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Neuropsychopharmacology > Week 1 - Drugs and physiology > Flashcards

Week 1 - Drugs and physiology Flashcards

1
Q

What is a ‘drug’?

A
  1. A substance used in the diagnosis, treatment , or prevention of a disease or as a component of a medication 2. such a substance as recognised or defined by Food and Drug Administration (TGA in Australia) 3. A chemical substance, such as a narcotic or hallucinogen, that effects the central nervous system, causing changes in behaviour and often addiction (american heritage dictionary)
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2
Q

In MIMS (Drugs guide), what is the ‘use’?

A

Use (main effect): what disorder is it used to treat

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3
Q

In MIMS (Drugs guide), what is the ‘Contraindications’?

A

Contraindications: Drugs or disorders that this drug should not be prescribed with/for

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4
Q

In MIMS (Drugs guide), what is the ‘Precautions’?

A

Take care when using with other drugs (e.g., with alcohol)

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5
Q

In MIMS (Drugs guide), what is the ‘
Adverse reactions
‘?

A

Unwanted effects

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6
Q 
In MIMS (Drugs guide), what is the '
side effects'?
A

Unwanted effects for one treatment yet may be wanted for another (e.g., sedative effect of antihistamines, slow GIT gastro-intestinal-track motility with Opiates)

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7
Q 
In MIMS (Drugs guide), what is the '
Pack'?
A

How the drug is packaged

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8
Q 
In MIMS (Drugs guide), what is the '
dose'?
A

what dose to prescribe depending no what it is used to treat

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9
Q

What is the LD50?

A

Dose at which 50% of ‘population’ found to be Lethal, keep below this does

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10
Q

What is the ED50?

A

Dose at which 50% of the ‘population’ found the drug to be Effective - therapeutic (intended) dosing)

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11
Q

Each drug has a ‘therapeutic index’, what does this mean? (what does a low therapeutic index and a high therapeutic index mean?)

A

A margin of safety, it is the difference between LD50 an ED50 (Stay within here)

Low therapeutic index - little marin for dosing, easier to overdose e.g., heroin (injectable results in lower therapeutic index)
High therapeutic index - Large margin for dosing, difficult to harm patient e.g., alcohol (orally results in higher therapeutic index)

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12
Q

What is drug potency?

A

Ability for drug to take effect (how much is needed?)

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13
Q

What is drug toxicity?

A

Potential to do irreversible harm to body functions - poisons or excessive amount of any substance

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14
Q

What dose is it generally considered safe to stay around?

A

ED50 (but depends on severity of the condition being treated and dosage curve)

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15
Q

What area of the brain is implicated in memory?

A

Hippocampus

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16
Q

What area of the brain is broadly implicated in vision?

A

Occipital Lobe

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17
Q

What area of the brain is broadly implicated in pain?

A

Thalamus and spinal cord

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18
Q

What area of the brain is broadly implicated in judgement?

A

Prefrontal cortex and Cingulate Gyrus

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19
Q

What area of the brain is broadly implicated in movement?

A

Motor cortex

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20
Q

What area of the brain is broadly implicated in sensation?

A

Parietal lobe - Somatosensory

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21
Q

What area of the brain is broadly implicated in Reward?

A

The basal ganglia circuit, specifically the mesolimbic pathway (ventral tegmental area and nucleus accumbens), is the center off the reward system yet there are more circuits and brain structures such as the anterior cingulate cortex, and midbrain dopamine pathways. The major neurochemical pathway of the reward system in the brain is the mesocorticolimbic pathway, which includes both the mesolimbic and mesocortical pathways. The ventral tegmental area (VTA) is a source of many dopamine pathways in the brain, which are neurons which use theneurotransmitter dopamine to transmit a signal to other structures. Dopamine acts on D1-like receptors or D2-like receptors to either stimulate (D1-like) or inhibit (D2-like) the production ofcAMP.[11]

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22
Q

What two components make up the peripheral nervous system?

A

Somatic (Sensorimotor) [touch, sensation]
Autonomic (Parasympathetic [digestion, growth, immune responses], Sympathetic [fight or flight, fright, fornicate])

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23
Q

In the autonomic component of the peripheral nervous system, what does the parasympathetic and sympathetic nervous systems do respectively?

A

Parasympathetic [digestion, growth, immune responses],

Sympathetic [fight or flight, fright, fornicate]

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24
Q

What brain parts for the main brain hormone system?

A
  • Hypothalamus leading to the…
  • Pituritary (and adrenals [atop of kidneys] - cortisone, adrenalen)
  • Pineal Gland (sleep and circadian rhythms)
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25
Q

Drugs targeting the PNS are generally _____ than those targeting hormones, which have a greater _____ but are _____.

A

Faster, range of effect, slower

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26
Q

What is homostasis?

A

The body naturally wants to promote homestasis (balance) - safe ranges of:

  • Oxygen
  • Rid waste products (Feaces, Urine, Co2)
  • Have good Nutrients
  • pH range 7.2
  • Temperature 37.2 C
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27
Q

What internal systems support oxygen homeostasis?

A
  • Respiratory (air inhale)
  • Cardio-vascular system (getting oxygen to cells via blood)
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28
Q

What internal systems held rid waste products?

A
  • Renal (liquids)
  • GIT (Faeces) including Liver
  • Respiratory (expel CO2)
  • Cardiovascular system (blood, drained to lymphatic system and waste is transported out)
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29
Q

What internal systems help keep nutrient homeostasis?

A
  • GIT
  • Cardiovascular (transport)
  • Renal (kidney, helps with electrolyte balance charged ions)
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30
Q

What internal systems help keep pH range around 7.2 (homeostasis)?

(level of acidity, changes in this can make neutrons fire erratically or stop - a measure of free charged ions, electrolytes)

A
  • Renal
  • Respiratory (reduces CO2)
  • Cardiovascular system (buffering [push in either direction] capacity other chemicals in the blood that helps to keep pH balanced)
  • GIT (brings in the chemicals that help the blood)
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31
Q

What internal systems help keep temperature around 37.2 C (homeostasis)?

A
  • Skin
  • Cardiovascular (blood moves closer to the skin), Respiratory (breathing out hot air)
  • Gastrointestinal (changing the temperature of the food we eat)
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32
Q

The effect of a drug is modulated by what four things? (pharmacokinetics - what happens to the drug once it has entered the body [fate])

A
  • Absorption (bioavailability - routes of administration)
  • Distribution (blood flow, tissue permeability)
  • Metabolism (biotransformation) - liver, enxymes in tissue
  • Excretion - Kidneys, lungs
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33
Q

What is bioavailability?

A

Fraction amount of drug which reaches its site of action (or biological fluid).

Once at site of action, drug may work for mins or hours (Depending on how well it binds and how much is given)

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34
Q

What are the 7 main routes of drug aministration (4 x parenteral [i.e., injectable], 3 x other)

A

INJECTABLES:

  • Oral (p.o) - first pass metabolism (must ass through the liver) going through the liver results in half-loss of drug, so only need half when injected.
    • Sublingual
    • Rectal (suppository)
  • Pulmonary absorption (inhalants)
  • Topical applications - transdermal, eye - via mucous membranes
  • Subcutaneous (S.c) ( parenteral [past the mouth] injectable) = Injection into the subcutis skin layer [below the dermis and epidermis i.e., below the cutis]
  • Intraperitoneal (i.p.) ( parenteral [past the mouth] injectable) - injection of a substance into the peritoneum (body cavity) [Large body fluid replacement, chemotheraphy and vetenarian treatments]
  • Intramuscular (i.m.) ( parenteral [past the mouth] injectable) - the injection of a substance directly into a muscle, limited to 2-5ml of fluid [often deltoid muscle in the arm, vastus lateralis muscle of the leg; and the ventrogluteal and dorsogluteal muscle of the buttocks]
  • Intravenous (i.v.) ( parenteral [past the mouth] injectable) - the infusion of liquid substances directly into a vein. (Intravenous therapy may be used to correct electrolyte imbalances, to deliver medications, for blood transfusion or as fluid replacement to correct, for example, dehydration. Intravenous therapy can also be used forchemotherapy. Compared with other routes of administration, the intravenous route is the fastest way to deliver fluids and medications throughout the body.)
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35
Q

What affects the pharmacokinetic of drugs?

A
  • Absorption (bioavailability - routes of administration)
  • Distribution (blood flow, tissue permeability)
  • Metabolism (biotransformation) - liver, enxymes in tissue
  • Excretion - Kidneys, lungs
  • Half-life = time to remove half of active drug amount, affected by all of the above
  • Pharmacokinetics are determine by chemical properties of the drug (e.g., liphophilicity [soluble in lipids-fat i.e., all cell membranes]
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36
Q

What are the disadvantages and advantages of oral administration of drugs?

A

Advantage

  • Most convenient, economical *safe*

Disadvantage

  • Variable absoption pattern - depends on food in stomach etc - e.g., 20-30minutes to work
  • Needs patient co-operation
  • No use for drugs that are poorly soluble, slowly absorbed, unstable or extensively metabolised by the liver
  • Emesis due to irritation of gastric mucosa
  • Drug metabolised by gut enzymes or high acidity in gut *enteric coating*
  • Metabolised by liver - must give higher dosage (half lost to liver)
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37
Q

What is sublingual drug administration? and what is it good for?

A

An enteral method of drug administration - Under the tongue dissolving -
dissolve quickly through mucosa (e.g., nitroglycerin) to vena cava (no first past) [straight into blood system]

Good for high lipophilic drugs.

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38
Q

What is rectal drug administration? and what are its advantages and disadvantages?

A

An enteral method of drug administration -
Drugs put in the rectal cavity.

Advantage:

  • Very good when patient can not take drugs orally (vommiting, unconscious).
  • 50% will bypass the liver

Disadvantage

  • 50% still goes through liver
  • Irregular absorption and many drugs irritate rectal mucosa. (therefore highly variable)
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39
Q

What does it mean when a drug has a low therapeutic index?

A

Small difference between LD50 an ED50
little margin for dosing, easier to overdose e.g., heroin (injectable results in lower therapeutic index)

40
Q

What does it mean when a drug has a high therapeutic index?

A

large difference between LD50 an ED50

Large margin for dosing, difficult to harm patient e.g., alcohol (orally results in higher therapeutic index)

41
Q

What is an enteric coating?

A

An enteric coating is a polymer barrier applied on oral medication. This helps by protecting drugs from the pH (i.e. acidity) of the stomach.

42
Q

An _________ is a polymer barrier applied on oral medication. This helps by protecting drugs from the pH (i.e. acidity) of the stomach.

A

Enteric Coating

43
Q

What is the technical name for oral/sublingal/rectal administration of drugs? (involving the esophagus, stomach, and small and large intestines (i.e., the gastrointestinal tract).

A

Enteral Administration

44
Q

What are the advantaged and disadvantaged of Intravenous (parenteral injection)?

A

Advantages

  • Limitations of absorption reduced (greater bioavailability)
  • Immediate and accurate effects (emergency use)
  • Permits titration of dose (slow release, or release on button) - because you get an instant response as to how the drug is working

Disadvantage

  • Increased risk of adverse effects overdose
45
Q

What are the advantaged and disadvantaged of Subcutaneous (parenteral injection)?

A

Advantages

  • Prompt action from solutions, slow release from repository preps
  • Good for insoluble suspensions and solid pellets

Disadvantages

  • Can’t use with large volumes (may cause necrosis)
46
Q

What are the advantaged and disadvantaged of Intramuscular (parenteral injection)?

A

Advantages

  • Prompt action from solutions, slow release from repository preps
  • Good for moderate volumes

Disadvantages

  • Can alter distribution by changing blood flow to the area (massage heat)
  • Not ideal in obese patients (where muscles can’t be found easily)
47
Q

What are the advantaged and disadvantaged of Inhalents?

A

Advantages

  • Use of gas exchange at lungs - very fast access to the circulation
  • Avoids hepatic first pass
  • Good for pulmonary disease, asthma (local effect)

Disadvantages

  • ?
48
Q

What are some routes of administration for Mucous Membrane Application (Topical)? What is the main advantage of this technique?

A

• Nasal, vaginal, colon, urethra - good for local effects (eg decongestants)

49
Q

What are some drug administration routes directly into the cerebrospinal fluid?

A
  • Intrathecal - Inject directly into the subarachnoid space (spinal anes)
  • Intracerebroventricular (intraventricular) - Inject directly into ventricles (brain tumours)
50
Q

What is the blood brain barrier? What can and can’t get through it?

A
  • The blood–brain barrier (BBB) is a highly selective permeability-barrier that separates the circulating blood from the brain extracellular fluid (BECF) in the central nervous system (CNS).
  • The blood–brain barrier is formed by capillary endothelial cells, which are connected bytight junctions.
    • Allows the passage of water, some gases (O2 and CO2), and highly lipophilic drugs (can cross the phospholipid membrane by passive diffusion), as well as the selective transport of molecules such as glucose (energy) and amino acids that are crucial to neural function.
    • May prevent the entry of low level lipophilic (disolving or combining in lipids or fats) [potential neurotoxins], large molecules and charged molecules.
51
Q

Why might you want to breach the blood-brain barrier with a drug?

A

All drugs that reach the brain effect the rest of the body (unless locally applied – intrathecal/intraventricular)

52
Q

Many drugs used in psychopharmacology increase or reduce _____________.

A

Neurotransmission

53
Q

What is neurotransmission?

A

neurons chemically communicating with neurons

54
Q

What are Neurons (Brain cell type)?

A

A neuron is an electrically excitable cell that processes and transmits information through electrical and chemical signals.

55
Q

What are NeuroGlial Cells (Brain cells)?

A

non-neuronal cells that maintain homeostasis, form myelin, and provide support and protection for neurons in the brain and peripheral nervous system.

56
Q

What are the four main functions of glial cells?

A

Four main functions of glial cells:

  1. To surround neurons and hold them in place
  2. To supply nutrients and oxygen to neurons
  3. To insulate one neuron from another
  4. To destroy pathogens and remove dead neurons.
57
Q

What type of Glial cell in the CNS provides support and insulation to axons ?

A

Oligodendrocytes

58
Q

What type of cells are Oligodendrocytes and what role do they perform?

A

Neuroglial cells, Their main functions are to provide support and insulation to axons in the central nervous system.

59
Q

What type of Glial cell in the CNS is star-shaped, the most abundant; and provides biochemical support of endothelial cells that form the blood–brain barrier, provision of nutrients to the nervous tissue, maintenance of extracellular ion balance, and a role in the repair and scarring process of the brain and spinal cord following traumatic injuries.

A

Astrocytes/Astroglia

60
Q

What type of cells are Astrocytes? and what roles do they perform in the CNS?

A

Neuroglial cells

  • Biochemical support of endothelial cells of the blood-brain barrier
  • Provision of neutrients to the nervous tissue
  • Maintencance of extra-cellular ion balance
  • repair and scarring process of the brain and spinal cord following traumatic injuries.
61
Q

What role does the Ependymal cells have in the CNS?

A

These cells line the CSF-filled ventricles in the brain and the central canal of the spinal cord. They are important for Neurogenesis.

Their apical surfaces are covered in a layer of cilia (slender protuberances, micro ‘eyelash’ like structures projecting from the much larger cell body), which circulate CSF around the CNS. Their apical surfaces are also covered with microvilli, which absorb CSF. Ependymal cells also produce CSF. Within the ventricles of the brain, a population of modified ependymal cells and capillaries together form a system called the choroid plexus, which produces the CSF.

62
Q

What is neurogenesis and what glial cells have an important role in it?

A

(birth of neurons) is the process by which neurons are generated from neural stem cells and progenitor cells. Ependymal (glial) cells.

63
Q

What role do microglia have in the CNS?

A

Remove dead or degenerating neutrons or glia via phagocytosis(eating of cells)

64
Q

Where does the action potential start in the neuron?

A

Axon hillock [where the cell body joins the acon tail]

65
Q

What determine if the cell will ‘fire’? i.e., has an action potential?

(describe location, excitatory threshold, resting potential, role of sodium and potassium - basically the whole process!)

A
  • The voltage at the axon hillock determines if a cell will fire, every neuron has a resting potential (normally -70mv) and an excitatory threshold above which it will fire (normally -50mv).
  • This voltage is influenced by Inhibitory Post-Synaptic Potential (IPSP) [neuron less likely to reach AP] AND **Excitatory Post-Synaptic Potential (EPSP) **[neuron more likely to reach AP].
  • Ion channels can open up on the neuron body enabling an action potential - sodium Na+ enters! - potential becomes more positive until an action potential occurs
  • The Sodium Potassium (K+) pup restores original ion values after firing.
66
Q

Are neurons generally positively or negatively charged?

A

Negatively charged, resting potential around -70mv

67
Q

(1) _____ = to make a neuron less negatively charged.
(2) _____ = To make a neuron more negatively charged.

A
  1. Depolarise
  2. Hyperpolarise
68
Q

What does an action potential lead to?

A

(simplified) Release of neurotransmitters.

69
Q

Axons + dendrites = _______

A

Neurites

70
Q

Describe the process of chemical communication via neurotransmitters….

(Bonus: what part can drugs affect?)

A

BONUS: all of the stages.

  1. Action potential to the presynaptic terminal
  2. Vesicle full of neurotransmitter docks with the presynaptic terminal wall. [Ions would change the polarisation of the neuron. For ions to pass through the phospholipid bilayer channels made of large protein molecules are needed ]
  3. **Exocytosis - Neurotransmitter is released into the synaptic cleft (exocytosis). **
  4. Neurotransmitters bind to their receptors on the postsynaptic terminal
  5. Endocytosis (Reuptake)- Neurotransmitters are released from their receptors and taken back **through the transporter to the presynaptic neuron **
  6. The postsynaptic neuron integrates the responses from the neurotransmission (which may be inhibitory or excitatory) in a process called neuronal integration. The amount of depolarisation following neuronal integration determines whether the neuron will send of an action potential.

7.

71
Q

How do neurotransmitters communitcate with the next neuron?

A
  • Receptors!
  • Release of a neurotransmitter binds to a receptor to tell the next neuron what to do
  • Allows for sophisticated (and quite complex!) transfer of information
  • Co-ordinated circuitry allows appropriate behavioural output to an environmental stimulus
72
Q

What is the phospholipid bilayer?

A

a Lipid bilayer making up part of the cell membrane of a neuron (outer layer/neuron ‘skin’) which DOES NOT allow ions to freely flow through it (will let uncharged molecules through!) - thereby ions can only flow along it, or be let through gated ion (protein) channels (as occurs in EPSP and IPSP [as in action potential process]).

Important to know, since lipophilic drugs can be made to pass through this layer or will need to be either transported (in a vesicle) or affect the outside of the neuron.

MORE INFO: http://classroom.synonym.com/brain-cells-lipid-bilayer-18002.html

73
Q

What are the two main types of receptors?

A

Iontrophic (ion Channels - affect whether AP will occur)

Metatrophic (Big proteins that cause a metabolic/chemical reaction on the inside)

(the type of receptor that a drug affects/binds-with will affect the speed and outcome of the drug)

74
Q

Generally speaking how do drugs influence chemical neurotransmission?

A

They bind to receptors, which changes the information sent to the next neuron in a chain. Either within a small region or between regions of the brain.

75
Q

Can all neurotransmitters bind to all receptors?

A

No, there are different receptors for different neurotransmitters (And some receptors found that don’t have neurotransmitters yet!)

76
Q

How many dopamine receptors are there?

A

5 (D1, D2[different isoforms - different lengths genetically], D3, D4, D5)

77
Q

How many oxytocin receptors have been found so far?

A

One! (OT)

78
Q

In receptor pharmacology: what is affinity and efficacy?

A

Affinity = the attraction that a drug has for a receptor site
Efficacy - the ability for a drug to induce a response once bound to the receptor site.

79
Q

In receptor phramacology, what are agonists?

A

Agonists are drug ‘keys’ that unlock the receptor ‘door’ They act like the neurotransmitters to open the door

80
Q

In receptor phramacology, what are antagonists?

A

Antagonists are drug ‘keys’ that fit the lock but can’t open the ‘door’ They compete with neurotransmitters for the keyhole

81
Q

(Fill in gaps using these words: Efficacy, Affinity)

  1. Agonists have ___ and ____
  2. Antagonists have _____ but NOT _____.
A
  1. Affinity, Efficacy
  2. Affinity, Efficacy
82
Q

In drug interaction: what is antagonism?

A

The effect of one drug (or neurotransmitter) minimised or abolished by another.

83
Q

____ is when the effect of one drug (or neurotransmitter) minimised or abolished by another.

A

Antagonism

84
Q

What are the 5 types of antagonism drug/neurotransmitter interactions?

A
  1. Receptor block “competitive” antagonism (most common)
  • Reversible
  • Irreversible
  1. Non-competitive antagonism (block occurs IN neuron or cell, not at receptor site)
  2. Chemical antagonism
  3. Pharmacokinetic antagonism
  4. Physiological antagonism
85
Q

What is ‘competive’ receptor block antagonism (Drug/neurotransmitter interaction) and what are its two sub-types.

A

A drug (or neurotransmitter) which blocks a receptor (i.e., outside of a neuron, it competes for who gets there first)

  1. Reversible (not permanent) - drug will bind to receptor but goes on and off
  2. Irreversible (e.g., as in poisons/toxins) - binds and never leaves
86
Q

What is ‘non-competive’ receptor block antagonism (Drug/neurotransmitter interaction)

A

block occurs IN neuron or cell, not at receptor site - does not compete with other neurotransmitters and drugs at the synapse - just goes straight in.

87
Q

What is chemical antagonism?

A

When two substances outside of the body have been put together in a medication that cancel each other out (even if they worked individually)…medicaly doesn’t work.

E.g., putting an active compound into a vehicle that cancels the drug out

88
Q

What is pharmacokinetic antagonism?

A

The effect of your drug is reduced or cancelled because of something in the body. E.g., interaction with other medication/ingested compound or broken down by gut and liver enzymes - e.g., Cytochrome P450 cycle [Oxidises drug (adds an oxygen atom to drug - inactivates)] (lots of different cycles this is just an example - this one just oxidises drugs)

MORE EXAMPLES:

First pass metabolism

Liver: CYP1, CYP2 CYP3 Enzymes

CYP1A2 oxidises caffeine
CYP2C9 oxidises ibuprofen
CYP2E1 oxidises alchohol - also needs alcohol dehydrogenase (not common in asian races)

89
Q

What is the first past effect (Also known as first-pass metabolism or presystemic metabolism)?

A

is a phenomenon of drug metabolism whereby the concentration of a drug is greatly reduced before it reaches the systemic circulation. (e.g., goes through the liver first!)

90
Q

What is physiological antagonism?

A

The physiological effect of two administered drugs counteract each other

E.g.,

ingest alcohol - leads to stupor at high doses
ingest methamphetamine - increases motor activation
Ingest BOTH

Alcoholic stupor requires greater alcohol consumption
Methamphetamine counteracts the effect of alcohol.

91
Q

In positive drug interactions, what is an additive interaction?

A

Sum of the effect of each drug to get ‘double’ the effect

92
Q

In positive drug interactions, what is an Synergistic interaction?

A

One drug potentiates (massively increases/facillitates the effect of another or each other) the effect of another (i.e., more than additive)

93
Q

What are some reasons why drugs become less effective after use?

A

Desensitisation (of receptors) and tachyphylaxis — loss of drug effect (gradually diminishes)
Tolerance/refractoriness/drug resistance (Drug doesn’t have enough receptors to work on anymore as they ‘hide’ like whack a mole lol)

  • Change in receptors (hiding)
  • loss of receptors
  • Exhaustion of neurotransmitters (unavailability of neurotransmitters [chemicals]
  • Increased metabolic degradation
  • Physiological Adaption (foreign chemical tries to help but upsets how the brain thinks it should be working.
94
Q

What is tachyphylaxis? Why does it occur?

A

Acute (sudden) decrease in the response to a drug after its administration.[1] It can occur after an initial dose or after a series of small doses. Increasing the dose of the drug may be able to restore the original response

(Also desensitisation, tolerance, refractoriness, drug resistance)

Can be due to:

  • Depletion or marked reduction of the amount of neurotransmitter responsible for creating the drug’s effect.
  • Depletion of receptors available to which the drug or neurotransmitter can bind. (This depletion is caused by the cells reducing the number of receptors in response to their saturation.)
95
Q

How can drugs alter how chemical neurotranmitters are…..?

A
  • Manufactured
  • Released
  • Effective at receptors
  • Removed from the Synapse
  • Metabolised
  • Stored

Neuropsychopharmacology (5 decks)

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