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Ultimate Sadness > Chapter 2: Basic Science Concepts > Flashcards

Chapter 2: Basic Science Concepts Flashcards

1
Q

Definition: substrate (ligand)

A

a substance that creates a signal or produces an effect by binding to a receptor, enzyme or transporter

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2
Q

Definition: endogenous

A

a substance that is produced by the body

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3
Q

Definition: exogenous

A

a substance that is produced outside of the body

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4
Q

Definition: agonist

A

a substance that combines with a receptor to initiate a reaction

can be endogenous or exogenous

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5
Q

Definition: antagonist

A

a substance that reduces or blocks a reaction

can be exogenous or endogenous

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6
Q

Definition: induction

A

when a substance iincreases the activity of an ezyme

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7
Q

Definition: inhibition

A

when a substnace decreases or blockss the activiity of an enzyme

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8
Q

central nervous system

A
  • includes brain and spinal cord
  • controls rest of body by sending signals to peripheral nervous system
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9
Q

2 main systmes of the peripheral nervous system

A
  • somatic: voluntary movememnt
  • autonomic: involuntary body functions (digestion, CO, BP)
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10
Q
A
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11
Q

neurotransmitters

A
  • body’s chemical messengers
  • released from presynaptic neurons into synaptic cleft to be picked up by post synaptic neurons
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12
Q

common neurotransmitters (5)

A
  • acetylcholine (ACh)
  • epinephrine (epi)
  • norepinephrine (NE)
  • dopamine (DA)
  • serotonin (5HT)
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13
Q

primary neurotransimitter involved in somatic NS

A

ACh: it binds to nicotinic receptors (Nn) in skeletal muscles

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14
Q

main divisions of autonomic nervous system

A
  • parasympathetic: “rest and digest”, releases ACh which binds to muscarinic receptors → SLUDD (Salivation, Lacrimation, Urination, Defecation, Digestion)
  • sympathetic: “fight or flight”, releases epi and NE which act on adrenergic receptors → increased BP, HR, bronchodilation (+ opposite of SLUDD)
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15
Q

Adrenergc receptors

A
  • alpha1
  • beta1
  • beta2
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16
Q

Definition: competitive inhibition

A

when an antagonnist binds to the same active site of a receptor as the endogenous substrate → prevent endogeous from binding

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17
Q

Definition: non-competitive inhibition

A

when the antagonist binds to the receptor a t asite other than the activve site (allosteric site) → changes shape of active site and prevent endogenous substrate from binding

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18
Q

ACh receptor(s)

A
  • muscarniic
  • nicotonic
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19
Q

Epi receptor(s)

A
  • alpha 1 (peripheral action)
  • alpha 2 (CNS action)
  • beta 1 (heart)
  • beta 2 (lungs)
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20
Q

NE receptor(s)

A
  • alpha 1 (peripheral action)
  • alpha 2 (CNS action)
  • beta 1 (heart)
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21
Q

DA receptor(s)

A

dopamine

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22
Q

5HT receptor(s)

A

5HT

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23
Q

muscarinic receptor
- agonist action
- drug agonists

A

increase in SLUDD
- salivation
- lacrimation
- urination
- defecation
- digestion

  • pilocarpine
  • bethanechol
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24
Q

muscarinic receptor
- antagonist action
- drug antagonists

A

decrease in SLUDD
- salivation
- lacrimation
- urination
- defecation
- digestion

  • atropine
  • oxybutinin
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25
Q

nicotonic receptor
- agonist action
- drug agnoists

A

increase HR and BP

nicotine

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26
Q

nicotinic receptor
- antagonist action
- drug antagonsits

A

neuromuscular blockade

NMBs (rocuronium)

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27
Q

alpha 1 receptor
- agonist action
- drug agonists

A
  • smooth muscle vasoconstirction
  • increased BP

  • phenylephrine
  • dopamine (dose dependent)
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28
Q

alpha 1 receptor
- antagonist action
- drug antags

A
  • smooth muscle vasodlation
  • decreased BP

alpha 1 blockers (doxazosin, carvedilol, phentolamine)

29
Q

alpha 2 receptor
- agonist action
- drug agonists

A
  • decreased release of epi and NE
  • decreased BP and HR

  • clonidine
  • brimonidine
30
Q

beta 1 receptor
- agonist action
- drug agonists

A
  • increased myocardial contractility
  • increased CO and HR

  • dobutamine
  • isoproterneol
  • dopamine (dose dependent)
30
Q

alpha 2 receptor
- antag actions
- drug antags

A

increased BP and HR

  • ergot alkaloids
  • yohimbine
31
Q

beta 1 receptor
- antag actions
- drug antags

A

decreased CO and HR

  • beta 1 selective blockers (metoprolol)
  • beta 1 non-selective blockers (propranolol, carvedilol)
32
Q

beta 2 receptor
- agoist action
- drug agonist

A

bronchodilation

  • albuterol
  • terbutaline
  • isoproterenol
33
Q

beta 2 receptor
- antag actions
- drug antags

A

bronchoconstriction

nonselective beta blockers: propranolol, carvedilol

34
Q

dopamine receptor
- agonist actions
- drug agonists

A

renal, cardiac, and CNS effects

  • levodopa
  • pramipexole
35
Q

dopamine receptor
- antag actions
- drug antags

A

renal, CNS, cardiac effects

  • many first gen antipsychotics (haloperidol)
  • metoclopramide
36
Q

serotonin receptor
- agonsit action
- durg agonists

A

platelet, GI, and psych effects

triptans (sumatriptan)

37
Q

serotonin receptor
- antag actions
- drug antags

A

platelet, GI and psych effects

  • ondansetron
  • second gen antipsychotics (quetiapine)
38
Q

Definition: enzyme

A

compound that speeds up (catalyzes) a reactoin

39
Q

acetylcholinesterase endogenous effect

A

break down ACh

40
Q

drugs that target acetylcholinesterase (and their action)

A

acetylcholinesterase inhibitors: donepezil, rivastigmine, galantamine

block acetylcholinesterase → increased ACh levels

41
Q

drugs that target angiotensin converting enzyme (and their action)

A

ACE inhibitors: lisinopril, ramipril

inhibit production of angiotensin II → decreased vasoconstriction and decreased aldosterone secretion

42
Q

angiotensin converting enzyme endogenous effects

A

convert angiotensin I to II

43
Q

Catechol-O-mathyltransferase endogenous effects

A

breaks down levodopa

44
Q

cyclooxygenase endogenous effects

A

convert arachidonic acid to
- prostaglandins (inflammmation)
- thromboxane A2 (plt aggregation)

45
Q

monoamine oxidase endogenous effects

A

break down catecholamines (DA, NE, epi, 5-HT)

46
Q

phosphodiesterase endogenous effects

A

break down cyclic guanosine monophosphate (cGMP)

47
Q

vitamin K epoxide reductase endogenous effects

A

convert vitK to active form (required for production of selective clotting factors)

48
Q

xanthine oxidase endgoenous effects

A

break down hypoxanthine into xanthine and then xanthine into uric acid

49
Q

drugs that target catechol-O-methyltransferase (and their action)

A

COMT inhibitor: entacapone

break down COMT enzyme → prevent peripheral breakdown of levodopa → increase duration of action of levodopa

50
Q
A
51
Q

drugs that target cyclooxygenase (and their action)

A

NSAIDs (asa, ibuprofen)

block COX enzymes → decrease prostaglandins and thromboxane A 2

52
Q

drugs that target monoamine oxidase (and their action0

A

MAOi:
- phenelzine
- isocarboxazid
- tranylcypromine
- selegiline
- rasagiline

block MAO → increase catecholamine levels (too high though and you get HTN crisis or serotonin syndrome)

53
Q

drugs that target phosphodisterase (and their action)

A

PDE-5 inhibitors: sildenafil, tadalafil

comeptitively bind to same active site as cGMP on PDE-5 → prevent breakdown of cGMP → prolong smooth muscle relxation

54
Q

drugs that target vitamin K epoxide reductase (and their action)

A

warfarin

block vitK epoxide reductase ezyme → reduce production of clotting factors II, VII, IX, and X

55
Q

drugs that target xanthine oxidase (and their action)

A

xanthine oxidase inhibitor: allopurinol

block xanthine oxidase enzyme → decrease uric acid production

56
Q

how may a MAOI contribute to hypertesnive crisis

A
  • MAOI: block breakdown of epi and NE
  • addition of other drugs/foods that increase catecholamines can lead to excess → HTN crisis

HTN crisis: HTN, tachycardia, agitation, death

57
Q

how may a MAOI contribute to serotonin syndrome

A
  • MAOI: block breakdwon of 5-HT
  • additiion of other durgs that increase 5-HT can lead to serotonin syndrome
58
Q

serotonin syndrome s/s

A
  • tremor
  • akathisia
  • clonus
  • hyperthermia, sweating
59
Q

Definition: stability

A

extent to whcih a product retains, within specified liits, and throught its period of storage and use, the same properites and characteristics it possessed at the time it was made

60
Q

reactions that cause drug degradation

A
  • oxidation-reduction
  • hydrolysis
  • photolysis
61
Q

Definition: oxidation and reduction

A

oxidation: compound loses electrons
- catalyzed by heat, light, and metal ions
- produces free radicals → can lead to oxidation chain reaction

reduction: compound gains electrons

62
Q

Definition: re-dox reaction

A

when one compound is oxidized and another reduced in the same reaction

63
Q

drugs that are most likely to oxidize contain what molecular structure

A

hydroxyl group directly bound to an aromatic ring

epinephrine, phenylephrine

64
Q

how to protect drug from oxidation

A
  • light protection: amber glass
  • temperature control
  • antioxidants (inhibit free radicals): VitC and vit E
  • chelating agetns (binds to catalyst → prevent reaction): common chelators have the letters ED
  • pH control: buffer
65
Q

Definition: hydrolysis

A

when water causes cleavage of a bond in a molecule

66
Q

functional groups most susceptible to hydrolysis

A
  • esters
  • amides
  • lactams
67
Q

how to protect a drug from hydrolysis

A

protect form moisture
- adsorbents (dessicants): absorb moisture that enters container
- lyophilized powders: store drug as powder and reconstitute when dispensing to reduce risk of hydrolysis
- hygroscopic salt (water absorbing salt): use salt form of a drug that is less hygroscopic
- light protection
- chelating agents
- temp control
- pH control

68
Q

Definition: photolysis

A

breakage of covalent bonds due to UV light expsure

Ultimate Sadness (13 decks)

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