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Flashcards

Pharmacology 2

GEORGIA SMITH Pharmacology English 200 cards

Cards in this deck (200)

  1. 1What is P-gpPermeability glycoproteins
  2. 2What is enterohepatic recirculationmoves through gut, absorption into blood, enters hepatic portal vein, transported to liver, transferred to gall bladder in bile, secreted into small intestine..
  3. 3Where can drugs eliminated in bile be reabsorbed?In the GI tract
  4. 4what are examples of drugs that undergo enterohepatic recirculation?morphine, erythromycin, oral contraceptives, lorazepam.
  5. 5what is first pass metabolismwhen drugs are metabolised straight away in the liver
  6. 6What factors affect the distribution of drugs?- ability to cross a cell membrane
    -blood perfusion of the tissue or organ
    -plasma protein binding ability
  7. 7Where would clearance from plasma by equal to clearance from tissue?At equilibrium
  8. 8What happens when a drug is highly bound to plasma proteins?The drug stays in plasma and has poor distribution
  9. 9What is a alpha 1 acid glycoprotein?An acute phase protein that increases diseases and inflammation
  10. 10What is the function of an alpha 1 acid glycoprotein?Binds mostly basic and some neutral drugs
  11. 11What is albumin (HSA)Binds mostly acidic and some neutral drugs causing a lack of malnutrition and cirrhosis
  12. 12How would you calculate (Vd) volume distribution?total amount of drug administered (dose)/ plasma drug concentration
  13. 13what does Vp mean?plasma volume of drug
  14. 14what is Vt?The apparent tissue volume of drug
  15. 15what does fu stand for?fraction unbound in plasma
  16. 16what does fu1 stand for?Fraction unbound in tissue
  17. 17An example of a highly plasma bound drug?Heparin
  18. 18What drug is highly plasma bound but distributes to the interstitiumwarfarin
  19. 19What drug will leave the bloodstream quickly and distribute to body water compartment meaning that very little will remain in the plasma?Ethanol
  20. 20What drug is super lipophilic, moves into body fat quickly and is lost from the bloodstream rapidly?chloroquine
  21. 21What mediates phase one metabolism?cytochrome P450
  22. 22What mediates phase 2 metabolism?UDP-glucuronosyltransferases
  23. 23What is the goal of phase 1 and phase 2 metabolism?To increase water solubility for accretion in the urine
  24. 24What is the active drug of dactyl morphine?Morphine
  25. 25What is the active drug of valaciclovir?Aciclovir
  26. 26What is the active drug of L-dopa?Dopamine
  27. 27What is the mechanism of drug elimination dependent on?The physiochemical properties of drug and metabolites
  28. 28How would volatile gases by eliminated?exhaled air
  29. 29How would water soluble, filtered out in kidney be eliminated?In the urine
  30. 30How would mass transport in gut be eliminated?In faeces
  31. 31How is secreted into glands eliminated?In breast milk and sweat
  32. 32What drug is excreted unchanged in urine and can be collected and reused?Penicillin
  33. 33What does Kel stand for?The elimination rate constant
  34. 34What is the elimination rate constantThe fraction of drug in the body that is removed per unit of time.
  35. 35What is the equation of half life?T1/2 = ln2/Kel
  36. 36What is half life?The time taken for the plasma concentration to reduce by one half
  37. 37What does fenestrated mean?Containing windows or perforated
  38. 38What is a prodrug?The inactive dorm of a drug that is metabolised into an active form within the body
  39. 39What does partitioning mean?The movement of unbound drug from the plasma to tissues
  40. 40What is elimination?Metabolism plus excretion
  41. 41What major systems are concerned with elimination?kidneys, hepato-billiary system, lungs
  42. 42oxidation, hydroxylation, dealkylation, deamination ans hydrolysis occurs in which phase of drug metabolism?Phase 1
  43. 43conjugation occurs in which type of metabolism?phase 2
  44. 44What are the results of decreasing lipid solubility?May increase pharmacological or toxicological activity.
  45. 45What are cytochrome P450 enzyme family?A large family of heme-cofactor containing enzyme
  46. 46Where are CYPs mostly found?In the intestine and liver
  47. 47Where are CYPs found in the cell?In the endoplasmic reticulum
  48. 48Where are small amounts of CYPs found?Kidney, white blood cells, nasal passages
  49. 49What is the exception of CYP metabolism?Ethanol metabolism
  50. 50How is ethanol metabolised?Ethanol is metabolised to acetaldehyde by alcohol dehydrogenase and CYP2e1
  51. 51How does Acetaldehyde become acetic acid?By aldehyde dehydrogenase
  52. 52Where do conjugation reactions target?large groups attached such as glucuronyl, sulphate, acetyl
  53. 53how is paracetamol metabolised?mainly by conjugation with sulphate and glucuronic acid, only a minor by CYP450 to toxic metabolite detoxified by glutathione
  54. 54What happens in paracetamol overdose?pathways of conjugation are saturated and co-factors are depleted so more is metabolised by CYP450. The metabolites react with liver proteins instead of being depleted causing tissue damage leading to necrosis.
  55. 55What endogenous facts affect drug metabolism?genetic constitution, age and disease
  56. 56What exogenous factors affect drug metabolism?drugs, smoking./alcohol, environment exposure
  57. 57What does fast metabolism mean for drug metabolism?-normal enzyme activity, lower plasma concentration of the parent drug, higher concentration of the metabolite, generally normally therapeutic response
  58. 58What does slow metabolism mean for drug absorption?Low enzyme activity, higher plasma concentration of the parent drug, lower concentration of the metabolite, may lead to exaggerated therapeutic response at normal doses.
  59. 59How are neonates affected by drug metabolismLow CYP and conjugating activity
  60. 60How are the elderly affected with drug metabolism?CYP activity declines slowly with age
  61. 61What do inducers do?increase synthesis of enzymes, increase metabolism
  62. 62What are examples of inducers?rifampicin, carbamazepine, ethanol and smoking
  63. 63What are the problems of induction?decreased drug effectiveness of chronic exposure, need to increase drug dose, multiple drug therapy causing withdrawal problems and basis of many drug -drug reactions.
  64. 64What happens when ethanol is consumed with paracetamol?CYP450 metabolised to a toxic metabolite enhanced by ethanol consumption
  65. 65What does inhibition of the CYP system do?reduce the rate of metabolism and increase the pharmacological effect.
  66. 66What does grapefruit juice do?inhibits CYP3A4 and the metabolism substrates for terfenadine and nifedipine
  67. 67What is cleared faster a metabolite or the parent compound?The metabolite
  68. 68What are the three major processes of renal excretion?glomerular filtration, tubular reabsorption and tubular secretion
  69. 69What are excreted unchanged through the kidneys?water soluble drugs/metabolites
  70. 70How much renal blood flow is filtered through the glomerulus?20 percent
  71. 71What does not affect glomerular filtration?lipid solubility and pH
  72. 72What factors affect the rate of entry into glomerular filtration?concentration of free drug in plasma, molecular weight
  73. 73How much renal blood flow passes onto peritubular capillaries of the proximal tubule?80 percent
  74. 74how are drug molecules transferred to tubular lumen?By two carrier systems which can transport against electrochemicall gradients
  75. 75What is the most effective mechanism for drug elimination?Active tubular secretion
  76. 76What happens to drug concentration as water is reabsorbed?Drug concentration increases
  77. 77What drugs have high tubular permeability and are slowly excreted?highly lipid soluble drugs
  78. 78What drugs have low tubular permeability and concentrate in urine (!00x in plasma)?highly water soluble drugs
  79. 79How does tubular reabsorption work?1. free drug enters glomerular filtrate
    2. active secretion
    3. passive reabsorption if lipid soluble, unionised drug which has been concentrated so that the intraluminal concentration is greater than that in the perivascular space
  80. 80What is tubular reabsorption dependent on?1. drug lipid solubility (pKa)
    2.pH of tubular fluid
  81. 81What happens if an acid drug becomes ionised and more alkaline?It becomes less lipid soluble so reabsorption diminishes
  82. 82What happens if a basic drug becomes unionised?its reabsorption increases
  83. 83What is pKa?The measure of the strength of an aid/base
  84. 84How much of the drug is ionised when pH of solution = pKa of drug?50 percent
  85. 85How do you work out the percentage ionised of the drug?pH - pKa
  86. 86What is pH partitioning?Acidic drug accumulate in basic fluid compartments and vice versa
  87. 87if aspirin is a weak acid with a pK a of 3.5 what happens in the stomach?it is mostly un-ionised so pass through the lipid membrane
  88. 88Where do weak acids accumulate?In compartments of high pH
  89. 89Where do weak bases accumulate?In compartments of relatively low pH
  90. 90A weak base is excreted in what urine?acidic
  91. 91A weak acid is more rapidly excreted in which urine?alkaline
  92. 92What will be the result of urinary acidification?The excretion of weak bases will be accelerated causing ion trapping
  93. 93What is the one compartment model?Over simplified model that a human consists of a single well stirred compartment that a drug is absorbed, immediately distributed and subsequently eliminated
  94. 94What will IV admin of a dose do to plasma concentration in the one compartment model?It will go from zero to steady state (Css)
  95. 95What do kinetic orders do?Relate the plasma concentration of a drug and its rate elimination from the body
  96. 96What is the first order?- it decreases in drug is dependent on the plasma concentration
    -concentration of the drug is the rate limiting factor
    - expotenial decrease
    -most drugs
  97. 97What is the two compartment model?Drugs will only enter the body tissues (peripheral) via the plasma (central)
  98. 98What does the two compartment model predict?The fast and slow phase of distribution between the compartments
  99. 99What is zero order (saturation)?Decrease in drug is independent of the plasma concentration, rate is constant due to limiting factor, straight line ,alcohol
  100. 100What is the difference with zero order?- concentration falls linearly rather than exponentially
    -rate of fall does not vary with dose
  101. 101How do you calculate the plasma concentration at time 0?Co = D/Vd
  102. 102What is the nervous system?A complex network of interconnecting neurones
  103. 103What are neurones?Electrically excitable cells which release neurotransmitters
  104. 104What is neuronal signalling?The transfer of information along and between neurones
  105. 105How does electrical signalling?- the cell body communicates with its terminal using electrical impulses (action potentials)
    -actions potentials are all or none
    - action potentials cause depolarisation of the terminal and release of neurotransmitters
  106. 106What is the pharmacological importance of of action potential?The site for drug action for local anaesthetics and anticonvulsants
  107. 107How many potassium ions are pumped in for every sodium pumped out2 potassium ions are pumped in for every 3 pumped out
  108. 108In resting membrane potential where are sodium and chlorine concentrated?Outside
  109. 109In resting membrane potential the potassium and anions are concentrated where?Inside
  110. 110How do neurones differ from all cells?They can rapidly alter their membrane potential
  111. 111What are neurones' membrane potential dependent on?Voltage gated ion channels
  112. 112How much is the membrane depolarised?-55mv
  113. 113What happens after hyperpolarisation?potassium channels close slowly,membrane potential falls below RMP
  114. 114What happens at action potential propagation?small area of membrane depolarises, odium moves out of the cell and is lost, local current in adjacent sections, membrane reaches threshold for AP, propagation of action potentials down the axon.
  115. 115What happens to sodium channels in refractory?They cannot be opened immediately
  116. 116In what direction does action potential propagate in?only one direction
  117. 117What channels do anaesthetics block?sodium
  118. 118What other drugs can be blocked by sodium channels?Anticonvulsants
  119. 119What are three monoamine neurotransmitters?noradrenaline, dopamine and 5-HT
  120. 120What are two amino acid neurotransmitters?glutamate and GABA (y-aminobutyric acid)
  121. 121What are the common features of neurotransmitters?synthesis, storage and release, interaction with target cell, termination of action
  122. 122How is dopamine synthesised?From tyrosine by tyrosine hydroxyls and DOPA decarboxylase
  123. 123Why are neurotransmitters sorted in vesicles?They are protected from metabolic enzymes and ready for release
  124. 124What does depolarisation of the terminal cause?calcium dependent exocytosis
  125. 125What occurs in calcium dependent exocytosis?voltage sensitive calcium channels open and vesicles fuse with presynaptic membrane and empty into the synaptic cleft
  126. 126What happens to chlorine when extra neuronal metabolism inactivates transmitter?chlorine is recycled
  127. 127What are the properties of a ligand-gated ion channel?receptor with binding site linked directly to an ion channel, by binding opens the channels so ions can enter or leave the cell changing the membrane potential
  128. 128Name 3 sodium./calcium excitatory channelsNMDA (Glutamate)
    nicotine (ACh)
    5-HT3
  129. 129What is an example of a chlorine inhibitory channel?GABAa
  130. 130What are the main features of a ligand-gated ion channel?-mediate fast neurotransmissions
    -alter membrane potential directly
    -small changes in potential summate
    -can induce action potential
  131. 131How does a G- protein linked receptor work>Binding to the receptor activates enzymes as second messengers and opens ion channels
  132. 132How fast are the effects of G-protein receptorsSlow and often modulatory
  133. 133How might drugs affect neurotransmission?By inhibition of synthetic enzymes
  134. 134How does storage and release of transmitter one work?vesicle disrupters cause initial increase in release then a decrease, releasing agents cause non-impulse dependent release
  135. 135What does termination of action 1 cause?A build up of transmitter in the synaptic cleft
  136. 136What does termination of action 2 cause?An increase in transmitter in the synaptic cleft
  137. 137What is the central dogma of the nervous system?Peripheral afferent
    central nervous system
    peripheral efferent
  138. 138what are the features of the sympathetic nervous system?pupils dilate, airway dilate, resp. increase, HR increase, salivary secretion reduces, brain activity alert
  139. 139What are the features of the parasympathetic nervous system?pupils constrict, airways constrict, res decrease, HR decrease, secretion normalise, brain activity normalise
  140. 140In the sympathetic nervous system is the pre or post ganglionic longer?The post
  141. 141What are the neurotransmitters for the pre and post ganglion for the sympathetic nervous system?PRE= Acetylcholine
    POST = noradrenaline
  142. 142What are the neurotransmitters for the pre and post ganglion for the parasympathetic nervous system?PRE= acetylcholine
    POST= acetylcholine
  143. 143How does the sweat gland differ by sympathetic nervous system?The post ganglion's neurotransmitter is acetylcholine
  144. 144What is the somatic neurotransmitter in the NMJ?acetylcholine
  145. 145What is CAT stand for?Cholineacetyl transferase
  146. 146What does AChE stand for/Acetylcholinesterase
  147. 147what does cholineacetyltransferase?An transferase enzymes that transfers an acetyl group synthesising acetylcholine
  148. 148What are the receptor interactions of Ach?muscarinic and nicotinic
  149. 149What is the role of acetylcholine esterase?To aid the termination in synapse
  150. 150Where are receptors located?In the postganglionic parasympathetic
  151. 151What is the structure of a g-protein coupled receptor?7-transmembrane spanning receptors
  152. 152what is the function of a g-protein coupled receptor?Coupled to intracellular system via a g-protien
  153. 153Name two nicotinic receptor subtypesneuronal type brain and autonomic ganglia excitatory and muscle type: NMJ excitatory
  154. 154What is the structure of ligand gated ion channels?4 to 5 subunit structure
  155. 155What is the function of a ligand gated ion channel?Couple directly to a ion channel
  156. 156What is the time scale of a ligand gated ion channel?Fast (milliseconds)
  157. 157What are muscarinic agonists known as?Parasympathomimetics
  158. 158What are muscarinic antagonists known as?Parasympatholytic
  159. 159What are clinical examples of muscarinic receptor agonists?pilocarpine and carbachol
  160. 160What is pilocarpine used for?to treat glaucoma
  161. 161How does pilocarpine work>causes ciliary muscle contraction focusing on near vision causing increase drainage of aqueous humour
  162. 162what is xerostomia?dry mouth/reduced saliva
  163. 163What causes xerostomia?radiation, antineoplastic drugs, side effects of many other drugs
  164. 164What are the side effects of pilocarpine?muscarinic sweating, nausea, minimal cardiovascular side effect
  165. 165What are the clinical uses of atropine?to decrease oral/respiratory secretions before oral procedures and to resuscitate bradycardia
  166. 166What is ipratropium?A muscarinic receptor antagonist that treats asthma
  167. 167What is hyoscine?A muscarinic receptor antagonist used to treat motion sickness
  168. 168Do nicotinic agonist activate sympathetic or parasympathetic NS?both causing autonomic confusion so they are not clinically useful
  169. 169What do nicotinic (hexamethonium) antagonists do?Cause a loss of sympathetic and parasympathetic reflexes, especially cardiac
  170. 170What do muscle type nACh do when the receptors are stimulated?Depolarisation occurs causing contraction of skeletal muscle
  171. 171What is an example of a muscle type nACH AGONIST?suxemethonium
  172. 172What is an example of a muscle type nACH ANTAGONIST?tubocurarine
  173. 173What is the effect of suxemethonium at NMJ?initial dep. causing muscle twitch and because it cannot be metabolised quick enough causes constant depolarising block meaning paralysis or muscle relaxation for surgery.
  174. 174What is the effect of a nicotinic antagonist tubocurarine?causes hyper polarisation and inhibition of EPPs causing non-depolarising blocker so paralysis for surgery
  175. 175What drug affects cholinergic transmission?Hemicholinium
  176. 176What does botulinum toxin and bungarotoxin do?causes parasympathetic and motor paralysis by preventing the release of Ach
  177. 177What inhibits acetylcholinesterase?Acetylcholinesterase's
  178. 178What is the role of acetylcholinesterase?To increase Ach transmission by blocking what metabolises it.
  179. 179Give two example of two anti cholinesterase?neostigmine and organopphosphates
  180. 180What are the ANS effects from an anti cholinesterase?increased transmission at the parasympathetic nervous system
  181. 181What are the effects on the NMJ from anticholinesteraseincreased tension causing depolarising block and so neostigmine can treat myasthenia gravis.
  182. 182How is noradrenaline terminated?uptake/recycling/metabolism by monoamine oxidase
  183. 183What receptors are noradrenaline split into?alpha and beta receptors
  184. 184Where are alpha noradrenergic repeats located?In effectors tissues/targets of the sympathetic nervous system,.
  185. 185What type of coupled receptors occur with alpha noradrenergic receptors?G-protein therefore a slow (seconds) response
  186. 186What are the sympathetic effects of alpha 1 receptors?pupil dilation
    blood vessel to visceral organs ad skin constrict
    brain activity general alertness
  187. 187What are alpha 2 receptors?presynaptic receptor, inhibits neurotransmission release (both NA, ACh...)
  188. 188What sympathetic effects are mediated by beta 1 receptors?Heart race increase
  189. 189What sympathetic effects are mediated by beta 2 receptors?lens for long distance view, lungs dilate, blood vessels to limb muscles dilate
  190. 190What are the sympathetic effects mediated by beta 3 receptors?Increase lipolysis
  191. 191What is a noradrenergic agonist example?Adrenaline
  192. 192What are the two main uses of adrenaline?To prolong an isolate local anaesthesia and mediate vasoconstriction in alpha 1
  193. 193What is an example of an alpha 2 agonist?Clonidine
  194. 194What is the clinical use of clonidine?To treat hypertension and treat withdrawal of morphine
  195. 195What is a beta 1 agonist example?Dobutamine
  196. 196What is dobutamine used for?To treat heart failure by mediating cardiac stimulation
  197. 197What is an example of a beta 2 agonist?Salbutamol
  198. 198What is salbutamol used for?To treat asthma causing bronchial smooth muscle relaxation
  199. 199what type of agonist is clenbuterol?beta 2 and beta 3 agonist
  200. 200what is clenbuterol used for?to treat asthma and increase muscle bulk in athletes

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Pharmacology Flashcards on Pharmacology 2, created by GEORGIA SMITH on 11/05/2017.
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GEORGIA SMITH
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