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* DIT each session > Day 1.1 Pharm > Flashcards

Day 1.1 Pharm Flashcards

1
Q

What is Km?

A

Substrate conc at 1/2 Vmax

Shows affinity of enz for substrate

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2
Q

If Km is decreased, what does this say abt affinity?

A

Affinity is increased if Km is decreased.

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3
Q

What is Vmax directly proportional to?

A

Enz conc

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4
Q

Lineweaver-Burke: What is the y-int?

A

1 / Vmax

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5
Q

Lineweaver-Burke: What is the x-int?

A

1 / -Km

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6
Q

Lineweaver-Burke: As the y-int increases, what happens to the Vmax?

A

Vmax decreases.

Y-int is 1 / Vmax. A bigger Y-int means a smaller number in the denominator.

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7
Q

Lineweaver-Burke: What happens as the x-int moves to the right?

A

Km increases.

X-int is 1 / -Km. As it moves to the right, it gets less negative. (So Km increases)

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8
Q

Lineweaver- Burke: If Vmax decreases, what happens to the y-int?

A

It increases.

Y-int = 1 / Vmax

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9
Q

Lineweaver-Burke: As Km increases, what happens to the X-int?

A

It increases.

X int = 1 / -Km

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10
Q

Lineweaver-Burke: What happens to the slope of the line when an uninhibited rxn gets a competitive inhibitor?

A

It increases.

Competitive inhibitors Cross Competitively. The Y-int stays the same (bc the Vmax stays the same), but the X-int increases (bc the Km increases)

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11
Q

Lineweaver-Burke: What happens to the slope of the line when an uninhibited rxn gets an non-competitive inhibitor?

A

It increases

The X-int stays the same (bc the Km stays the same) but the Y-int increases (bc the Vmax decreases)

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12
Q

What happens to Km with a competitive inhibitor?

A

It increases. (You need more substrate to get to 1/2 Vmax)

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13
Q

What happens to Vmax with a competitive inhibitor

A

It stays the same. The reaction can still go at the same max rate, you will just need more substrate (a higher Km) to get there.

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14
Q

With a competitive inhibitor, how does affinity change?

A

Affinity decreases. When Km goes up (as with competitive inhibition), affinity goes down.

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15
Q

With a competitive inhibitor, how does potency change?

A

Decreased potency.

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16
Q

T/F Competitive inhibitors can be overcome by increased substrate.

A

True

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17
Q

What effect do non-competitive inhibitors have on Vmax?

A

Vmax is decreased. The rxn can’t get to the same max rate, no matter how much substrate there is (bc the non-comp inhibitor doesn’t bind to the active site)

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18
Q

What effect does a non-comp inhibitor have on Km?

A

No change in Km. The amount of substrate needed to get to 1/2 Vmax is the same, it’s only that the Vmax itself is smaller.

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19
Q

How is non-competitive inhibition related to efficacy?

A

Non-competitive inhibitors decrease efficacy.

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20
Q

T/F Km is a measure of affinity

A

True.

Note: As Km is decreased, there is MORE affinity. (You don’t need as much substrate to get to Vmax)

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21
Q

What is the slope of the Lineweaver-Burke plot?

A

Km / Vmax

Slope = y / x
Y = 1 / Vmax
X = 1 / -Km
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22
Q

Equation for Vol of Distribution

A

Vd = amt of drug given IV / plasma conc of drug

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23
Q

Equation for Clearance

A

CL = 0.7 x Vd / t1/2

or CL = K x Vd where elim constant K = 0.7 / t1/2

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24
Q

Equation for loading dose

A

LD = Cp x Vd

Cp, or Css - it’s the plasma conc, or the desired conc at steady state

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25
Q

Equation for maintenance dose

A

MD = Cp x CL

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26
Q

How does renal dz affect LD and MD?

A

Renal dz = decreased CL.

LD (Cp x Vd) is unchanged, bc not affected by CL.

MD (Cp x CL) will decrease with decreased clearance.

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27
Q

What units are used to measure Vd

A

Liters (or any unit of volume)

If given L/kg, determine Vd by factoring in the weight of the pt in kg.

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28
Q

Half life

A

The amt of time needed for a drug conc to reach 50% when infused at a constant rate. Conversely, the time needed for 50% of a drug to be eliminated.

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29
Q

How long does it take a drug to reach 94% of steady state if constantly infused?

A

4 half lives

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30
Q

concentrations and # of half lives needed to get there

A

50% one half life
75% two
87.5% three
94% four

It takes between four and five half lives for a drug to reach steady state (or to be eliminated completely)

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31
Q

Bioavailability

A

Amt of drug that actually reaches blood after metabolism (1st pass in liver, etc). If given IV, F = 1 (100%). If given orally, usu not. If given F other than 100%, just divide the equations by F. (e.g. LD = Cp x Vd / F)

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32
Q

Zero-order elimination

A

Rate of elim is CONSTANT, regardless of amount. Conc decreases linearly with time. A constant amount is eliminated.

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33
Q

Drugs w/ Zero-order elim

A

PEA:
Phenytoin (anti-epileptic)
Ethanol
Aspirin

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34
Q

First-order elimination

A

Rate of elim is PROPORTIONAL to the drug conc- a constant fraction is eliminated. Cp decreases exponentially with time.

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35
Q

If a constant amount of drug is eliminated, what order elim is this?

A

Zero-order

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36
Q

If a constant fraction of drug is eliminated, what order elim is this?

A

First-order

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37
Q

Urine pH: why do ionized species get trapped in urine?

A

Bc ions can’t easily cross the plasma mbr. (Uncharged molecules do cross)

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38
Q

Are weak acids charged or uncharged?

A

Uncharged. Weak acid = HA

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39
Q

For acids, bases:

Is the protonated form charged?

A

Acids: No. Protonated form = HA
Bases: Yes. Protonated form = BH+

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40
Q

For acids, bases:

Is the unprotenated form charged?

A

Acids: Yes. Unprotonated = H+ and A-
Bases: No. Unprotonated = H+ and B

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41
Q

Are weak bases charged or uncharged?

A

Charged. Weak base = BH+

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42
Q

Uncharged molecules can cross the plasma membrane. Which form of acid and which form of base will cross the membrane?

A

Uncharged acid: Protenated form HA

Uncharged base: Dissociated form H+ and B

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43
Q

What is pKa

A

Acid dissociation constant. The pH at which protenated = unprotenated

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44
Q

If the pH is decreased below the pKa, what happens?

A

Low pH = acidic. So EVERYTHING will be in protenated form. For acids, this means they will be HA (uncharged), and for bases, it means they will be BH+ (charged). So bases will be trapped since they are charged.

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45
Q

If the pH is increased above the pKa, what happens?

A

High pH = basic. So EVERYTHING will be dissociated. For acids, this means they will be H+ and A- (charged), and for bases, it means they will be H+ and B (uncharged). Thus, acids will be trapped since they are charged.

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46
Q

Rx for aspirin overdose

A

Aspirin is a weak acid, so give NaHCO3 to make the urine basic and trap the acidic drug in basic urine.

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47
Q

Rx for amphetamine overdose

A

Amphetamines are basic, so give NHCl4 to make the urine acidic- trap the basic drug in acidic urine.

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48
Q

Drug metabolism: by what processes do Phase I rxns usually occur?

A

Reduction
Oxidation
Hydrolysis
Usually uses a Cytochrome P450 enz.

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49
Q

What kind of metabolites are produced in Phase I metabolism?

A

Slightly polar, water-soluble metabolites; they are often still active.

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50
Q

T/F Phase I and Phase II drug metabolism occur in a specific order.

A

False. They are non-sequential. You can have Phs II before Phs I or Phs I before Phs II.

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51
Q

T/F Phase I and II metabolism can both activate or inactivate drugs.

A

True.

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52
Q

Drug metabolism: by what processes do Phase II rxns generally occur?

A 
GAS:
Glucuronidation
Acetylation
Sulfation
Usually occurs using conjugation.
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53
Q

What kind of metabolites are produced in Phase II rxns?

A

Very polar, inactive metabolites. Often, these metabolites are renally excreted.

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54
Q

Which phase of drug metabolism do eldery pts usually lose first?

A

Phase I.
Elderly pts have GAS (GAS = Phase II processes, Glucuronidation, Acetylation, Sulfation) They have GAS, so they don’t have Phase I.

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55
Q

Where does Phase I and II drug metabolism take place?

A

Mostly in the liver

Also in the kidney

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56
Q

What is efficacy?

A

The maximum effect a drug can produce.

Vmax

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57
Q

What is potency?

A

The amount of drug needed.

Km

58
Q

What determines efficacy?

A

The Vmax

59
Q

What determines potency?

A

The Km

Note: Higher Km = LESS potency

60
Q

What happens to efficacy if the Vmax is lowered?

A

The efficacy is lowered.

In the case of a non-competitive inhibitor, Vmax would be lowered, so the efficacy would also be lowered.

61
Q

What happens to potency is the Km is increased?

A

The potency is reduced.

In the case of a competitive inhibitor, Km is increased, which means potency is lowered.

62
Q

What is the difference b/t a competitive and non-competitive inhibitor?

A

Competitive competes for the same active site. Non-comp binds elsewhere and changes the confirmation of the active site so that the enz can’t bind.
Non-comp = Irreversible inhibitor. (same thing)

63
Q

What effect does a competitive inhibitor have on potency?

A

Competitive inhibitors increase Km. An increase in Km means that potency is lowered.

64
Q

What effect do irreversible inhibitors have on efficacy?

A

An irreversible inhibitor (aka a non-competitive inhibitor) decreases the Vmax. Decreased Vmax means decreased efficacy.

65
Q

What effect does a partial agonist have on Vmax?

A

It always lowers Vmax (and thus always lowers efficacy.)

66
Q

What effect does a partial agonist have on Km?

A

It depends on the agonist. It can either increase Km (so decrease potency), or it can decrease Km (so increase potency). Potency is an independent variable.

67
Q

What is the therapeutic index?

A

TI = LD50 / ED50

The dose that kills 50% / the dose that is effective (treats) 50%

68
Q

Is it better to have a high or low therapeutic index?

A

Higher = safer drug

69
Q

How can you get a high TI?

A

High TI when LD50 is high (so the dose it takes to kill 50% is really big), or when ED50 is low (so the amount needed to treat is small)

70
Q

Which drugs have a low TI (meaning they are unsafe and need to be monitored)?

A

Phenobarbital (for seizures)
Lithium (bipolar)
Digoxin
Coumedin/Warfarin

71
Q

What drugs inhibit Cytochrome P450?

A 
PICK EGS:
Protease inhibitors
Isoniazid
Cimetidine
Ketoconazole

Erythromycin
Grapefruit juice
Sulfonamides

72
Q

What are the characteristics of a good clinical trial?

A

Randomized
Controlled
Double-blinded

73
Q

What is a Phase I clinical trial?

A

“Is it safe?”
Testing healthy volunteers
Test for safety, toxicity, pharmacokinetics

74
Q

What is a Phase II clinical trial?

A

“Does it work?”
Testing pts with dz
Efficacy, dosage, side effects

75
Q

What is a Phase III clinical trial?

A

“Does it work better?”
Testing pts w dz
Compare to existing Rx/Standard of Care

76
Q

What is a Phase IV clinical trail?

A

Post-market surveillance

77
Q

How long does the process of Phase I to III take for clinical trials?

A

5-10 years

78
Q

What systems are affected by autonomic drugs?

A 
The SNS and PNS systems. The drugs can:
Activate PNS
Inactivate PNS (NOT the same as SNS)
Activate specific receptors of SNS
Inactivate specific receptors of SNS
79
Q

What is a cholinomimetic?

A

Stimulates the PNS Ach Muscarinic (?M) receptor

80
Q

Cholinomemetics: How do direct cholinergic agonists work?

A

They bind to the PNS Muscarinic Ach receptor and stimulate it.

81
Q

Cholinomimetics: How do indirect agonists work?

A

They inhibit the AChE, which means that the ACh is degraded at a slower rate.
Aka anti-acetylchoinesterases

82
Q

What does AChE do?

A

Breaks down ACh into choline and acetate (thus inactivating it)

83
Q

-chol is what drugs?

A 
Cholinergic agonists (at the PNS muscarinic receptor)
eg Bethanechol, Carbachol
84
Q

Bethanechol

A

Cholinomimetic - Direct Agonist of M ACh receptor.
Used for post-op ileus, neurogenic ileus, urinary retention
(makes you more leaky)

85
Q

Carbachol

A

Cholinomimetic - Direct Agonist of M ACh receptor.

Used for glaucoma, pupillary contraction, and rls of interocular prs (so basically, glaucoma)

86
Q

What is glaucoma?

A

Elevated interocular pressure

87
Q

Pilocarpine

A

Cholinomimetic - Direct Agonist of M ACh receptor.
Used for glaucomic emergencies. Also stim’s sweat, tears, saliva (makes you more leaky)
Contracts ciliary musc of eye for open angle glauc, contracts pupillary spincter for narrow angle glauc.
Resistant to AChE

88
Q

Methacholine

A

Cholinomimetic - Direct Agonist of M ACh receptor.

Used as a challenge test for asthma- causes bronchoconstriction. (so get asthma symptoms when you take it)

89
Q

Neostigmine

A

Cholinomimetic - Indirect Agonist of M ACh receptor. (Anti-AChE)
Used for post-op ileus, neurogenic ileus, urinary retention, MysGrav, reversal of NMJ blockade post-op.
NEO = NO CNS penetration

90
Q

-stigmine

A

AChE inhibitor (Indirect agonist)

91
Q

What is Myasthenia Gravis?

A

Ab to the ACh receptor. Px with ptosis (droopy eyelid) or diplopia (dbl vision) which worsens throughout day.

92
Q

What are the paralyzing agents (anesthesia)?

A

Succanylcholine
Rocuronium
Vecuronium
These cause NMJ blockade. Use neostigmine to reverse their effect.

93
Q

Pyridostigmine

A

Cholinomimetic - Indirect Agonist of M ACh receptor. (Anti-AChE)
Used for MysGrav (long-term)
No CNS penetration.
Gets “rid” of MysGrav

94
Q

Edrophonium aka Tensilon

A

Cholinomimetic - Indirect Agonist of M ACh receptor. (Anti-AChE)
Dx MysGrav, v short acting- if sympt of MysGrav go away when you give it, pt has MysGrav

95
Q

Myasthenia Gravis is related to problems with which organ?

A

Thymus
50% of MG pts have thymic hyperplasia
20% have thymic atrophy
15% have thymoma

96
Q

What is a myasthenic crisis?

A

rapidly progressing weakness, esp in respi muscles (diaphragm)

97
Q

Rx for Myasthenia Gravis?

A

AChE inhibitors
Corticosteroids
Thymectomy
Plasmapheresis (wash out Ab)

98
Q

Physostigmine

A

Cholinomimetic - Indirect Agonist of M ACh receptor. (Anti-AChE)
Phys Phyxes (fixes) atropine OD.
Also used for Glaucoma
Crosses BBB

99
Q

Echothiophate

A

Cholinomimetic - Indirect Agonist of M ACh receptor. (Anti-AChE)
For Glaucoma

100
Q

Cholinesterase inhibitor poisoning (excess PNS)

A 
DUMBBELSS:
Diarrhea
Urination
Miosis
Bronchospasm
Bradycardia
Excitiation of CNS and smth musc
Lacrimation
Sweating
Salivation
Abd cramping
101
Q

What causes cholinesterase inhibitor poisoning (excess PNS)?

A

Organophoshates = Insecticides = Parathion

Usu in farmers/gardeners

102
Q

What is Parathion?

A

Insecticide, causes DUMBBELSS symptoms

103
Q

How do you treat excess PNS / cholinesterase inhibitor poisoning /organophosphates / parathion?

A

Pralidoxime (regenerates AChE) and atropine

104
Q

What are the anti-AChE durgs used in Alzheimer’s? (Alz = decreased ACh)

A

Donepezil
Galantamine
Rivastigmine

105
Q

“trop” drugs

A

Muscarinic antagonist aka anit-cholinergic

106
Q

What happens if you inhibit PNS activity?

A 
Hot as a hare
Dry as a bone
Red as a beet
Blind as a bat
Mad as a hatter 
Bloated as a toad
Incrsd body temp, dry/flushed skin, cycloplegia, delirium/disorientation, constipation & urinary retention
107
Q

What receptors do the anti-cholinergics inhibit?

A

Muscarinic receptors.

Aka muscarinic antagonists

108
Q

What are the muscarinic antagonists? (list)

A 
Atropine, homatropine, tropicamide
Benztropine
Scopolamine
Ipratroprium
Oxybutynin
Glycopyrrolate
Methscopolamine, propantheline
109
Q

What anti cholinergics (muscarinic antagonists) are used to treat urge-type incontinence?

A

Oxybutynin
Tolterodine
Darifenacin and solifenacin
Trospium

110
Q

What does atropine do?

A 
Muscarinic antagonist (anti-cholinergic)
Eye: increases pupil dilation, cycloplegia
Airway: decreased secretions
Stomach: decresased acid secretion
Gut: Decreased motility
Bladder: decreased urgency in cystitis
111
Q

Side effects of atropine?

A

Increased body temp, rapid pulse, dry mouth, dry flushed skin, cycloplegia, constipation, urinary retention, delirium/disorientation.

112
Q

What is cycloplegia?

A

Paralysis of the ciliary muscles of the eye, causing lack of accomodation and therefore blurry vision

113
Q

Contraindications for atropine

A 
Elderly pts
Glaucoma
BPH or any urinary retention
GI obstruction/ileus
Pts w dementia, delirium
Infants w fever (can cause hypothermia)
114
Q

Atropine, homatropine, tropicamide

A

Muscarinic antagonists, used to produce mydriasis (dilation) and cycloplegia in eyes

115
Q

Benztropine

A

Muscarinic antagonist, used in CNS for Parkinson’s

Park my Benz

116
Q

Scoploamine

A

Muscarinic antagonist, used for motion sickness (ear patch) or in end of life care

117
Q

Ipratroprium

A

Muscarinic antagonist, used for Asthma, COPD

I Pray I can breathe soon!

118
Q

Oxybutinin

A

Muscarinic antagonist used for Genitourinary sympt - reduces urgency in mild cystitis, reduces bladder spasm

119
Q

Glycopyrrolate

A

Muscarinic antagonist, genitourinary and also used to decrease airway secretions

120
Q

Methscopolamine, propantheline

A

Muscarinic antagonist- GI, used for peptic ulcer treatment

121
Q

What happens to the level of ACh in:
Parkinson’s?
Alzheimer’s?
Huntington’s?

A

Parkinson’s = Increased ACh

Alz and Huntington’s = Decreased ACh

122
Q

Categorize: Physostigmine

A

-stigmine = Cholinomimetic: Indirect agonist (Anti-AChE)

123
Q

Categorize: Pilocarpine

A

Cholinomimetic: Direct muscarinic agonist

124
Q

Categorize: Echothiophate

A

Cholinomimetic: Indirect agonist (Anti-AChE)

125
Q

Categorize: Oxybutinin

A

Muscarinic antagonist (urge incontinence)

126
Q

Categorize: Atropine

A

trop = Muscarinic antagonist

127
Q

Categorize: Donepezil

A

Cholinomimetic: Indirect agonist (Anti-AChE) for Alzheimer’s

128
Q

Categorize: Pralidoxime

A

AChE regenerator (So inhibits ACh) Use after organophosphate poisoning.

129
Q

Categorize: Bethanechol

A

-chol = Cholinomimetic: Direct muscarinic agonist

130
Q

Categorize: Neostigmine

A

-stigmine = Cholinomimetic: Indirect agonist (Anti-AchE) for Alz

131
Q

Categorize: Darifenacin

A

Muscarinic antagonist (urge incontinence)

132
Q

Categorize: Ipratroprium

A

trop = Muscarinic antagonist

133
Q

Categorize: Tropicamide

A

trop = Muscarinic antagonist

134
Q

Categorize: Benztropine

A

trop = Muscarinic antagonist

135
Q

Categorize: Scopolamine

A

Muscarinic antagonist

136
Q

Categorize: Edrophonium

A

Cholinomimetic: Indirect agonist (Anti-AchE). Tensilon test for MG.

137
Q

Categorize: Tolterodine

A

Muscarinic antagonist (urge incontinence)

138
Q

Categorize: Trospium

A

Muscarinic antagonist (urge incontinence)

139
Q

Categorize: Rivastigmine

A

-stigmine = Cholinomimetic: Indirect agonist (Anti-AchE) for Alz

140
Q

Categorize: Homatropine

A

trop = Muscarinic antagonist

141
Q

Categorize: Pyridogstigmine

A

-stigmine = Cholinomimetic: Indirect agonist (Anti-AChE)

142
Q

Categorize: Carbachol

A

-chol = Cholinomimetic: Direct muscarinic agonist

* DIT each session (34 decks)

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