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PDA 2 > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

aspirin

A

Cox1 > Cox2 inhibitor

antipyretic/analgesic/anti-inflammatory

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2
Q

acetaminophen

A

COX2 inhibitor
metabolized to endogenous cannabinoid –>reduces pain signaling
antipyretic/analgesic
weak anti-inflammatory

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3
Q

naproxen

A

non specific COX inhibitor
NSAID
antipyretic/analgesic/anti-inflammatory

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4
Q

methyl salicylate

A

wintergreen oil, (bengay, icy hot)
counter irritant- stimulates pain receptors to elicit warming effect, “swamps out” pain impulses, metabolized to salicylic acid-ASA (COX inhibitor w/o binding to COX)

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5
Q

triethanolamine (trolamine) salicylate

A

metabolized to salicylate acid

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6
Q

menthol

A

cooling effect
counter irritant/analgesic
mild antimicrobial

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7
Q

capsaisin

A

vanilloid receptor (TRPV1) agonist that overwhelms nerves w/ a burning sensation to reduce pain transmission = counter irritant

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8
Q

hydrocortisone

A

topical corticosteroid

decreases inflammatory factors from immune cells

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9
Q

triamcinolone, betamethasone, fluticasone, mometasone

A

nasal/topical corticosteroid

decreases inflammatory factors from immune cells

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10
Q

ketotifen

A

H1 blocker- antihistamine

opthalmic

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11
Q

pheniramine

A

H1 blocker- antihistamine

ophthalmic, nasal

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12
Q

diphenhydramine and doxylamine

A

H1 blocker- antihistamine

CNS penetrating- sedating

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13
Q

cetirizine

A

H1 blocker- antihistamine

CNS penetrating- somewhat sedating

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14
Q

loratadine

A

H1 blocker- antihistamine

low CNS penetrating- non sedating

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15
Q

fexofenadine

A

H1 blocker- antihistamine

low CNS penetrating- non-sedating

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16
Q

MOA of H1 blockers

A

block H1 receptors in periphery
block H1 receptors in CNS=drowsiness
->decreases pruritis, flushing, vasodilation, vascular permeability, pain potentiation, swelling

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17
Q

Cromolyn

A

nasal inhaler
stabilizes mast cells that release inflammatory mediators
nasal spray and opthalmic

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18
Q

Dextromethorphan

A

antitussive, opioid like (l-isomer=potent opioid), blocks medullary cough center

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19
Q

Decongestants and MOA

A 
phenylephrine
pseudoephedrine
naphazoline
oxymetazoline
tetrahydrozoline

alpha1 agonists = vasoconstrict

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20
Q

Guaifenesin

A

expectorant-increases vol/reduces viscosity of bronchial secretions

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21
Q

Local anesthetics and MOA

A

lidocaine/Xylocaine
benzocaine
dyclonine

block pain neurotransmission through fast voltage gated sodium channels (VGSGs)

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22
Q

Neosporin

A

neomycin: gram - partial gram +
polymyxin B: gram -
bacitracin: gram +

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23
Q

Docosanol

A

(Abreva) antiviral

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24
Q

carbamide peroxide

A

oxidizing agent, broad spectrum antimicrobial

mouth sores, earwax removal, mild earaches

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25
Q

phenol

A

local anesthetic, antimicrobial

sore throat

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26
Q

permethrin

A

insecticide from chrysanthemum

lice treatment

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27
Q

terbinafine

A

athlete’s foot (tinea pedis)

ringworm (tinea corporis)

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28
Q

clotrimazole

A

athlete’s foot, ringworm, thrush, vaginal yeast infections

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29
Q

miconazole

A

athlete’s foot, ringworm, jock itch (tinea cruris) vaginal yeast infection

30
Q

zinc pyrithione

A

dandruff/psoriasis

31
Q

cetylpyridium

A

Cepacol

antiseptic

32
Q

H2 blockers and MOA

A

block H2 receptors in the parietal cells of stomach-reduce stomach acid
ranitidine, famotidine

33
Q

Proton Pump Inhibitors and MOA

A

block proton pump (H+/K+ATPase) on parietal cell to reduce gastric acid secretions
omeprazole

34
Q

Antacids and MOA

A

neutralize stomach acid

calcium, magnesium/aluminum hydroxide

35
Q

Anti-gas agent and MOA

A

anti-foaming agent that reduces the surface tension on gas bubbles, not systemically absorbed
symethicone

36
Q

Loperamide

A

opioid w/ no analgesic properties, acts on mu opioid receptors to reduce intestinal tone, normally low CNS penetration

37
Q

bismuth subsalicylate

A

bismuth has antibacterial activity

subsalicylate is a reivative of a salicyclic acid (ASA)

38
Q

Fiber

A

draws water into stool and adds bulk

39
Q

polyethylene glycol 3350

A

Miralax

osmotically draws water into stool

40
Q

bisacodyl

A

stimulates bowel movement/local irritation

41
Q

senna

A

stimulate bowel movement/local irritation

42
Q

docustate

A

stool softener/surfactant that makes it easier to pass

43
Q

Benzoyl peroxide

A

peeling agent = increases skin turn over = reduces bacterial count

44
Q

salicyclic acid

A

peeling agent, antibacterial, lyses pimples

45
Q

Where are “fast” action potentials found in the heart?

A

atria
ventricles
Purkinje fibers
have all phases of cycle

46
Q

Where are “slow” action potentials found in the heart?

A

SA and AV node

responsible for automaticity, no phase 1 and no real phase 2

47
Q

During an effective refractory period…

A

time for voltage gated Na+ channels to go from “inactive” to “closed”
second AP can’t be generated

48
Q

During a relative refractory period…

A

some of the Na+ channels are back to “closed”

a second AP can be generated but at a much greater depolarization than normal

49
Q

Parasympathetic effect on the SA and AV nodes

A 
decreases Ca++ channels
activates K+ channels
decreases 
I-f currents
decreases 
slow APs
decreases HR
50
Q

Sympathetic effect on SA and AV nodes

A

increases Ca++ currents

increases HR

51
Q

ibuprofen

A

non-selective COX inhibitor, NSAID

antipyretic, analgesic, anti-inflammatory

52
Q

glucocorticoid/corticosteroid MOA

A

acts on GR (transcription factor) affects a panel of genes, decreases release of pro-inflammatory cytokines, at higher doses, can inhibit the growth of immune cells

53
Q

Electrical system in the heart flow

A

impulse generated in SA node
spreads through atria via gap junctions
AP depolarize AV node then goes to Bundle of His
Impulse then travels down bundle branches
at apex impulse spreads through Purkinje fibers and up ventricle, depolarizing

54
Q

ECG: P wave

A

atrial depolarization

55
Q

ECG: QRS complex

A

ventricle depolarization

56
Q

ECG: T wave

A

ventricle repolarization

57
Q

In general what is after depolarization (ADP) arrhythmia?

A

activity coupled with previous AP

58
Q

Early ADPs

A

depolarizations occur in phase 3 (can be due to prolonged phase 3 or low HR)

59
Q

Delayed ADPs

A

depolarizations in phase 4

can be due to increased [Ca++]/HR

60
Q

Impulse conduction block

A

abnormal conduction through AV node, bundle of His or bundle branch

61
Q

Impulse re-entry

A

impulse re-enters and excites an area twice, can be due to abnormal anatomy (Wolf-Parkinson White) or damage to cardiac tissue

62
Q

Vaughn-Williams Classification: Type IA

A

MEDIUM affinity for Na+ channels

Bind/block pore of Na+ channel and block it

63
Q

Heart effects of Vaughn-Williams Classification: Type IA

A

decreased conduction velocity
increased refractoriness
decreased automaticity through Na+ channels
prolongs QT interval- can cause Torsades de Pointes

64
Q

Vaughn-Williams Classification: Type IB

A

low affinity for Na+ channel-rapid on/off of drug channel

increases effect on depolarized tissue, little effect on normal tissue

65
Q

Vaughn-Williams Classification: Type IC

A

HIGH affinity for Na+ channels-slow on/off of drug on channel
decreased conduction, little effect on refractoriness
block K+ channels

66
Q

ADRs of Type IC

A

very arrhythmogenic, particularly in damaged hearts b/c of high affinity

67
Q

Vaughn-Williams Classification: Type II

A

Decreases sympathetic effects on Ca++ channels
in SA»AV node and in re-entry circuits
supress exercise induced tachycardia
can slow ventricular response to AFIB

68
Q

Vaughn-Williams Classification: Type III

A

delayed rectifier K+ channel blockers

69
Q

Drugs for Type IA

A

procainamide, disopyramide, quinidine (blocks K+ channels)

70
Q

Drugs for Type IB

A

lidocaine

71
Q

Drucs for Type IC

A

propafenone, flecainide

72
Q

Drugs for Type II

A

Beta blockers- propranolol, metoprolol, esmolol

PDA 2 (3 decks)

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