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ICPP correction > ICPP correction fc > Flashcards

ICPP correction fc Flashcards

1
Q

which adrenoreceptors are present in the heart + lungs?

A

1 heart + 2 lungs pneumonic
heart = beta-1
lungs = beta-2

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2
Q

what happens in phase I of drug metabolism (removal)?

A

phase 1 enzymes (CYP450s) catalyse REDOX, dealkylation and hydroxylation reactions
CYP450s are generalists - metabolise wide range of metabolites

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3
Q

what happens in phase II of drug metabolism?

A

phase II enzymes (cystolic enzymes) enhibit more rapid kinetics than CYP450s
phase ii metabolised drugs increases ionic charge enhancing renal elimination

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4
Q

how many transmembrane domains do GPCR have?

A

7

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5
Q

What are the differences in function between Gi, Gq and Gs G coupled proteins?

A

Gq - stimulates phospholypase C
Gs - stimulates adenyl cyclase
Gi - inhibits adenyl cyclase

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6
Q

What is the correlation between potency and EC50?

A

EC50 is irreversibly proportional to potency

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7
Q

What is the relative refractory period of an action potential?

A

The relative refractory period is the time in which some of the Na+ channels are inactivated, and some are in a closed state

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8
Q

what are the different routes of drug administration?

A

OI IT IS SIR
1. oral
2. intravenous
3. intramuscular
4. transdermal
5. intranasal
6. sublingual
7. subcutaneous
8. inhalation
9. rectal

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9
Q

what are the different physiological and physiochemical factors which affect drug absorption in the gut?

A

physiological:
* blood flow
* GI motility
* food/pH

physiochemical:
* density of SCL e.g. OATs or OCT
* surface area
* drug pKa or liphophilicity

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10
Q

what are the 2 major categories of drugs which passively diffuse into GI capillaries?

A

weak acid / bases
lipophilic drugs

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11
Q

where does first pass metabolism take place?

A

gut lumen by enzymes
gut wall epithelia by phase I + II enzymes
liver by phase I + II enzymes

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12
Q

what are the different capillary types based on their permeability and where are they located?

A
  1. continuous - CNS, muscle
  2. fenestrated - intestine, kidney
  3. sinusoid - liver, bone marrow
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13
Q

how do phase I + II enzymes metabolise drugs?

A

Increase ionic charge by:
Phase I = modify existing side groups by REDOX dealkylation and hydroxylation
Phase II = add larger charged groups by conjigation

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14
Q

what are the three primary processes by which drug is excreted / moved in the kidneys?

A

glomerular filtration
active tubular secretion
passive tubular reabsorption

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15
Q

what are the 4 different biological solutes in order of permeability?

A

hydrophobic molecules
small uncharged polar molecules
large polar molecules
inorganic/organic ions

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16
Q

what properties of lipids affect their lipid membrane permeability?

A

relative electrical charge (greatest influence)
molecular weight or size

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17
Q

what is the difference between pores and ion channels?

A

pores = always opened
ion channels = open when signal is applied

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18
Q

what are the two types of signals which activate ion channels?

A

voltage or ligand gated

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19
Q

how do ion channels and carrier transporters differ in function?

A

gated ion channels are open and carry current as long as signal is present
carrier transporters undergo series of conformational changes to transport solute across the membrane

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20
Q

what are the different transporters involved in transporting glucose into and out of intestinal epithelial cells?

A

into: SGLT1 on apical surface transports 2 Na+ and 1 glucose into cell
out: GLUT2 on basaolateral surface transports glucose into blood
(Na+/K+ATPase also is involved to regulate Na+)

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21
Q

what energy source does SGLT1 use to transport glucose into epithelial cell?

A

symporter + secondary active transporter - uses electrochemical gradient of Na+ to drive glucose into cell

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22
Q

what energy source does GLUT2 use to drive glucose out of cell into blood?

A

uniporter + facilitated diffusion - uses concentration gradient between epithelial cells and capillaries of hepatic portal vein

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23
Q

what makes SGLT1 so efficient?

A

uses 2 Na+ to transport 1 glucose against its gradient

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24
Q
  1. what is the target location of the antidiabetic drug dapagliflozin?
  2. what is the action of this drug?
  3. what is its energy source?
  4. how does this drug decrease glucose concentration?
A
  1. acts in early proximal tubule of nephron to inhibit SGLT2 Na+/glucose symporter
  2. acts as an allosteric non-competitive inhibitor
  3. electrochemical gradient for Na+
  4. glucose is not taken back up into epithelia and is excreeted in urine
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25
Q

which glucose transporters are involved in the transport of glucose across the blood brain barrier?

A

GLUT1 across capillary wall
GLUT3 acroos the neuronal membrane

26
Q

how does insulin lead to an increase in glucose uptake into adipose tissue?

A
  1. insulin binds to tyrosine kinase receptor
  2. active dimer forms
  3. bound kinase receptor triggers cytoplasmic phosphorylation signalling cascade
  4. GLUT4 receptors stored in cytoplasmic secretory vesicles fuse with membrane
  5. increased num of GLUT4 increases glucose uptake into adipose tissue
  6. glucose is converted to G-6-P then glycogen
27
Q

which transporter is responsible for preventing a decrease in cytoplasmic pH?

A

Na+/H+ exchanger
* charge transfer is 1:1 so has no effect on membrane potential
* a type of secondary active transporter so uses electrochemical gradient for Na+

28
Q

which transporter is responsible for preventing a increase in cytoplasmic pH?

A

AE2 transporter
* transports HCO3- outwards + exchanging it for a Cl- ion

29
Q

where in the nephron are OATs found?

A

proximal collecting tubule

30
Q
  1. what is the typical resitng membrane potential in neurones?
  2. what is the typical resting membrane potential in cardiac myocytes?
  3. what is the typical resting membrane potential in skeletal muscle myocytes?
  4. what is the resting membrane potential in smooth muscle cells?
A
  1. -70mV
  2. -80 to -85mV
  3. -90mV
  4. -50mV
31
Q

what effect does depolarisation + hyperpolarisation have on smooth muscle cells?

A

depolarisation = contraction
hyperpolarisation = relaxation

32
Q

what effect does GABA have on membrane potential?

A

agonist for GABAa receptors
when it binds it opens the channel and allows Cl- currents which hyperpolarises the membrane potential

33
Q

why is the resting membrane potential negative relative to the outside of the cell?

A

movement of potassium outwards leaves behind large impermeant anions that results in a nett negative potential

34
Q

what limits the effect of GABA on the synapse?

A

re uptake of Na+ coupled GABA transporters back across into releasing neurone

35
Q

in VGSC + VGPC the 4th transmembrane segment has a special role, what is this role?

A

act as voltage sensors
* contains lost of +vely charged amino acid residues that are sensitive to local changes in electric field

36
Q

in a VGSC, what is the loop that connects the repeats 3 + 4 of the α subunit?

A

inactivation particle - prevents further inward current flow of Na+
rapid inactivation + activation of the sequence gives rise to the distinct spike in AP

37
Q

what is the absolute refractory period?

A

period immediately following an action potential during which it is impossible to fire another AP no matter how strong the stimulus (approx 1ms)
this is because once the VGSC has been inactivated it must be fully closed before it can fire another AP

38
Q

what is the relative refractory period?

A

follows from the absolute refractory period, nerve fibre can fire an action potential it just needs a stronger stimulus to do so
the opening of VGPC opens + causes hyperpolarisation

39
Q

what effect does myelination have on an axon?

A

increases resitance and reduces capacitance

40
Q

what is the relation between velocity + fibre diameter in a myelinated vs unmyelinated axon?

A

myelinated: velocity is proportional to fibre diameter
unmyelinated: velocity is proportional to square root of fibre diameter

41
Q

what are the 2 types of neuromuscular relaxants used in surgery?

A

depolarising blockers = act as competitive agonists at the nAChR receptors, result in prolonged depolarisation that keeps VGSC in inactivated state (e.g. succinyl choline)
non-depolarising blockers = act as competitive anatagonists and block the action of ACh (e.g. vecuronium)

42
Q

what is the primary inhibitory neurotransmitter in the CNS and spinal column?

A

CNS = GABA
spinal column = glycine

43
Q

A patient with epilepsy is prescribed Lamotrigine by her neurologist. Which of the following best describes the pharmacological action of Lamotrigine within the CNS?

A

It prolongs the duration of the VGSC in the in activated state

44
Q

Both GPCRs and the Receptor Type that Insulin acts on, share a feature with regards the scale and efficiency of how the intracellular signal propagates. What is this sahred feature?

A

amplification of original signal - few molecules can have a much larger response

45
Q

what 2 features increase sensitivity of target cells to allow drugs to act at lower concentrations?

A

spare receptors - increases chance of binding with a receptor or target protein
amplification - few molecules can have a huge effect

46
Q

what shift will be seen on a response - [agonist] graph to indicate an agonist with higher potency?

A

shift to the left

47
Q

what shift will be seen on a response - [agonist] graph to indicate an agonist with higher potency?

A

shift to the left

48
Q

what shift will be seen on a response - [antagonist] graph to indicate an increasing [anatagonist]?

A

shift to the right
eventually the maximal response will also decrease since there are no spare receptors

49
Q

what is efficacy or Emax of a drug?

A

max physiological or biological response achievable from a drug within a particular cell or tissue in body

50
Q

what is EC50 of a drug?

A

The concentration of drug that elicits half the maximal physiological or biological response of a full agonist.

51
Q

what is intrinsic efficacy of a drug?

A

measure of how effective a drug or ligand is in inducing the active conformation of the target protein.
competitive antagonist = 0%
full agonist = 100%
partial agonist = 0 - 100%

52
Q

what is Kd of a drug?

A

dissociation constant for the binding of a ligand to a receptor – it is 50% of Bmax
lower Kd = higher affinity

53
Q

what is potency of a drug?

A

The dose of drug required to produce a specific effect of given intensity (usually the EC50) as compared to a standard reference

54
Q

what causes SLUDGE symptoms and how is it treated?

A

caused by: drug overdose, ingestion magic mushrooms or insecticides
treated with: atropine or pralidoxine

55
Q

what is enteral vs paraenteral drug administration?

A

enteral - delivered through GI tract
paraenteral - delivered through routes other than the GI tract

56
Q

decreased activity of what enzyme can make codeine ineffective?

A

CYP2D6

57
Q

what change in composition can increase fluidity of bacterial membrane?

A

more cis-double bonds

58
Q

what effect does increased M2 muscarinic receptors have?

A

couple to Gαi receptor which decreases adenyl cyclase which decreases cAMP which decreases PKA

59
Q

what is the main inhibitory neurotransmitter in the brain?

A

GABA

60
Q

how do parasympathetic and sympathetic neurones differ in terms of myelination and length?

A

parasympathetic: pre-ganglionic neurones are long + myelinated but post-ganglionic neurones are short + unmyelinated
sympathetic - pre-ganglionic neurones are short + unmyelinated but post-ganglionic neurones are long + myelinated

ICPP correction (1 decks)

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