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phar24 > week 6 > Flashcards

week 6 Flashcards

1
Q

define ion channels

A

hole in membrane - have a pore that once opens allows ions to flow in and out of the cell based on electrochemical & osmotic gradients

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2
Q

selectivity of ion channels

A

each channel is selective to the specific ion e.g., sodium, potassium, calcium

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3
Q

what five drivers move ions through channels

A

ions move toward electrochemical equilibrium through:

  1. electricity
  2. diffusion
  3. v-gated ion channels
  4. transporters
  5. passive
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4
Q

how to ions move through channels via electricity

A

= ions will move across a membrane if you introduce an electrical field. ions carry charge & pos NA will move towards negative terminal (inside cell) & likewise, neg CI will move towards pos terminal (outside cell)

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5
Q

ions moving through membrane via facilitated diffusion

A

= ions will move across the membrane passively provided channels are present & there is a concentration gradient i.e. more salt outside than in or vice versa

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6
Q

examples of channels that aren’t as selective/structured

A
  1. n-AChR conducts K, Na, Ca = 5-fold symmetry

2. chloride channel = 2 fold symmetry = ion pathway less obvious

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7
Q

three activations of ion channels

A
  1. voltage-gated
  2. ligand-gated ion channel
  3. G-protein coupled receptor
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8
Q

the steps of the movement of ions in a voltage gated sodium, potassium channel

A
  1. cell membrane depolarises
  2. sodium channels open = sodium rushes into the cell
    • massive inward flow of charged sodium = changes
      membrane to positive potential
  3. causes potassium channels to open or activate = potassium starts flowing out of the cell carrying its positive charge with it = repolarising the membrane
    • causes membrane to move back closer to resting
      neg membrane potential
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9
Q

what does the rapid movement of ions across the cell membrane cause

A

causes “action potentials” to propagate from one cell body, down axons to the synapse where they initiate release neurotransmitters

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10
Q

steps in APs & V-gated channels & transporters working together

A

step 1: membrane “resting” = sodium, potassium pump is closed, sodium & potassium channel closed (but still some passive movement)

step 2: rapid membrane depolarisation = sodium & potassium pump closed, sodium channel opens & sodium flows in

step 3: membrane repolarises = potassium channel opens, sodium channel starts closing (potassium flows out, sodium stops flowing)

step 4: membrane returns to rest = sodium & potassium pump open, sodium & potassium channel closed (sodium & potassium flows to equilibrium)

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11
Q

examples of functions of calcium channels

A

memory, neurotransmitter release, pace making action potentials, adrenaline/insulin secretion, contraction muscle tone

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12
Q

example of ion channel diseases

A
  • cycstic fibrosis, epilepsy, cancer, heart disease
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13
Q

define channelopathies & 2 causes

A

= defects in ion channels

  1. genetic factors = mutations that lead to malfunction of ion channels can cause multiple diseases such as epilepsy
  2. environmental factors = continuous exposure to pain or certain drugs may cause channels to malfunction leading to chronic pain for example
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14
Q

How do calcium T-type regulate sodium, potassium driven action potentials

A
  1. injury occurs
  2. chemicals called cytokines are released
  3. this activates G-protein coupled receptors
  4. this activates protein kinases
  5. this hyperpolarises & activates T-type protein calcium channels
  6. the influx of highly positive calcium into the cell creates a deploarising event, triggering the sodium channel threshold causing the action potential to commence
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15
Q

how is ionic movement effected

A

by changes in the open/closed state as well as speed of open/closed state of channel (activation & inactivation kinetics)

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16
Q

channels activate & inactivate in response to

A

changes in membrane voltage

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17
Q

how can ionic movement be controlled

A

ion channel conformation can be controlled through drugs i.e. keep open/closed, active/inactive = bind to channel & restrict/reduce flow or opposite increase affinity

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18
Q

example of drugs that control ionic movement

A
  1. sodium channels e.g. AEPs, anaesthetics

2. calcium channel blockers e.g. DHPs, VDs

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19
Q

what does the movement of ions generate

A

electrical signals called action potentials that are tiny electrical units of information that connect neural circuits & instigate release of neurotransmitters

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20
Q

how much of hospital admission are estimated to be medicine -related causing significant morbidity & mortality

A

2-3%

1.4% likely to be due to adverse drug reaction

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21
Q

define therapeutic index

A

used to compare the therapeutic does to the toxic does of a pharmaceutical agent

= dose vs response in the population

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22
Q

define ED50

A

the drug dose that produces a therapeutic response in 50% of the population

23
Q

define TD50

A

drug does that produces a toxic response in 50% of the population

24
Q

equation for therapeutic index

A

TD50 divided by ED50

25
Q

the lower the TI the …

A

the less safe the drug = the difference between the effects of the two concentrations is small

26
Q

define therapeutic window

A

mostly determined by plasma concentration of the drug verse the response in the pop

= range of steady-state concentrations of drug that provide therapeutic efficacy with minimal toxicity

27
Q

does therapeutic window guarantee safety & efficacy

A

no

28
Q

what does therapeutic window indicate

A

indicates at which doses the probability of efficacy is high & adverse effects is low

29
Q

drugs with low therapeutic index are especially likely to be involves in …

A

adverse drug reactions

30
Q

2 types of adverse effects and their subheadings

A
  1. predictable = overdose, side effect or withdrawal

2. unpredictable = allergy/hypersensitivity

31
Q

what characteristic of drugs can you predict the adverse reaction

A

drugs with low TI

32
Q

examples of drugs with low TI

A

anticoagulants (warfin), lithium & hyperglycemia drugs (drugs for diabetes)

33
Q

3x characteristic of predictable adverse reactions from drugs

A

mostly preventable & reversible & dose related

34
Q

4x characteristics of unpredictable adverse drug reactions

A

less common & most serious (requires drug withdrawal) & not dose related (may occur at low doses) & idiosyncratic

35
Q

define predictable adverse drug reactions

A

consequence of main pharmacological effect (pk)

36
Q

define unpredictable adverse drug reactions

A

unrelated to the known pharmacological action of the drug (off target)

37
Q

define idiosyncratic

A
  • unique to individual, if it is known it becomes predictable
38
Q

6 classifications of ADRs (adverse drug reactions)

A
  1. Dose-related (augmented)
  2. non-dose related (Bizarre)
  3. dose-related & time related
  4. time related
  5. withdrawal
  6. unexpected failure of therapy
39
Q

examples of dose-related ADRs

A

toxic effects = digoxin & SSRIs

side effects = anticholinergic effects of TCA

40
Q

examples of non-dose related ADRs

A

immunological reactions: penicillin hypersensitivity

idiosyncratic reactions: malignant hyperthermia (reaction to general anaesthetic

41
Q

examples of dose related & time related ADRs

A

hypothalamic - pituitary - adrenal axis suppression by glucocorticoids

42
Q

examples of time related ADRs

A

teratogenesis (thalidomide, valproate) –> affects foetal

carcinogenesis –> causes cancer

43
Q

examples of withdrawal ADRs

A
  • opiate withdrawal syndrome

- myocardial ischemia (beta-blocker)

44
Q

examples of unexpected failure of therapy ADRs

A
  • inadequate dosage of oral contraceptive, particular when used with enzyme inducers
45
Q

meaning of predisposition to ADRs

A

patient related factors

46
Q

examples of factors that increase predisposition to developing ADRs - patient related factors

A
  • age (very young, or very old)
  • gender
  • underlying disease
  • hepatic & renal function
  • body weight & fat distribution
  • genetic factors
47
Q

examples of factors that increase predisposition to developing ADRs - other drug related factors

A
  • other drugs taken (smoking, alchohol, polypharmacy)
  • route of administration
  • dose of the drug and frequency
48
Q

define drug to drug interactions

A

the modification of the action of one drug by another

49
Q

type of drug-drug interactions

A
  1. behavioural (altered compliance)
  2. pharmaceutic (outside the body)
  3. pharmacokinetic (altered concentration)
  4. pharmacodynamic (altered effect)
50
Q

2 types of pharmacodynamic interactions

A

= most common

  1. additive effect = drugs have similar actions e..g, alcohol & bezodiazepine (both CNS depressants)
  2. opposite effects = drugs cancel each others effects
    e. g., beta-blockers (heart condition) with beta-agonists (asthma)
51
Q

meaning of pharmacokinetic interactions

A

change in concentration leading to clinical consequences

52
Q

3 types of pharmacokinetic interactions

A
  1. altered bioavailability = oral contraception & antibiotics
  2. altered distribution = displacement of drug bound to plasma albumin
  3. altered clearance = metabolism, prodrugs, excretion (penicillin & probenecid)
53
Q

how to manage poisoning

A
  1. assessment & examination
  2. prevent further absorption
  3. specific antidotes
  4. increase elimination
54
Q

what is the three state model of voltage-gated ion channels

A
  1. closed = at the resting potential, the channel is closed
  2. open = in response to a nerve impulse, the gate opens and sodium enters the cell
  3. inactivated = for a brief period following activation, the channel does not open in response to a new signal

phar24 (12 decks)

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