Pharmacology Flashcards

1
Q

pharmacokinetics?

A

how the body affects the drug; Absorption, Distribution,

Metabolism and Excretion (ADME)

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2
Q

pharmacodynamics ?

A

how the drug affects the body

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3
Q

receptor types?

A

ligand gated ion channels (eg, nicotinic ACh), G coupled receptors (eg, beta adrenoceptors), kinase linked receptors (eg, GF) and cytosolic receptors (eg, steroids)

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4
Q

potency?

A

measure of how well a drug works

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5
Q

affinity?

A

how well a ligand binds to the receptor

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6
Q

efficacy?

A

how well a ligand activates the receptor?

antagonists have 0 efficacy

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7
Q

isoprenaline?

A

non-selective beta adrenoceptor agonist so it activates B1 in the heart and B2 in the lungs

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8
Q

salbutamol

A

selective B2 adrenoceptor agonist

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9
Q

eg of enzymes as drug targets?

A

NSAIDS that inactivate COX responsible for the breakdown of
arachidonic acid to prostaglandin H2
(aspirin irreversibly blocks the active site)

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10
Q

transporters as drug targets eg?

A

PPI (omeprazole) irreversibly inhibit proton pump

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11
Q

ion channels as drug targets eg?

A

CCB eg, amlodipine

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12
Q

bio-availability?

A

amount of drug taken up as a proportion of the amount

administered

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13
Q

aspirin in the gut?

A

Aspirin is acidic
• In the stomach the acidic tablet dissolves but it then becomes less
ionised due to the fact that a weak acid (such as aspirin) becomes less ionised in lower pH and movement of un-ionised aspirin across gut is rapid.

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14
Q

which molecules are distributed where?

A

Proteins/large molecules are only active in the plasma compartment (5L) eg, warfarin
- Water soluble molecules are active in plasma and interstitial compartment
(5L + 15L) eg, NSAIDS
- Lipid soluble molecules are only active in the intracellular fluid (45L) eg, paracetamol

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15
Q

volume of distribution equation?

A

Volume of distribution = Total amount of drug in body ➗ Concentration
of drug in plasma

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16
Q

clearance?

A

The volume of plasma that can be completely cleared of drug per unit
time (mls minute-1 (ml/min))

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17
Q

water soluble v larger molecules in kidney elimination?

A

Water soluble molecules which pass through the glomerular endothelia
gap are eliminated by glomerular filtration
• Larger water soluble molecules can be eliminated by active tubular
secretion

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18
Q

hepatic extraction ratio?

A

The proportion of drug removed by one passage through the liver

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19
Q

phase I reaction - where do they occur?

A

95% of phase I reactions are in liver smooth endoplasmic

reticulum

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20
Q

what is phase 1 reactions?

A

make the drug more hydrophilic so that it can be excreted by the kidneys - it does this by adding a hydroxyl group to the drug

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21
Q

cytochrome p450?

A

microsomal enzyme found in liver SER and involved in phase 1 reactions

22
Q

phase 2 reactions?

A

conjugation reactions, glucuronodiation and used if drug is very hydrophobic

23
Q

somatic NS neurotransmitter

A

ACh

23
Q

somatic NS neurotransmitter

A

ACh

24
Q

autonomic NS neurotransmitter?

A

ACh and NAd

25
Q

ACh - parasympathetic NS receptor?

A
  • muscarninc Ach receptors (M1,M2,M3)
26
Q

ACh - sympathetic NS receptor?

A
  • ACh mediates release of Ad and NAd
27
Q

ACh in somatic NS?

A

-nicotonic receptors at neuromuscular junction

28
Q

adverse effects of muscarninic agonists?

A

DUMBELS
muscarninc = parasympathetic
diarrhoea, urination, miosis, bradycardia, emesis, lacrimation and salvation/sweating

29
Q

catacolamine synthesis?

A

TYROSINE > DOPA > dopamine > noradrenaline > adrenaline

30
Q

alpha 1 adrenergic receptors?

A

causes vasoconstriction, pupil dilation and bladder contraction
BLOOD VESSELS AND BLADDER

31
Q

alpha 2 Adrenergic receptors?

A

presynaptic inhibition of noradrenaline

32
Q

beta 1 adrenoceptor?

A

increased force of heart contraction, increases heart rate and increased electrical conduction in heart
IN HEART!

33
Q

beta 2 adrenoceptor?

A

bronchodilator, vasodilation and reduces GI motility

BRONCHIAL SMOOTH MUSCLE - LUNGS

34
Q

beta 3 adrenoceptor?

A

increases lipolysis and relaxes bladder

BLADDER

35
Q

nociceptive pain?

A

Inflammatory chemicals reach nerves to stimulate pain

36
Q

neuropathic pain?

A

Where the nerve is directly inured - pain originates in nervous system

37
Q

pain pathway?

A

Noxious stimulus

  1. Nociceptors
  2. Spinal cord (ascending pathway)
  3. Spinal cord modulation
  4. Thalamus
  5. Cortical areas, somatosensory cortex & prefrontal cortex
  6. Pain experience & memory
38
Q

tissue injury pathway?

A

The breakdown of membrane lipids leads to the formation of arachidonic acid under the action of the enzyme phospholipase A2

  • Arachidonic acid is then converted to prostaglandins under the action of the enzyme cyclooxygenase (Cox)
  • Prostaglandins are irritants to nerve fibres and stimulate pain
39
Q

nerve fibres transmitting pain?

A

C and A delta fibres

40
Q

C fibres?

A

Unmyelinated

Characterised by diffuse dull intense pain

41
Q

A delta fibres?

A

Small and myelinated

Conduct localised sharp sensation

42
Q

Gate control theory

A

If A beta fibres ARE stimulated then the pain signal is halted and
does not reach the brain and is thus not perceived
- This means that low intensity stimulation of the skin or peripheral
nerves or vibration in order to stimulate the A beta fibres will
generate analgesia

43
Q

Type A - adverse drug reaction?

A

Augmented eg, anti-coagulants causing bleeding

44
Q

Type B - adverse reactions?

A

Bizarre; unexpected, unrelated and unpredictable

45
Q

Type C - adverse reactions?

A

chronic eg, steroids predispose to hypoglycaemia - resulting in diabetes

46
Q

Type D - adverse reactions?

A

delayed

47
Q

Type E - adverse reactions?

A

End of use; withdrawal reactions

48
Q

oral contraceptives and antibiotics?

A

interaction causing motility changes

49
Q

oral availability of morphine?

A

50%