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MSII Unit II > Pharm II > Flashcards

Pharm II Flashcards

1
Q

M2/M4/alpha2 receptor couples to __ and cause ___?

A

Gi/decrease in cAMP or hyperpolarization

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2
Q

M1/M3/M5/alpha1 receptor couples to ___ and cause ___?

A

Gq/increase DAG and IP3

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3
Q

Beta1/2/3 receptor couples to ___ and cause ___?

A

Gs/increase in AC and increase in cAMP

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4
Q

What is autoreceptor?

A

Presynaptic receptor that response to the NT released/usually inhibitory

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5
Q

What is heteroreceptor?

A

Presynaptic receptor that response to the NT other than the one released

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6
Q

What is the normal state of Fe in hemoglobin?

A

Ferrous 2+

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7
Q

What is the route of CO’s absorption and excretion?

A

Respiration

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8
Q

How do we know if it methylene chloride that is causing the CO poisoning?

A

CO levels rises after removal from the source

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9
Q

What is carboxyhemoglobin?

A

CO + hemoglobin

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10
Q

Carboxyhemoglobin shifts the O2 dissociation curve to the ___?

A

Left

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11
Q

Does the level of carboxyhemoglobin cause all the toxic effect of CO poisoning?

A

No

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12
Q

Which enzyme in mitochondria does CO binds to?

A

Cytochrome oxidase—>inhibit cellular respiration

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13
Q

How is peroxynitrites form?

A

CO displaces nitric oxide from platelets—>free radical damage

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14
Q

What are some severe CO acute clinical findings?

A

Coma/seizures/HoTN/MI

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15
Q

What does the CO late effect cause?

A

Neurologic effects from lipid peroxidation

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16
Q

The __ you are the higher risk for delayed neurologic effect of CO

A

Older

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17
Q

What is O2 saturation for CO poisoning?

A

Falsely normal for pulse oximetry

Co-oximeter for arterial blood gas is appropriate (if use old blood gas machine then it is falsely normal)

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18
Q

How to treat CO poisoning?

A

Give O2 to shorten CO half life/hyperbaric (2.8 atm)—>shorten CO half life and prevent lipid peroxidation

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19
Q

When do we give HBO?

A

LOC/GCS

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20
Q

What do we see on the brain MRI for delayed neurological effect of CO?

A

Bilaterally low density areas of the globus pallidus

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21
Q

Why is there an increase of lactate (>10mmol/L) in cyanide poisoning?

A

CN binds to cytochrome A3—>no ATP—>lactate level goes up

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22
Q

Why do we use nitrite (e.g. sodium nitrite) for CN poisoning?

A

Nitrite convert hemoglobin to methemoglobin (Fe 3+)—>CN prefer Fe3+ therefore ditch cyt A3 to bind with methemo—>forms cyanometHb—>don’t bind O2, better than no ATP

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23
Q

What role does thiosulfate play in CN poisoning?

A

enhance normal metabolism of CN

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24
Q

Why can’t we use nitrite for CN AND CO poisoning?

A

MetHb further lowers O2 carrying capacity

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25
Q

What does H2S gas do?

A

Similar to CN but its binding is reversible

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26
Q

What is hyroxycobalamin?

A

Bind to CN and form cyanocobalamin (vitamin B12)—>also increase BP a bit—>usually used with thiosulfate

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27
Q

How many antidote do we use for CN crystal poisoning?

A

Nitrite/thiosulfate/hydroxycobalamin

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28
Q

Sign of MetHb poisoning?

A

O2 doesn’t help/pulse oximetry is falsely lower/co-oximeter is appropriate

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29
Q

What is the antidote for methemoglobinemia?

A

Methylene blue

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30
Q

What is the mechanism of methylene blue?

A

Cofactor for NADPH reductase (reduce MetHb to normal)—>gain e- from NADPH—>give it to MetHb

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31
Q

Why pt with G6PD deficiency does not respond to methylene blue?

A

G6PD is needed to convert methylene blue back to the reduced form (working form)

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32
Q

What is sulfHb?

A

Sulfer + Hb—>can’t carry O2—>similar to MetHb

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33
Q

How to distinguish sulfHb/MetHb?

A

Give pt CN—>if CN levels drops then it is MetHb

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34
Q

Bronchoconstriction is driven by M_ receptor?

A

M3

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35
Q

What are the 2 kinds of cholinoceptor stimulants?

A

Direct and indirect (inhibit acetylcholinesterase)

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36
Q

What are the features of Bethanechol?

A

Muscarinic selective/stable/relieve urinary paralysis after surgery/poorly absorbed by CNS because of quaternary ammonium group

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37
Q

Which muscarinic receptor mediate the production of EDRF (endothelial derived relaxing factor)?

A

M3 on endothelial cell—>NO—>cGMP—>decrease Ca2+—>vasodilate

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38
Q

How does the indirect acting carbamate drugs inhibit cholinesterase?

A

By covalent bond to the enzyme and temporarily occupy it (takes a while for it to be hydrolyzed)

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39
Q

How does the indirect acting non-ester drugs inhibit cholinesterase?

A

Bind to the enzyme as long as it is not metabolized

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40
Q

How does the indirect acting organophosphate drugs inhibit cholinesterase?

A

Irreversibly inactivate the enzyme

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41
Q

What does pralidoxime do?

A

Reverse the damage done by the organophosphate drugs—>regenerate cholinesterase (can’t regenerate the enzymes that have gone through aging process—>can’t bring the enzyme level back to 100%)

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42
Q

What happens if you give too much cholinesterase inhibitors to a pt?

A

Muscle strength would go up and then paralysis (for both healthy and Myasthenia gravis pt)—>edrophonium (short lived) is used to determine under or overdosing

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43
Q

What is SLUDGE (too much ACh activation)?

A

Salivation/lacrimation/urination/defecation/GI distress/emesis

44
Q

What is atropine?

A

ACh analog—>competitively inhibit muscarinic receptor

45
Q

Why used tropicamide instead of atropine to dilate your pupils?

A

Tropicamide has a shorter half life

46
Q

What do we use for overdose of direct acting muscarinic agonist?

A

Atropine

47
Q

What do we use for overdose of indirect acting muscarinic agonist?

A

Atropine and pralidoxime

48
Q

Which receptors are most sensitive to atropine?

A

autoreceptor in the heart (react to low dose of atropine)

49
Q

How to treat children with atropine overdose (atropine fever)?

A

Treat symptoms rather than using AChE inhibitor

50
Q

What is the similarity between Succinylcholine and Mivacurium?

A

Both short lived

51
Q

Cholinesteras inhibitor can reverse the effect of non or depolarizing NMJ blocker?

A

Nondepolarizing blocker (since it was competitively inhibited)

52
Q

Malaria enters the body and goes to __ first?

A

Liver

53
Q

Primaquine induce anemia in pt with ___ deficiency?

A

G6PD

54
Q

P. malariae/knowlesi does not have any resist to ___

A

Chloroquine

55
Q

Use ___ for falciparum/malariae/knowlesi

A

Chloroquine

56
Q

Use ___ for vivax/ovale

A

Chloroquine + primaquine (prevent relapse)

57
Q

For chloroquine resist falciparum, use ____

A

Atovaquone + proguanil (chloroguanide)

58
Q

For chloroquine resist vivax, use ____

A

Quinine + doxy or tetra + primaquine

59
Q

What is the rate limiting layer of the skin for percutaneous absorption?

A

Corneum through con. gradient

60
Q

Topical drug is absorbed via ___?

A

Passive diffusion

61
Q

2 factors that can enhance percutaneous absorption?

A

Hydration/skin disease (eczema)/some disease might hinder like ichthyosis vulgaris

62
Q

What are the 3 categories of vehicles and their examples?

A

Monophasic: powder/oil/liquid
Biphasic: lotion (powder + liquid)/paste (ointment + powder/cream (oil + liquid)

63
Q

Features of powder?

A

absorb moisture and reduce friction/can increase friction if clumped

64
Q

Features of gels?

A

Liquid that is converted into semisolid/used in hairy areas

65
Q

2 way to prepare cream?

A

Oil in water (evaporate/drying)/water in oil

66
Q

Features of ointment?

A

Little to no water

67
Q

Risk of class I topical steroid?

A

Can cause steroid atrophy (decreased collagen)/cause glaucoma if applied near the eye

68
Q

What is occlusion for dermatology?

A

Wear something over the topical medication to drive it into the skin

69
Q

Systemic affect of topical steroid is?

A

Suppression of hypothalamic-pituitary-adrenal axis

70
Q

What kind of UV light is used for psoriasis treatment?

A

UVA and UVB (UVC is absorbed by the ozone layer)

71
Q

Long term treatment of UVA leads to ___?

A

Skin cancer

72
Q

What does the UV light do treating psoriasis?

A

Immune suppress (for inflammatory conditions)

73
Q

Why is psoralens (naturally in lime) used with UV light?

A

Enhance absorption

74
Q

Can medication be photosensitizing?

A

Yes

75
Q

What does sunscreen do and what is SPF

A

Scatter and absorb UV rays/for example: it takes 2 hours for you to get red in the sun, SPF 15 will take 2x15=30 hours for you to get red

76
Q

How often should you reapply sunscreen?

A

around 2 hours

77
Q

Does sunscreen prevent you from getting Vitamin D?

A

Yes

78
Q

Why use MTX for psoriasis?

A

Psoriasis: increase skin cell turn over
MTX: inhibit cell growth

79
Q

What percentage of MTX is bound to plasma protein?

A

50%

80
Q

Psoriasis is a ___ disease

A

Systemic

81
Q

Side effects for biologic treatment (DMARD/TNF alpa inhibitor and what not)?

A

Risk of infection/site reaction/unmasking neurologic diseases

82
Q

Don’t use MTX for psoriasis if the pt has?

A

Liver/GI/want babies/pulmonary diseases

83
Q

Don’t use UV for psoriasis if the pt has?

A

History of skin cancers

84
Q

What does retinoid do for psoriasis?

A

Normalize epidermal differentiation

85
Q

Retinoid causes?

A

Fetal abnormality (don’t give to pregos)

86
Q

Phase of inflammatory responses?

A

Acute (increase capillary permeability)—>subacute (leukocytes infiltration)—>chronic (necrosis)

87
Q

What does histamine do?

A

Capillary dilation/increase post-capillary venule permeability/sensitizing sensory neurons (itching)

88
Q

Difference and similarity between kinins and histamine?

A

Similar effect/kinin is more long term/kinin also increase arachidonic acid release

89
Q

Difference and similarity between COX1 and COX2?

A

Both metabolize arachidonic acid/COX1 is always been made/COX2 is made during inflammation

90
Q

Goals for NSAIDs?

A

Relieve pain/slow tissue damage/inhibit COX1/2

91
Q

How does aspirin work?

A

Put an acetyl group onto COX1/2 and irreversible block the making of eicosanoids

92
Q

Salicylic acid (hydrolyzed form of acetylsalicylic acid) can ___

A

Reversibly inhibit COX1/2

93
Q

Effect of aspirin?

A

anti-inflammatory/analgesic/antipyretic/inhibit TXA2—>increase bleeding time

94
Q

Dosage progression of aspirin

A

Anti-platelet (low dose)—>analgesic and antipyretic—>anti-inflammatory

95
Q

Acetaminophen overdose is resulted from the depletion of ___?

A

Glutathione

96
Q

Indomethacin should not be used for___?

A

Children

97
Q

Selective COX2 inhibitor is not ___ like traditional NSAIDS

A

anti-platelet

98
Q

Where is norepi converted to epi?

A

In adrenal medulla

99
Q

Difference between norepi and epi (besides epi can bound to beta 2)

A

Norepi is a NT/epi is a neurohormone

100
Q

Alpha methyl tyrosine ___ the synthesis of NE

A

Decreases

101
Q

Beta 1 increase ___ and ___?

A

HR and force of contraction

102
Q

Beta 3 increases ___?

A

Lipolysis

103
Q

Beta is more ___ than alpha, therefore low dose affect ___ first? and high dose affect ___ more? (skeletal muscle)

A

Beta is more sensitive/low dose (body) affect beta first/high dose (drug) affect alpha more

104
Q

Which is more potent for all receptors, NE or epi?

A

Epi

105
Q

Iso/NE/epi, who is the most potent for beta receptors?

A

Iso

106
Q

Why does NE release decrease if you keep giving tyramine?

A

NE pool is gradually depleted

107
Q

What chemical structure predict indirect acting drugs?

A

OH group on benzene ring and acyl side chain

MSII Unit II (8 decks)

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