxiety, stress
  • In Low amounts can cause; Depression and lethargy
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2
Q

Dopamine.

A
  • An excitatory neurotransmitter
  • Pleasure centre!
  • ‘Reward centre of the brain’
  • In High amounts can; anxiety and psychosis
  • In Low amounts can; depression and lethargy
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3
Q

Serotonin.

A
  • Inhibitory neurotransmitter
  • Stabilizes our mood, feelings of well-being, and happiness
  • ‘Happy hormone’
  • High amounts can cause; Mood Swings
  • Low amounts can cause; Anxiety and Insomnia
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4
Q

GABA (Gamma-aminobutyric acid).

A
  • Inhibitory neurotransmitter
  • Increases Cl- influx which promotes decreased cellular activity
  • Reduces neuronal excitability by inhibiting nerve transmission
  • High amounts can cause; Lethargy, Confusion, Sedation and Amnesia
  • Low amounts can cause; Anxiety and Insomnia
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5
Q

Glutamate.

A
  • Excitatory neurotransmitter
  • Responsible for sending signals between nerve cells
  • Plays an important role in learning and memory
  • High amounts can cause; Anxiety
  • Low amounts can cause; Low focus, Retention
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6
Q

Substance P.

A
  • Excitatory neurotransmitter

- Pain sensation

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7
Q

Neurotransmission.

A

The transmission of nerve impulses between neurons

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8
Q

Process of Neurotransmission.

A

When a stimulus reaches the threshold stimulus it causes the axon membrane to depolarize, the rapid change in polarity across the membrane generates an action potential.

  1. Action Potential arrives at the axon terminal
  2. Voltage-gated Ca+ channels open
  3. Ca 2+ enters the presynaptic neuron
  4. Ca 2+ signals to neurotransmitter vesicles
  5. Vesicles move to the membrane and dock
  6. Neurotransmitters released via exocytosis
  7. Neurotransmitters bind to receptors
  8. Signal initiated in the postsynaptic cell
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9
Q

What occurs in the synaptic cleft during neurotransmission?

A

The neurotransmitters bind to their respective receptors after binding either an excitatory or inhibitory response will be delivered.

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10
Q

What occurs to the excess neurotransmitters?

A

The excess needs to be removed from within the cleft wither by enzymatic degradation or reuptake.

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11
Q

Enzymatic Degradation.

A

Enzymes such as; COMT, MAO and cholinesterase are released to degrade to excess waste.

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12
Q

Re-Uptake.

A

Neurotransmitter molecules that have been released at a synapse are reabsorbed by the presynaptic neuron that released them. Reuptake is performed by transporter proteins in the presynaptic membrane.

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13
Q

Which neurotransmitters are expelled through re-uptake?

A
  • Dopamine
  • Serotonin
  • Norepinephrine
  • Epinephrine
  • Glutamate
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14
Q

Preganglionic Neurons.

A

Are a set of nerve fibres of the autonomic nervous system that connect the central nervous system to the ganglia.

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15
Q

Postganglionic Neurons.

A

Are a set of nerve fibres that are present in the autonomic nervous system which connects the ganglion to the effector organ.

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16
Q

Physical Dependence.

A

Physical dependence is a physical condition caused by chronic use of a tolerance-forming drug, in which abrupt or gradual drug withdrawal causes unpleasant physical symptoms.
*The body adapts to the presence of the exogenous substance and creates a tolerance *

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17
Q

Weening Protocol.

A

The protocol is initiated when a patient is ending treatment. Meaning that the substance is slowly decreased until the regular function is restored.

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18
Q

Psychological Dependence,

A

This occurs when the patient WANTS the drug and it is not related to the treatment of a diagnosis.

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19
Q

What are the Signs of Drug Abuse and Psychological Dependence

A
  • Spending a great deal of time acquiring, using and recovering from the use of the substance
  • Disruption of important activities because of substance use
  • Using more than intended
  • Compulsive use despite harm
  • Tolerance – requiring more drugs over time
  • Withdrawal symptoms if without drug
  • Unsuccessful efforts to cut down
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20
Q

Define Headache.

A

Pain or discomfort in the head is caused b various factors. Described as; throbbing, pounding, painful etc.
headache is ONLY a symptom

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21
Q

How to treat a headache?

A

DO NOT treat without investigating, DO NOT treat of unsure. There are many underlying factors to a headache and they need to examine before administering treatment.

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22
Q

Migraine.

A

Chronic headache disorder. They last for more than 15 days per month for 3 months.

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23
Q

Pathology Sequealea for Migraine.

A

Trigeminal nerve irritation, inflammation within meningeal vasculature. (the headache is intense and within the meninges).

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24
Q

Two main Categorizations for Migraines.

A
  1. Without Aura- most common

2. With Aura- more pronounced visual disturbances precede the headache (symptoms occur before the migraine sets in)

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25
Q

Signs and Symptoms of Migraine.

A
  • Prodrome fatigue
  • Irritability (pre-migraine)
  • Nausea and vomiting
  • Intense headache
  • Hypersensitivity to stimuli
  • Sensory disturbances
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26
Q

Treatment of Migraines.

A
  1. Analgesiscs: NSAIDs, Tylenol
  2. Triptan (Serotonin agonists which induce calming sensations)
  3. Botox (Decreases the release of acetylcholine and acts as an anti-inflammatory)
  4. Caffeine
  5. Antiemetics
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27
Q

NSAIDs.

A

Non-steroidal anti-inflammatory drugs (NSAIDs) decrease prostaglandin response (which contributes to inflammation), they also decrease platelets aggregation.

  • Given as an anti-inflammatory
  • Given as an antipyretic
  • Given as an analgesic
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28
Q

Common Side Effects of NSAID use.

A
  • Nausea
  • Easy Bruising
  • Vomiting
  • Diarrhea
  • Tarry stools
  • Coffee ground emesis
  • Dizziness
  • Liver Failure
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29
Q

Which patients should avoid NSAID usage?

A

-Patients with peptic ulcer disease (increases risk of GI bleed)
-Patients with asthma or pulmonary disease (increased risk of bronchospasm)
-Patients with pre-existing clot history such as; DVT, MI, CVA(increases risk for thrombosis)
-

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30
Q

Mecanisme of Action: Tylenol

A

Acetaminophen has analgesic and antipyretic properties. However, acetaminophen lacks peripheral anti-inflammatory properties. Instead, it inhibits the COX pathway in the central nervous system but not peripheral tissues.

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31
Q

Psychiatric Disorders.

A

disorders characterized by a change in thoughts, moods or behaviour which interferes with the person’s life.

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32
Q

Hallucinations.

A

An experience involving the apparent perception of something not present.

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33
Q

Two Categories of Hallucinations.

A
  1. Visual hallucinations: involve seeing things that aren’t there. The hallucinations may be of objects, visual patterns, people, or lights. For example, you might see a person who’s not in the room or flashing lights that no one else can see.
  2. Neuronal Dysfunction: Certain hallucinations are caused by neuronal overstimulation or neuronal damage!
    * we classify hallucinations based on the sensory classification: visual, auditory, tactile or olfactory *
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34
Q

Delusions.

A

A person cannot tell what is real from what is imagined. The main feature of this disorder is the presence of delusions, which are unshakable beliefs in something untrue.

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35
Q

Etiology of Delusions.

A

Delusions can be triggered by sleep disturbance and extreme stress, but they can also occur in physical conditions, including brain injury or tumour, drug addiction and alcoholism.

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36
Q

Psychosis.

A

Hallucinations, delusions ack of awareness and judgement, mood alterations

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37
Q

Etiology of Psychosis.

A
  • Mental health illnesses
  • Drug side effects/toxicity (OD)
  • Electrolyte imbalances
  • Sepsis (in elderly): due to immune system decrease
38
Q

Schizophrenia.

A

A long-term mental disorder of a type involving a breakdown in the relation between thought, emotion, and behaviour, leading to faulty perception, inappropriate actions and feelings, withdrawal from reality and personal relationships into fantasy and delusion, and a sense of mental fragmentation.

39
Q

3 Types of Schizophrenic Behaviour.

A
  1. Disorganized: incomprehensible speech: invented words, disconnected words & thought processes, disconnected/disorganized words
  2. Psychotic (positive symptoms): hallucinations, delusions (paranoias; disorganized thought processes), agitation
  3. Negative symptoms: withdrawal & apathy, lack of motivation/happiness
    Most difficult to treat; worse prognosis
40
Q

Etiology of Schizophrenia.

A
  • Structural alterations in brain present on MRI
  • Genetic Predisposition
  • Dopamine Excess
41
Q

Diagnose Schizophrenia.

A

Does the patient present…

  • Difficulty communicating thoughts verbally.
  • Difficulty in discerning and maintaining the usual communication pattern.
  • Disturbances in cognitive associations (e.g., perseveration, derailment, poverty of speech, tangentiality, illogicality, neologism, and thought blocking).
  • Inappropriate verbalization.
42
Q

Treatment for Psychiatric Disorders.

A

Antipsychotic (neuroleptics).

43
Q

Mecanisme of Action: Antipsychotics

A

These drugs block selective D2 dopamine receptors in the limbic system. It will also block non-selective receptors. Such as; serotonin receptors (5HT) and acetylcholine receptors (Ach).
Inhibiting the excitatory neurotransmission will allow an overall calming effect on the mood, behaviour and emotions.

44
Q

Side Effects of Antipsychotics.

A

Extrapyramidal side effects (drug-induced movement disorders)

  • Tardive dyskinesia (tongue mov’t)
  • Parkinsonism (rigidity), tremors
  • Restlessness, dystonias (muscle spasm)
45
Q

Neuroleptic Malignant Syndrome toxic reaction.

A

ALERT: hyperthermia, unstable BP, diaphoresis, incontinence. When this occurs STOP medication administration IMMEDIATELY.

46
Q

Typical Antipsychotic Drugs.

A

Mainly used in the treatment of psychotic conditions. They sit ontop of the D2 receptor sites and antagonize the dopamine molecules. By inhibiting dopamine from binding to the receptor sites there is a decrease in its effects.

  • Despite their effects, these drugs carry a lot of side effects and cause extrapyramidal motor control debilities. It may also induce body stiffness and chills.
  • It’s also important to watch for neuroleptic malignant syndrome with these drugs
47
Q

Drug Class for Typical Anti-psycotic Drugs.

A

Phenothiazines:
- (Chlorpromazine)
Non-Phenothiazines (chemically different than phenothiazines):
-Haloperidol (Haldol)

48
Q

Atypical Drugs.

A

Atypical antipsychotics, also known as new generation antipsychotics, are known to have fewer side effects. They also have less sedation effects than typical drugs.

49
Q

Depression.

A

a common mental disorder that presents with depressed mood, loss of interest or pleasure, decreased energy, feelings of guilt or low self-worth, disturbed sleep or appetite, and poor concentration.

50
Q

Signs and Symptoms of Depression.

A
  • Loss of interest in activities
  • Inability to experience pleasure
  • Decreased concentration
  • Sleep alterations
  • Hallucinations and Delusions
  • Appetite Alterations
  • Suicidal Ideation
51
Q

Etiology of Depression.

A

Most commonly caused by the lack of serotonin and norepinephrine in the brain.

52
Q

Treatment for Depression.

A

Antidepressants.

53
Q

Types of Antidepressants.

A
  1. Selective Serotonin Re-Uptake Inhibitors
  2. Serotonin and Norepinephrine reuptake inhibitors
  3. Tricyclic Antidepressants
  4. MAO inhibitors
54
Q

Selective Serotonin Re-Uptake Inhibitors.

A

1st line of treatment!
Increase Serotonin levels
- Fluvoxetine (Prozac), Sertraline (Zoloft), Paroxetine (Paxil)

55
Q

Serotonin & Norepinephrine reuptake (Antidepressants)

A

SNRI’s - increase Serotonin & Norepi

-Mirtazapine (Remeron), Bupropion (Wellbutrin)

56
Q

Tricyclic Antidepressants.

A

Serotonin, norepinephrine, dopamine reuptake inhibitors

-Imipramine (Impril)

57
Q

MAO inhibitors.

A

Treat depression by preventing the breakdown of the brain chemicals serotonin, dopamine, and norepinephrine. Therefore causing an overall increase in levels.

58
Q

Cognitive behavioral therapy.

A

This type of counselling/ psychotherapy with a mental health counsellor (psychotherapist or therapist).

59
Q

Side Effects of Antidepressant.

A 
Serotonin Syndrome: a condition that occurs when there's too much serotonin within the body
Causes:
- Changes in LOC 
- Fever
- Nausea
- Hypothermia or signs of Shock
- Muscle rigidity
60
Q

Important Considerations for Antidepressant

Medications.

A

Drug-Drug Interactions with CNS medications!

61
Q

Mood Stabilizers.

A

A type of adjunct treatment, given PRN (as needed). This kind of therapy is usually given to reduce the risk of suicide and erratic behaviours.

62
Q

Lithium (Lithonate) Mecanisme of Action.

A

increases Serotonin and other neurotransmitters, as well as decreases Na+ cellular influx. It decreases impulsivity and decreases mood swings.

63
Q

Important Considerations of Lithium.

A
  • Narrow TI: serum monitoring
  • Toxicity
  • High Vd
  • Slow onset of action (1- 3 weeks)
  • Drug-drug interactions!!!
  • Compliance
64
Q

Dementia.

A

A deficit in short & long-term memory; is associated with deficits in higher cortical functions such as judgement, or a personality change.

65
Q

Diagnosis for Dementia.

A

The microscopic changes that occur are not testable and cannot be diagnosed for certain. Therefore, ruling other factors is the first step towards making a decision.

Rule Out: drug side effects, depression, metabolic disease (e.g. hypothyroidism), declining sensory perception (e.g. vision, hearing), brain lesion (e.g. tumour), infection, anemia.

66
Q

Signs and Symptoms of Dementia.

A
  • Memory loss, is usually noticed by someone else.
  • Difficulty communicating or finding words.
  • Difficulty with visual and spatial abilities, such as getting lost while driving.
  • Difficulty reasoning or problem-solving.
  • Difficulty handling complex tasks.
  • Difficulty with planning and organizing
67
Q

Alzheimer’s Disease.

A

A brain disorder that slowly destroys memory and thinking skills and, eventually, the ability to carry out the simplest tasks.
Progressive loss of neurons and synapses. This is a progressive/intense form of dementia

68
Q

Signs and Symtpoms of Alzheimer’s Disease.

A

Mild forgetfulness
Behavioural changes
Inability to complete ADLs

69
Q

Etiology of Alzheimer’s Disease.

A

Caused by the accumulation of beta-amyloid deposits. It is formed from the breakdown of a larger protein, called amyloid precursor protein. In the Alzheimer’s brain, abnormal levels of this naturally occurring protein clump together to form plaques that collect between neurons disrupt cell function and cause cell necrosis. It will also decrease the amount of acetylcholine.

70
Q

Treatment of Alzheimer’s Disease.

A

Cholinesterase Inhibitors! These medications decrease the breakdown of acetylcholine causing an increase in levels. Normally acetylcholine is broken down by acetylcholinesterase, but this molecule is inhibited therefore inhibiting the breakdown of the neurotransmitter.

71
Q

Parkinson’s Disease.

A

Parkinson’s disease is a brain disorder that leads to shaking, stiffness, and difficulty with walking, balance, and coordination. It is caused due to inadequate dopamine transmission causing an inadequate CNS function.
- A neurodegenerative disorder

72
Q

Etiology of Parkinson’s Disease

A

Destruction of Dopamine neurons => reduced Dopamine transmission in Basal Ganglia = inability to filter out extra movements & focus purposeful movement.

73
Q

Treatement for Parkinson’s Disease.

A

There is no cure however, increasing dopamine levels will manage side effects and symptoms caused by the neuronal damage.

74
Q

Catecholamines.

A

Catecholamines help the body respond to stress and prepare the body for “fight-or-flight” reactions. The main catecholamines are epinephrine (adrenaline), norepinephrine (noradrenaline), and dopamine.
- End Result: Stimulates the SNS

75
Q

Cholinomimetics.

A

Inhibiting acetylcholinesterase, therefore increasing the endogenous acetylcholine concentration in synaptic clefts. The excess acetylcholine, in turn, stimulates cholinergic receptors to evoke increased responses.
-End Results: Stimulates the PNS

76
Q

Anticholinergics.

A

Block the action of acetylcholine!

-End Result: Decrease PNS stimulation, Increase SNS

77
Q

Adrenergic Antagonists.

A

Compounds that inhibit the action of adrenaline (epinephrine), noradrenaline (norepinephrine), and other catecholamines that control autonomic outflow and some functions of the central nervous system at the adrenergic receptors or inhibit their release.

78
Q

Nicotine Agonists.

A

A nicotinic agonist is a drug that mimics the action of acetylcholine (ACh) They activate acetylcholine at nicotinic receptors.

79
Q

Side Effects of Nicotine Agonists.

A
  • Increased Alertness
  • Increased BP
  • Peripheral Vasoconstriction
  • Decreased GI activity
80
Q

Amphetamines.

A

Stimulant drugs speed up the central nervous system. They stimulate the RAS and increase focus.

81
Q

Drug Class of Amphetamines.

A

Methylphenidate.

82
Q

Side Effects of Amphetamines.

A
  • Appetite Decrease
  • Weight Loss
  • Tachycardia
  • Irregular Pulse
  • Increased Temperature
83
Q

Scopolamine.

A

Used to treat nausea and vomiting. Anticholinergic in the CNS blocks acetylcholine. Causes CNS depressant effects.

84
Q

Mecanism of Action scopolamine.

A

Scopolamine acts as a competitive inhibitor at postganglionic muscarinic receptor sites of the parasympathetic nervous system, and on smooth muscles that respond to acetylcholine but inhibit cholinergic innervation.
Scopolamine prevents communication between the nerves of the vestibule and the vomiting center in the brain by blocking the action of acetylcholine.

85
Q

Side Effects of Scopolamine.

A
  • Dilated Pupils
  • Blurred Vision
  • Increased Sensitivity to light
  • Confusion
  • Amnesia
  • Sedation
  • Unconsciousness
86
Q

Curare.

A

Curare is poison. An anticholinergic and acts as a neuromuscular blocking agent by binding to the acetylcholine receptor (AChR) at the neuromuscular junction and preventing nerve impulses from activating skeletal muscles.

87
Q

Important Considerations for Curare.

A

In toxic amounts, this drug can cause respiratory muscle paralysis.

88
Q

Botulism.

A

A rare illness caused by a toxin that attacks the body’s nerves and causes difficulty breathing, muscle paralysis, and even death. This toxin is made by Clostridium botulinum.

89
Q

Clostridium Botulinum Infection.

A

A gram+, anaerobic bacteria.
The neurotoxin inhibits acetylcholine at the somatic neuromuscular junctions! Causing an overall decrease in CNS function.

90
Q

Treatment for Botulism.

A

A drug called an antitoxin, which prevents the toxin from causing any more harm. Antitoxin does not heal the damage the toxin has already done. Nitrites are also used as they inhibit the growth of the pathogen!

Pharmacology (27 decks)

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