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year 1 foundations > biochemical basis > Flashcards

biochemical basis Flashcards

1
Q

what is an example of reversible competitive antagonist?

A

propranolol

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2
Q

what is example of irreversible antagonist?

A

aspirin

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3
Q

what are the 4 super-families of receptors?

A
  1. ligand-gated ion channel
  2. G-protein coupled receptors
  3. kinase-linked receptors
  4. nuclear receptors
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4
Q

what are ligand-gated ion channels?

A

super efficient signalling systems
- ion channel opens and allows ions to move in/out of cell
- hyperpolarisation and depolarisation
- neurotransmitters bind to the channel that changes conformation to open

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5
Q

what is an example of ligand-gated ion channels?

A

nicotonic & ACh receptor
(nicotine acetyl choline receptor = permeable to Na+. K+. Ca2+ = non-specific = modulate fast synaptic excitation)
-> through cholinergic synapse

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6
Q

what is positive of ligand-gated ion channels in comparison to other receptor classes?

A

time scale!
- takes milliseconds for ligand-gated ion channels (G-protein coupled takes seconds and kinase-linked & nuclear receptors take hours)

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7
Q

what is G-protein coupled receptor?

A

membrane-bound receptors that then have downstream action

G -proteins interact with other molecules, 2 categories:
- adjacent enzymes - activate or inhibit - the enzymes would evoke second cascade which would lead to response
- adjacent ion channels, example/ beta-adrenoceptors, always activate certain molecules

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8
Q

what are G-proteins and how are they activated/inactivated?

A

proteins coupled to receptors in G-coupled receptors
- made of alpha, beta & gamma subunit
- when alpha binds to GDP - 3 subunits remain together & inactive
- when alpha binds to GTP- alpha subunit seperates from beta & gamma and is free to activate/inhibit other proteins

to inactivate again - alpha subunit consumes energy from GTP and turns it into GDP

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9
Q

what is process of alpha-1 adrenoceptor?

A

-catecholamine binds to adrenoceptor
- stimulates Gq to release GDP & bind to GTP, activating alpha Gq
-activated Gq activates phospholipase C (PLC)
- PLC cleaves PIP-2 to IP3 & DAG

IP3 = moves to ER and opens calcium channels, calcium moves into cytoplasm -> depolarisation

DAG = binds to PKC (which needs calcium to function) and PKC phosphorylates & activates proteins which triggers cellular response = MLCK activity(enzyme involved in the regulation of smooth muscle contraction) & vasoconstriction

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10
Q

how does 1 molecule make big response in G-protein coupled receptor?

A

signal amplification

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11
Q

what are the G proteins for each adrenoceptor?

A

alpha 1 = Gq
alpha 2 = Gi
beta 1, 3 & 3 = all Gs

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12
Q

(principal transduction = like the start bit of process)

what is principal transduction for the beta adrenoceptors?

A

they all have the same principal transduction
= G alpha s stimulates adenylyl cyclase which increases cyclic AMP

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13
Q

what is principal transduction of alpha adreno-ceptors?

A

alpha 1 = Gq activates phospholipase C which increases IP3 and DAG

alpha 2 = Gi inhibits adenylyl cyclase which decreases cAMP and calcium channels and increases K+ channels

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14
Q

what is physiological effect of alpha 1 adreno-ceptors?

A

vasoconstriction of blood vessels

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15
Q

what is physiological effect of alpha 2 adreno-ceptors?

A
  • presynaptic inhibition of noradrenaline
  • when in GI tract they can contribute to the inhibition of gastrointestinal motility and secretion (since digestion is not key for fight or flight response)
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16
Q

what is physiological effect of beta 1 adreno-ceptors?

A

increased heart rate & cardiac muscle contraction

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17
Q

what is physiological effect of beta 2 adreno-ceptors?

A

dilation of bronchi
- increased heart rate & cardiac muscle contraction (less than B1)
- also decreased gut motility

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18
Q

what is physiological effect of beta 3 adreno-ceptors?

A

thermogenesis in skeletal muscle, lipolysis

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19
Q

what affect does adrenaline have on adrenoceptors?

A

binds/activates all adrenoceptors
= full sympathetic physiological response

20
Q

what affect does isoprenaline have on adrenoceptors?

A

binds/activates beta 1 & 2 adrenoceptors
= tachycardia (big side effect)
= bronchodilation

21
Q

what affect does salbutamol have on adrenoceptors?

A

binds/activates beta 2 adrenoceptors
= bronchodilation
= desired therpeutic effect for asthma

22
Q

what is the process of alpha 2 adrenoceptors?

A
  • adrenaline etc bind and changes conformation of adrenoceptor
  • stimulates Gi to release GDP & bind to GTP, activating Gi
    -activated Gi inhibits adenylyl cyclase
  • negative feedback on effect of Gs which important for inactivation of un-important cells for fight or flight
  • also inhibits noradrnaline release -> relaxation of GI tract
    *G beta gamma (part of G protein) reacts with K+ channel

(beta 2 and alpha 2 both relax Gi tract, just through different mechanisms)

23
Q

what is process of beta receptors?

A
  • beta receptor coupled with Gs
  • binding of adrenaline etc changes conformation of adrenoceptor
  • stimulates Gs to release GDP & bind to GTP, activating Gs
  • activated Gs, activates adenyl cyclase which converts ATP to cAMP
  • cAMP moves through cytoplasm causing phosphorylation of PKA which inhibits MLCK activity
  • cellular response triggered = depens on what beta receptor
24
Q

what is salbutamol?

A
  • given as an inhaler, beta 2 adrenoceptor
  • it will phosphorylate PKA, cAMP = gives bronchodilation
25
Q

what is phosphodiesterase function?

A

terminates action of cAMP

26
Q

what is theophylline function?

A

phosphodiesterase inhibitor
- maintains bronchodilation as phosphodiesterase inactivates cAMP and cAMP needed for cascade of bronchodilation

27
Q

what is kinase-linked receptor general process?

A

-also called enzyme-coupled receptors
binding to receptor (cytokine receptor)
- protein phosphorylation
- gene transcription
- protein synthesis
- cellular effects

has MULTIPLE PARALLEL signalling pathways
(insulin= example)

28
Q

what is an example of kinase-binding receptor and what is process?

A

insulin receptor

  • insulin secreted after meal
  • results in cellular responses
  • tyrosine residues phosphorylated
  • ATP floating around and ATP drops off phosphate group at tyrosine
  • phosphorylates this part of protein that allows attachment of relay proteins to receptor = now ready to activate lots of different pathways like GLUT4 -> glucose enter cell
29
Q

what are the different cellular responses of insulin?

A

insulin receptor = kinase-linked receptor = multiple signalling pathways

  • recruitment of glucose transporters
  • increased formation of glycogen
  • increased formation of fat
  • changes in gene expression
  • decreased formation of glucose from glycogen
  • increased formation of protein
30
Q

what are nuclear receptors general process?

A

intra-cellular receptors that are generally bound by steroid hormones
- these receptors are protein monomers located in nucleus of target cell and contain DNA-binding domains that allow for control for gene transcription

31
Q

what type of molecule is for nuclear receptors?

A

agonist that can get into plasma membrane - must be very lipophillic
like steroid hormones (example - osetrogen)

32
Q

what process do steroid hormones initiate in nuclear receptors?

A

2-step process:

  1. Activated hormone-receptor complex forms within the cell
  2. The complex binds to DNA & activates specific genes ->Gene activation leads to production of key proteins
33
Q

what is structure of nuclear receptor?

A
  • part that binds to sterioid (agonist, signalling molecule)
  • part that binds to DNA
34
Q

what are examples of receptor molecules for nuclear receptors?

A
  • androgen, testosterone ligand
  • oestrogen
  • glucocorticoid
  • progesterone
  • mineralocorticoid, aldosterone ligand

all lipophillic so easily pass through membrane

35
Q

what is process of aldosterone hormone (mineralocorticoid)?

A
  • aldosterone promotes increase in ENaC(sodium channel) expression (by binding to receptor that changes gene expression) which increases sodium absorption therefore increasing blood pressure
  • aldosterone normally secreted in response to hyponatremia (where you get resistance to thiazides - which are used to lower arterial blood pressure by blocking sodium reabsorption)
36
Q

what is mechanism of action of ibuprofen?

A

has NSAID which inhibits COX-1 and COX-2 therefore decreases fever & gastric protection

*COX-2 converts arachidonic acid to prostaglandin E2 which leads to pain pyrexia (fever)
COX-1 converts arachidonic acid to prostanglandin G2 which leads to gastric protection

37
Q

what type of drug is ibuprofen?

A

non steroidal anti-inflammatory drug
- act’s at cyclooxegenase enzymes (COX)

38
Q

what is mechanism of action for amlodipine?

A

calcium channel blocker - which reduces cardiac contractibility, drugs interact with channels ->reduction in arterial blood pressure

39
Q

How is calcium involved in cardiac contractibility?

A

because Ca2+ involved in cardiac cell contraction and propagation of cardiac impulse - contraction of vascular smooth muscle cells requires influx via Ca2+ voltage-gated channels so increased Ca2+ which -> activation of myosin & actin -> muscle contraction

40
Q

what are SSRI’s?

A

selective serotonin re-uptake inhibitors
- anti-depressant drugs (inhibit re-uptake of serotonin so have more serotonin in body)

*you might think of amitryptyline - it works in similair way but amitryptyline is tricycline anti-depressant which is different family that is less common than SSRI’s as more side effects

41
Q

what are some examples of SSRI’s?

A
  • citalopram
  • escitalopram
  • fluoxetine
  • fluvoxamine
  • paroxetine
  • sertraline
42
Q

what is negative of SSRI’s?

A

lots of adverse side-effects

43
Q

what is sodium valproate an example of?

A

a drug that can have multiple mechanisms of action

44
Q

what is formoterol?

A

= beta blocker

  • commonly used as a maintenance medication for the long-term management of asthma and chronic obstructive pulmonary disease (COPD)
  • It is used to provide sustained bronchodilation and control of symptoms = it has higher potency than salbutamol
45
Q

what happens if taking sertraline & ibuprofen at the same time?

A

sertraline inhibits enzyme that metabolises ibuprofen so increasing plasma conc of ibuprofen which inhibits cox-1 which evokes GI side-effects

46
Q

what is relationship between Ki and affinity?

A
  • Ki = the concentration of a drug needed to occupy half of the available receptors
  • lower Ki indicates higher affinity but as pKi it means opposite since -ve so higher pKi indicates higher affinity

year 1 foundations (36 decks)

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