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Neuro II > Pharm > Flashcards

Pharm Flashcards

1
Q

What is an inert binding site

A

Binding site that doesn’t change function when a drug binds

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2
Q

Describe a covalent bond drug receptor interaction

A

Irreversible; drug removal requires new synthesis of a receptor or enzymatic removal of the drug

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3
Q

List the bonds in order of strongest to weakest

A

Ionic (btw positive and negative), hydrogen (btw net positive charge of hydrogen and negative charge of electronegative atom), hydrophobic (hydrophobic regions of drug and receptor), van der waals

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4
Q

How do you plot a dose response curve

A

Dose on x axis and drug effect on y axis (makes a hyperbolic curve)

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5
Q

What kind of curve do you get when you plot a concentration-effect curve (logarithm of drug vs response)

A

Sigmoidal

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6
Q

What is Emax

A

Maximal effect produced by a drug

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7
Q

What is ED50

A

Effective dose: dose of a drug that produces 50% of its maximal effect

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8
Q

What is a graded dose response curve

A

Answers: “how much?”

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9
Q

What does a quintal response require

A

Pre-defined response

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10
Q

What are the types of quantal dose responses

A

Non-cumulative: # or % of ppl responding to a certain dose and only at that dose
Cumulative: # or % of ppl responding to a certain dose and at all doses lower than that dose

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11
Q

What is the therapeutic index

A

TD50/ED50 = TI; higher the TI, safer the drug

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12
Q

What is the therapeutic window

A

Range of doses of a drug in a bodily system that provides for safe and effective therapy

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13
Q

What is the parameter that describes affinity

A

Kd = drug concentration at which 50% of the drug receptor binding sites are occupied by the drug; unit used is molar concentration; lower Kd = higher affinity

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14
Q

What is the intrinsic activity of a drug

A

Ability of the drug to change a receptor function and produce a physiological response upon binding; agonists have intrinsic activity

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15
Q

What is a full agonist

A

Fully activate receptors, produce maximal pharm effect when all receptors occupied, maximal intrinsic activity

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16
Q

What is a partial agonist

A

Partially activate the receptor, produce sub-maximal pharm effect when all receptors occupied, intrinsic efficacy varies but is always submaximal

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17
Q

What is an inverse agonist

A

Decrease receptor signaling, decrease response at receptors, intrinsic activity is present and related to inhibition of receptor function

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18
Q

What is pharmacologic antagonism (receptor)

A

Action at the same receptor as endogenous ligands or agonist drugs

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19
Q

What is chemical antagonism

A

When the chemical antagonist makes other drug unavailable

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20
Q

What is physiologic antagonism

A

Occurs btw endogenous pathways and regulated by different receptors

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21
Q

What is the difference between a competitive and non-competitive antagonist

A

Competitive: can be displaced from receptor by other drugs
Non-competitive: inactivation not surmountable; two types: irreversible (occluded agonist site via covalent bonds) and allosteric (binds to site other than agonist site)

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22
Q

Describe what competitive antagonism does to the dose response curve

A

Increases EC50 but does not change E max

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23
Q

Describe what non competitive antagonism does to the dose response curve

A

Decrease Emax but EC50 does not change

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24
Q

What is drug potency

A

Amount of drug required to produce specific pharm effect; higher affinity drugs are more potent, lower ED50, more potent the drug, determines drug dose used clinically

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25
Q

What is drug efficacy

A

Describes max pharm effect that drug can produce; represented by Emax; greater Emax = more efficacious drug; related to total number of receptors available to bind the drug; determines clinical effectiveness

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26
Q

What do TF regulate the recruitment of

A

RNA polymerase

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27
Q

What do TF bind to

A

Response element

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28
Q

What are the GPCR ligands

A

Biogenic amines, peptides/proteins, amino acids, lipids, nucleotides

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29
Q

What are the classes of GPCRs

A

Gs: activates adenylyl cyclase and Src tyrosine kinase
Gi: inhibits adenylyl cyclase but activates Src tyrosine kinase
Gq: activates phospholipase C

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30
Q

What are the GPCR ligands

A

Biogenic amines, peptides/proteins, amino acids, lipids, nucleotides

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31
Q

What is different about insulin and IGF RTK

A

They contain 2 polypeptide chains

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32
Q

What are examples of JAK STAT receptors

A

Growth hormone, erythropoietin, leptin, interferons, interleukins 2-10 and 15

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33
Q

What is unique about the effects of nuclear receptor drugs

A

Effects can last even after agonist concentration has been reduced to zero

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34
Q

Describe the mechanism of hormone receptor activation

A

In unbound state, heat shock protein 90 is bound to receptor; binding of hormone dissociates the heat shock protein and converts to active configuration

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35
Q

What drugs inhibit Na+ voltage gated channels

A

Local anesthetics, antiarrythmia drugs, epilepsy drugs

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36
Q

What is the difference between the actions of excitatory and inhibitory NT in terms of channels they open

A

Excitatory open cation channels, inhibitory open anion channels

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37
Q

What are GABA-A receptors a target for

A

Inhalation anesthesia, IV anesthesia, ethanol, and anxiety benzodiazepines

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38
Q

What is pharmacogenomics

A

Different response based on different genetics

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39
Q

How are individuals defined in terms of their metabolizing ability

A

0=PM
.5=IM
1-2=EM
>2=UM

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40
Q

Which CYP2D6 alleles are nonfunctional

A

3-6; 10,14,71 have reduced function, and 1-2 are fully functional

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41
Q

What is the active metabolite of codeine

A

Morphine

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42
Q

How is codeine converted to morphine

A

CYP2D6

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43
Q

What does CYP2C19 metabolize

A

Acidic drugs (PPI, antidepressants, antiepileptics and antipltls

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44
Q

Which CYP2C19 alleles are nonfunctional

A

2 and 3; 1 is fully functional; 17 is increased function (but cannot make up for non functioning; therefore heterozygous will be IM; seen in Europeans )

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45
Q

What is dihydropyrimidine DH

A

Elimination for chemo agents; 2A is nonfunctional; ie: fluorouracil (must be IV)

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46
Q

What is uridine 5 diphosphoglucoronysyl transferase an example of

A

Phase II enzyme; 28/28 allele = Gilbert syndrome ; can cause unconjugated bilirubin buildup

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47
Q

What is the strategy for eliminating compounds

A

Converting to more polar and water soluble derivatives (easier to excrete in urine)

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48
Q

What are the consequences of bio transformation

A
  • inactivation (aspirin ->acetic acid+salicylate)
  • active compound -> active compound (diazepam->oxazepam)
  • activation (L-dopa->dopamine)
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49
Q

What is an example of a first pass effect that limits the bioavailability

A

Morphine

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50
Q

What happens during the phase I reactions vs phase II reactions

A

Phase I: makes it inactive (oxidation, reduction, hydrolysis); catabolic; products can be more reactive and toxic
Phase II: makes it more water soluble and increases molecular weight (anabolic)

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51
Q

What is unique about the metabolism of isoniazid

A

Phase II Reaction first

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52
Q

What carries out phase I reactions

A

Mixed function oxidases or monooxygenases (CYP, flavin containing monooxygenase (FMO), epoxide hydrolases)

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53
Q

Where are phase I enzymes located

A

Lipophilic ER membrane of liver

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54
Q

What are examples of phase II enzymes

A

UGT, GST, NAT (n acetyltransferase), TPMT (thiopurine methyltransferase), SULT (sulfotransferase)

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55
Q

What are some enzyme inducers in drug metabolism

A

Phenobarbital, chronic ethanol, aromatic hydrocarbons (benzopyrene - smoke), rifampin, St. John’s wort, carbamazepine, phenytoin

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56
Q

What is glucose 6 phosphate DH deficiency

A

Can’t produce NADPH and therefore cant reduce glutathione from its oxidized form; cells can’t be protected from oxidative damage -> hemolytic anemia in presence of oxidants

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57
Q

What causes malignant hyperthermia

A

Inhalation of succinylcholine activates ryanodine receptor -> increased calcium leading to muscle contraction and formation of heat -> rhabdomyollysis

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58
Q

What is the acute toxicity test

A

Determine the no effect dose and the lethal dose in two species and via 2 routes

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59
Q

What is the subacute toxicity effect

A

Three doses, 2 species

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60
Q

What is the chronic toxicity test

A

Rodent and non rodent species for > 6 months; requires when drug intended to be used for long duration

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61
Q

What is the carcinogenic potential

A

Two years on two species

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62
Q

What is the no effect dose

A

Maximum dose and which a toxic effect is not seen

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63
Q

What is a surrogate endpoint

A

Ex: tumor size instead of survival

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64
Q

What was the outcome in the Vytorin vs simvastatin study

A

Vytorin had greater reduction of LDL but no overall reduction of CV events

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65
Q

What is dobutamine

A

B agonist that activates GPCR; used as a model for desensitization via GRK

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66
Q

What do SH2 and 3 bind to, respectively

A

2: tyrosine kinases
3: proline rich

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67
Q

What is SOS

A

Encodes Guanine nucleotide exchange factor; activates Ras

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68
Q

What are targeted anti cancer drugs to RTK signaling

A

Abs to GF receptors or GFs; multikinase inhibitors

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69
Q

What kind of receptor does mineralcorticoid aldosterone have

A

Nuclear

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70
Q

What is spironolactone

A

Aldosterone antagonist; suppresses expression of ENaC and Na/K pump, decreases reabsorption reduces BP and alleviates heart failure

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71
Q

What is verapamil?

A

Calcium channel blocker used to treat atrial and supraventricular arrhythmia, angina pectoris, HTN; adverse affect: constipation (relaxes gut mm)

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72
Q

What are the effects of digoxin

A

Vomiting and diarrhea (increases contractility of smooth m), disorientation, confusion, visual disturbances (increases vagal activity)

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73
Q

What is etoposide

A

Topoisomerase inhibitor -> activates p53 (because causes DNA damage)

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74
Q

What are the different types of antagonism

A

Pharmacological: action at the same receptor as endogenous ligand or agonist drug; receptor* antagonist
Chemical: when a chemical antagonist makes the other drug unavailable
Physiologic: endogenous pathways regulated by different receptors

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75
Q

When are calculations for pharmokinetics used

A

On drugs with narrow therapeutic index and concentration dependent efficacy and toxicity

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76
Q

What are the passive routes of absorption of drugs

A
  • Filtration: through pores or channels; determined by osmotic and hydrostatic pressure
  • Diffusion: through cell membranes determined by concentration gradient***most common
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77
Q

What do the names of weak bases/acidic drugs end in

A

Bases: chloride, acetate, hydrochloride, sulfate
Acids: sodium, potassium

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78
Q

What are the features of ionized compounds

A

Lower lipid solubility (more water soluble); do not cross membrane

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79
Q

What are the features of unionized compounds

A

Higher lipid solubility (not water soluble) cross bilateral

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80
Q

What does the ionization status depend on

A

PKa of med and pH of membrane

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81
Q

The lower the pka the ______ the acid

A

Stronger

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82
Q

What are the characteristics of active absorption

A

Saturable (competitive inhibition by other drugs), move against gradient
-Facilitated diffusion is dfft because only one that doesn’t require energy and doesn’t move against a gradient

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83
Q

What does alpha represent

A

Unbound fraction of a drug; small alpha equal small unbound portion

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84
Q

Are drugs with high alphas more or less effected by drug-drug interaction

A

Less; not as much bound so don’t have to compete

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85
Q

How do you calculate a drug-drug interaction in terms of bound vs unbound proportion

A

Percentage drug displacement x bound, add that to free; take that value - original free/original free x 100

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86
Q

What are some inhibitors of P450

A

Fluoxetine, omeprazole, cimetidine, isoniazid, ketoconazole

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87
Q

What are the process of renal elimination

A
  • passive glomerular filtration: blood flow dependent
  • passive tubular diffusion: proximal or distal tubules; ionization and concentration status dependent
  • active tubular secretion: acids/bases secreted
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88
Q

What is the rate elimination of first order kinetic drugs

A

Proportional to plasma concentration

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89
Q

What are the kinetic properties of zero order drugs

A

Saturable; rate of elimination NOT proportional to concentration in plasma; amount of drug removed is same over time; percentage of total amount does not stay the same over time

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90
Q

What is Tmax

A

Onset of activity

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91
Q

What is Cmax

A

Maximum drug concentration

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92
Q

What is MTC

A

Maximum therapeutic concentration

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93
Q

Between what two values does the therapeutic window reside

A

Maximal therapeutic concentration and minimum effective concentration

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94
Q

What does F=1 mean

A

100% absorbed

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95
Q

How do you calculate bioavailability

A

AUCoral/AUCiv x 100

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96
Q

What are the 3 things that determine the amount of a drug absorbed

A

Dose, bioavailability, salt factor

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97
Q

What do you have to do to Vd before putting it in an equation

A

Multiply by body weight in kg

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98
Q

What is the formula for ideal body weight for males and females

A

Female: 45 kg + (2.3 kg x heigh in inches - 60 inches))
Male: 50 kg + (2.3 kg x height - 60)

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99
Q

What is clearance

A

Volume of blood per unit of time that is cleared of the drug

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100
Q

What is tau

A

Dosing interval in hours (ie: q8h, tau=8)

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101
Q

What is the tau for continuous infusion

A

1

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102
Q

What is Kel

A

Elimination rate constant; fraction of drug removed per unit time

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103
Q

What is the equation for amount of drug absorbed

A

S x F x Dose

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104
Q

What is the equation for dose of different dosage form

A

Amount absorbed from current form/S x F of new form

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105
Q

What is the equation for concentration in plasma

A

(S x F x Dose)/ Vd

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106
Q

What is the equation for loading dose

A

(Vd)(Cp)/SxF

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107
Q

What is the equation for supplemental loading dose

A

(Vd)(Cp desired - Cp initial)/ SxF

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108
Q

What is the equation for clearance

A

(S)(F)(dose/tau)/Cp

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109
Q

What is the equation for maintenance dose

A

(Cl)(Cp)(tau)/(S)(F)

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110
Q

What is the equation for elimination rate. Constant

A

Cl/Vd OR (ln Cpt1 - ln Cpt2)/(t2-t1)

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111
Q

What is the equation for half life

A

.693/Kel

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112
Q

What is the equation for creatinine clearance

A

[(140-age) x IBW / (72 x Scr)

*multiply by .85 if patient is female

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113
Q

What are choline esters

A

Acetylcholine, carbachol, Bethune howl; poor absorption; less active when given PO; hydrolyzed by cholinesterase but at diff rates (acetylcholine most rapid); MOA: agonist on cholinergic receptors

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114
Q

What are alkaloids

A

Ex: muscadine, nicotine, pilocarpine; uncharged tertiary amines; well absorbed through most sites; muscadine is highly toxic when ingested and can enter brain; excreted by kidneys (acidification of urine excelerates clearance); MOA: agonist on cholinergic receptors

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115
Q

What are the muscarinic receptor types

A 
M1: on nerves; Gq
M2: heart, nerves, smooth m; Gi (activates K channels)
M3: glands, smooth m, endothelium; Gq
M4: CNS; Gi
M5: CNS; Gq
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116
Q

How do muscarinic agonists cause smooth m relaxation around bv

A

Causes them to release EDRF -> increases cGMP

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117
Q

What is the effect of small doses of Ach versus large doses

A

Small: vasodilation and reflex increased heart rate
Large: bradycardia and hypotension

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118
Q

What mAChR is required for direct activation of smooth m contraction

A

M3

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119
Q

What cholinergic receptors are seen in difft parts of the CNS

A

Brain -> mAChRs

SC -> nAChRs

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120
Q

What are excitatory vs inhibitory mAChRs involved in the CNS

A

Excitatory: increased cognitive function and seizures
Inhibitory: tremors, hypothermia, analgesia

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121
Q

What do different doses of nAChRs cause in the brain

A

Moderate -> alertness, high -> tremor, emesis, respiratory stimulation; lethal -> convulsions and coma (insectiside)

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122
Q

What are the effects of stimulation of nAChR on the PNS

A

CV: sympathomimetic (HTN)

GI/GU: parasympathomimetic

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123
Q

what are the uses for direct acting cholinergic agonists

A

Glaucoma (contracts culinary body which facilitates outflow of aqueous humor and reduces pressure), accommodative esotropia (misalignment of eyes), GI/GU tract disorders (bethanechol; used for stony of bowel, mega colon, urinary retention, esophageal reflux (increases tone), must be certain no obstruction before use, piocarpine and cevimeline increase salivary secretion (sjogren)

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124
Q

What are the toxic effects of muscarinic stimulants

A
  • Overdose of pilocarpine and choline esters -> NVD, urgency, salivation, sweating, vasodilation, bronchial constriction); blocked by atropine
  • mushrooms of genus inocybe contain alkaloids -> muscarinic poisoning
  • contraindications = asthma, hyperthyroidism, coronary insufficiency, acid-peptic dz
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125
Q

What are the toxic effects of nicotinic stimulants

A

-Acute: CNS stimulation (convulsions->coma->resp arrest), skeletal m depolarization -> blockade -> resp paralysis, HTN, cardiac arrhythmia
Treat with atropine and diazepam; blockade is not responsive to pharm treatment
-Chronic: increased risk of vascular dz and peptic ulcers

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126
Q

What is Ach used for

A

Intraocular use during surgery; not given systemically

127
Q

What is methacholine used for

A

Inhaled for bronchial airway hyperactivity who don’t have asthma; rarely used

128
Q

What is bethanechol used for

A

Urinary retention and heartburn; selective mAChR agonist; can produce UTI if sphincter fails to relax

129
Q

What is carbachol used for

A

Nonspecific cholinergic agonist used to treat glaucoma or to produce miosis during surgery

130
Q

What is cevimeline used for

A

Oral; treats dry mouth in sjogren

131
Q

What is pilocarpine used for

A

Xerostomia in sjogren or head and neck CA; miosis, glaucoma (topical); pure mAChR agonist

132
Q

What is varenicline used for

A

Smoking cessation; partial agonist binds to nicotinic receptors in brain; releases dopamine to reduce craving; eliminated in urine as unchanged drug nausea, changes in behavior, agitation, depression, suicide

133
Q

What are the indirect acting cholinergic agonists

A

Cholinesterase inhibitors

  • alcohol
  • carbamic acid esters
  • organophosphates
134
Q

What is the difference between binding of alcohols/carbamic acid esters and organophosphates to AChE

A

Organophosphates bind covalently and irreversibly; opposite for alcohols and carbamic acid

135
Q

What is special about the negative side effects of organophophates

A

Lipid soluble and therefore CNS toxic

136
Q

What is the only organophosphate that doesn’t have effects on CNS

A

Echothiophate

137
Q

What is irontecan

A

Topoisomerase I inhibitor prodrug; chemo combined with 5 FU; metabolized into SN-38; UGT1A polymorphisms at increased risk for toxicity (b/c breaks down SN-38 which is highly toxic)

138
Q

What is thiopurine s methyltransferase

A

Phase II enzyme; deactivates thiopurine drugs; ex; azathiorprine (prodrug of 6-MP), 6-MP and G-Tg;

139
Q

What are the classifications of G6PD deficiencies

A

I most severe, V no deficiency (enhanced activity); III is hemolysis with stressors

140
Q

How is glucose-6PDH deficiency inherited

A

X linked

141
Q

What is rasburicase

A

Urate oxidase enzyme used for chemo; produces hydrogen peroxide during metabolism; don’t give to G6PDH deficiency

142
Q

What population is most at risk for G6PDH

A

African

143
Q

What is the OATP1B1 transporter

A

Organic anion transporter; encoded by SLCO1B1; located on absolute real side of hepatocytes and up takes acidic drugs (statins, methotrexate and bilirubin); most common variant increases systemic exposure of simvastatin -> lower dose to reduce this problem

144
Q

What is the breast cancer resistance protein

A

BCRP (encoded by ABCG2); efflux transporter in ABC family; decreased function found in Asians -> associated with changes in response to xanthine oxidase inhibitor (allopurinol) and rose a statin

145
Q

Which drugs are associated with hypersensitivity reactions

A

Methotrexate, NSAIDs, sulfonamides, abx, steroids, Anti-epileptic; hypersensitivity attributed to HLA polymorphisms

146
Q

What is abacavir

A

Nucleoside reverse transcriptase inhibitor used in HIV; causes Steven Johnson syndrome in people with HLAB 57:01 polymorphisms (more common in European); abacavir is a prodrug -> activated to arborvitae triphosophate; hypersensitivity reaction may involve CD8 cells (HLA B 57:01 presents it to CD8 cells)

147
Q

What is flucloxacillin

A

Causes hypersensitivity reaction that causes liver toxicity; polymorphism in HLAB 57:01

148
Q

What polymorphism is associated with ximelagatran induced liver injury

A

HLA DRB1 07:01

149
Q

What are genetic variants in IFNL3 (IL-28B) associated with

A

Predicts success of HCV treatment response to iFN alpha and ribavirin

150
Q

What is CYP2C9

A

Phase I metabolized acting on acidic drugs (warfarin, phenytoin, and NSAIDs)

151
Q

What is the target of warfarin

A

Inactivates VKORC1; polymorphism can cause increased sensitivity to warfarin

152
Q

What is an example of a prodrug

A

Chlorazepate

153
Q

What is the important part about pharmacotherapeutics

A

Evidence based

154
Q

What is pharmaceutical equivalence

A
  • same active ingredients
  • same dosage form/route of administration
  • same strength/concentration of active ingredient
  • meet same standards for quality/purity
155
Q

What are pharmaceutical alternatives

A

Same active drug, but different salt/complexes or different dosage forms or strengths

156
Q

What does bioequivalence mean

A

Similar rate and extent of absorption (80%-125%)

157
Q

What is therapeutic equivalence

A

Must be pharmaceuticals equivalent and bio equivalent; also expected to have the same clinical effect and safety profile

158
Q

What are the equivalency ratings

A

A: equivalent
B: not equivalent

159
Q

What are the classifications of legend drugs

A
  • drugs that needs a script
  • Non-scheduled/non-controlled: NO abuse potential (ex: furosemide, cephalexin, amoxicillin, propranolol)
  • scheduled/controlled: Based on abuse potential; ie: morphine, codeine, amphetamine, diazepam; CI agents have no FDA approved indications; CV = not as abusive (lower number, higher risk of addiction)
160
Q

How many mcg are in a mg

A

1000

161
Q

What is mEq

A

Milliequivalent

162
Q

How many pounds is one kg

A

2.2

163
Q

How many tsps are in one tbsp

A

3; tsp is 5 ml; tbsp is 15 ml

164
Q

How many ml is in one ounce

A

30 ml; 2 tbsps, 6 tsps

165
Q

How many ounces is in one cup

A

8

166
Q

How many cc are in one liter

A

1000

167
Q

How many pints are in a quart

A

2

168
Q

How many ounces is in one pint

A

16 oz

169
Q

How many ml is one quart

A

946

170
Q

How many ml is one pint

A

473

171
Q

How many liters is in a gallon

A

3.79

172
Q

What does qhs stand for

A

Every night at bed time

173
Q

What does ac mean

A

Before meals; pc is after meals

174
Q

What are the abbreviations used for administration in eyes

A

Od: right eye
Os: left eye
Ou: both eyes

175
Q

What are the abbreviations for administration of drugs in ears

A

Ad: right ear
As: left ear
Au: both ears

176
Q

What are the quarternary and charged AChE inhibitors

A

Neostigmine, pryidostigmine, edrophonium, echothiophate, ambenonium; not soluble in lipids = poor absorption; IV administration; no CNS distribution; duration of effect determined by stability of inhibitor:enzyme complex NOT by metabolism

177
Q

What are the tertiary uncharged AChE inhibitors

A

Well absorbed from all sites, distributes in CNS, more toxic than quaternary; physostigmine, donepezil, tacrine, rivastigmine, galantamine

178
Q

How do alcohols bind to AChE

A

Reversibly; short lived therefore short duration of action as AChE inhibitor

179
Q

How do carbamic acid esters act as AChE inhibitors

A

Hydrolyze to analogue of ACh; second step forms covalent bond btw enzyme and carbamic acid group of inhibitor; * requires 30 min-6 hrs to hydrolyze

180
Q

How do organophosphates act as AChE inhibitors

A

Phosphorus-enzyme bind highly stable and hydrolysis at a slow rate; undergoes aging (breaking of oxygen-P bond of inhibitor which further strengthens the bond)

181
Q

Where do quaternary AChE inhibitors mainly work

A

NMJ

182
Q

Which AChE inhibitors are most commonly used to reverse paralysis during surgery

A

Neostigmine and edrophonium

183
Q

Which drugs are used to treat Alzheimer’s

A

Donepezil, rivastigmine, galantamine, physostigmine

184
Q

What are the side effects of anti cholinergic drugs

A

Cutaneous vasodilation, anhydrotic hyperthermia, nonreactive mydriasis, delirium, hallucinations, etc

185
Q

What is given to reverse anticholinergic toxicity

A

Phsyostigmine

186
Q

What happens if you give AChE inhibitors and systemic corticosteroids to someone with myasthenia Travis

A

Enhances muscle weakness

187
Q

How do you treat AChE inhibitor poisoning

A

Atropine and cholinesterase regenerator (pralidoxime) -> can regenerate enzyme by removal of phosphorous group from the active site

188
Q

What is pyridostigmine

A

Prophylaxis treatment for AChE inhibitor poisoning

189
Q

What are the tertiary amines vs quaternary amines of anticholinergic drugs

A

Tertiary: atropine, tropicamide, benztropine; used for effects on eye and CNS
Quaternary: charged - exert effects in periphery; ipratropium, glycopyrrolate

190
Q

Is atropine selective

A

No

191
Q

What are the side effects of scopolamine

A

Drowsiness

192
Q

What is cycloplegia

A

Inability to accomodate(results from anti muscarinic agents)

193
Q

Which muscarinic receptor is found on the bladder

A

M3; targeted for overactive bladder; ex: trospium, oxybutynin, darifenacin, solifenacin, tolterodine (last 3 have fewer side efffects)

194
Q

What is atropine contraindicated in

A

Glaucoma and men with BPH

195
Q

What is pirenzepine

A

Selective for M1; inhibits gastric secretion - treats ulcers

196
Q

What is mecamylamine

A

Tertiary amine that blocks ganglion

197
Q

What do ganglionic blockers do

A

Enhance sympathetic tone; cause sedation, cycloplegia, decreased BP, inhibited motility of GI, urinary retention

198
Q

What are the GPCRs associated with each of the dopamine receptors

A

D1 and D5: Gs; all others GI

199
Q

Where are alpha 1 receptors located

A

Vascular smooth m, pupillary dilator m, prostate, and heart (increases force of contraction)

200
Q

Where are alpha 2 receptors located

A

Postsynaptic CNS neurons, platelets, adrenergic and cholinergic nerve terminals (inhibits transmitter release), vascular smooth m, fat cells (inhibits lipolysis)

201
Q

Where are B1 receptors located

A

Heart and juxtaglomerular cells

202
Q

Where are beta 2 receptors located

A

Lungs, uterine, vascular smooth m (Relaxation), skeletal m(potassium uptake), liver (activates GNG and glycogenolysis)

203
Q

Where are beta 3 receptors located

A

Bladder (Relaxes detrusor) and fat cells (activates lipolysis)

204
Q

Where are D1 vs D2 receptors located

A

D1: smooth m (dilates renal arteries)
D2: nerve endings (modulates transmitter release)

205
Q

What are the indirect acting adrenomimetics

A

Cocaine, phenelzine (MAOI), amphetamines, ephedrine

206
Q

What are the alpha agonists

A

Clonidine (alpha 2) and phenylephrine (alpha 1)

207
Q

What are the mixed alpha and beta agonists

A

Norepinephrine (more alpha than beta) and epi (alpha=beta)

208
Q

What are the beta agonists

A

Dobutamine (beta 1), isoproterenol (both), terbutaline (beta 2), albuterol (beta 2)

209
Q

What are the dopamine agonists

A

Dopamine and fenoldopam

210
Q

What are the effects of epi on the heart

A

Increased contraction (positive inotropic effect), increase HR, increases conduction velocity

211
Q

What are the effects of epi on vascular tone

A

Increase sytosolic BP, but decrease diastolic BP and PVR, MAP unchanged

212
Q

What are the effects of epi on the respiratory system

A

Relaxes bronchial muscle, decreases secretion via alpha 1

213
Q

What are the effects of epi on skeletal m

A

Muscle tremor (beta2), increases K+ uptake (B2); elevates blood glucose (B2), increases FFA and increases renin release

214
Q

What are the effects of norepi

A

Cardiac stimulant but reduces heart rate; vasoconstrictor; no beta 2 effects; increases BP (baroreceptor reflex)

215
Q

What does phenylephrine do

A

Mydriasis and decongestant, vasoconstriction, decreased HR

216
Q

What is the effect of clonidine

A

Decreases symp outflow, reduces BP, bradycardia, locally -> vasoconstriction b/c causes release of NE from presynaptic neurons (its an alpha 2 agonist)

217
Q

What does isoproterenol do

A

Positive inotropic and chronotropic affect (B1), vasodilator, decreases BP (B2), and causes bronchodilation

218
Q

What does dobutamine do

A

B1 with alpha 1 activity; potent inotropic action

219
Q

What do terbutaline and albuterol do

A

Both B2; bronchodilation and relaxation of uterus

220
Q

What is the effect of dopamine

A

D1: vasodilation (high density in renal, cerebral, mesenteric, and coronary aa); D2 suppresses NE release; B1 activation at higher doses, alpha agonist at even higher doses

221
Q

What is ephedrine

A

Releasing agent and direct adrenergic agonist

222
Q

What are characteristics of indirect adrenergic agonists

A

More lipophilic and cross BBB

223
Q

What is tyramine

A

Indirect acting adrenergic agonist; product of tyrosine metabolism from cheese and meets; releases NE from presynaptic terminals if IV administration; metabolized by MAO (can cause increased BP in patients taking MAO inhibitors)

224
Q

What adrenergic agonists would you use in hypotensive emergencies

A

NE and phenyephrine

225
Q

What adrenergic agonist would you use for chronic hypotension

A

Ephedrine

226
Q

What adrenergic agonists would you used to treat cardiogenic shock (due to MI)

A

Dopamine; dobutamine

227
Q

What adrenergic agonists would you use for heart failure

A

Acute: dobutamine

Severe with decreased renal perfusion: dopamine

228
Q

What adrenergic agonists would you use for complete AV block and cardiac arrest

A

Epi and isoproterenol

229
Q

What adrenergic agonist do you use for narcolepsy

A

Amphetamines and methylphenidate

230
Q

What adrenergic agonists inhibit appetite

A

Phentermine, ephedrine, amphetamines

231
Q

What do you use to treat anaphylaxis

A

Epi

232
Q

What adrenergic agonist do you use to treat glaucoma

A

Alpha 2 selective agonist; apraclonidine, brimonidine

233
Q

What are adverse effects of adrenergic agonists

A

Elevated BP, worsening heart failure, tachycardia, insomnia, convulsions and hemorrhagic stroke (cocaine)

234
Q

What are the indirect acting anti adrenergic drugs

A

Metyrosine (inhibits tyrosine hydroxylase so cant make dopamine), guanethidine (prevents storage and depletes NE)

235
Q

What are the non selective alpha antagonists

A

Phentolamine and phenoxybenzamine

236
Q

What are the alpha 1 selective antagonists

A

Prazosin, terazosin, tamsulosin, doxazosin, alfuzosin, silodosin

237
Q

What is the difference between phentolamine and phenoxybenzamine

A

Phentolamine: reversible competitive antagonist; shorter acting
Phenoxybenzamine: non-competitive irreversible alpha antagonist; longer acting

238
Q

What do alpha antagonists do

A

Decrease BP, reflex tachycardia, relax prostate and bladder; relaxation of pupillary dilator m

239
Q

When would you use alpha antagonists

A
  • Pheochromocytoma: treat with phentolamine or phenoxybenzamine
  • HTN: -osin
  • ED: phentolamine and vasodilator papaverine
  • BPH: tamsulosin, silodosin
240
Q

What are the adverse effects of alpha antagonists

A

Seen more with alpha 2; postural hypotension (ant of alpha 1 on venous sm); tachycardia, retention of fluid and salt, impaired ejaculation, nasal stuffiness

241
Q

What are the mixed adrenergic blockers

A

Labetalol and carvedilol (beta and alpha1 antagonist)

242
Q

What are the non selective beta blockers

A

Propranolol, pindolol, nadolol, penbutolol

243
Q

What are the beta 1 blockers

A

Metoprolol, betaxolol, acebutolol, atenolol

244
Q

What are the partial agonists of beta receptors

A

Acebutolol, labetalol, penbutolol, pindolol

245
Q

What are the inverse agonists of beta receptors

A

Carvedilol and metoprolol

246
Q

What are beta blockers with ISA

A

Intrinsic sympathomimetic activity; they are partial agonists at beta receptors; block symp effect but have submaximal effects of their own (blunted symp); use for less risk of inducing bradycardia, increases VLDL/HDL

247
Q

What are the effects of beta blockers

A

Negative inotropic, negative chronotropic, initial rise in PVR but with chronic use decrease in PVR; inhibits renin release, increases airway resistance, reduces production of aqueous humor, inhibits lipolysis

248
Q

Which beta blockers are used after an MI

A

Timolol, propranolol, metoprolol

249
Q

Which beta blockers are given for heart failure

A

Metoprolol, bisoprolol, carvedilol *contraindicated in acute CHF

250
Q

What beta blockers are used to treat glaucoma

A

Timolol and betaxolol NOT propranolol

251
Q

Which beta blocker is used to treat hyperthyroidism

A

Propranolol

252
Q

What should you switch to if the beta blocker administered causes a hypoglycemic episode

A

Seen more in patients with T1DM; Beta 1 selective (also switch to this if it causes HTN or increases airway resistance)

253
Q

What does s.l. Stand for

A

Sublingually

254
Q

What does s.q. Stand for

A

Subcutaneously

255
Q

What does p.r. Stand for

A

Per rectum

256
Q

What does NGT and OGT stand for

A

NGT: nasogastric tube and oro-gastric tube

257
Q

What does ut.dict. Stand for

A

As directed

258
Q

What does t.r.a stand for

A

To run at

259
Q

What does k.v.o stand for

A

Keep vein open

260
Q

What does NS stand for

A

Normal saline *.9% NaCl

261
Q

How many phases of clinical trials need to be conducted in order to be approved by the FDA

A

I-III

262
Q

What is a lead compound

A

Chemical compound that has pharmacological or biological activity and who’s chemical structure is used as a starting point for chemical modification in order to improve efficacy, potency, or selectivity

263
Q

What happens after identification of a lead compound

A

Drug is screened and studied in vitro and in vivo leading candidate then undergoes preclinical and toxicity testing before human evaluation

264
Q

What is the purpose to in vitro studies

A

Esablishes the drugs target and effects; tested in cellular system that best represents the disease state the therapy is tarteting

265
Q

When can the lead compound be submitted for approval to test in human

A

If the pharmacological properties are safe and adequate and if the compound produces the expected result

266
Q

What is the no effect dose

A

Max dose at which a specified toxic effect is not seen

267
Q

What is a crossover design

A

Patients receiving each therapy in sequence (serve as own controls)

268
Q

What is phase 0 of clinical trial

A

Study subpharmacological doses of drug; low cost

269
Q

What is phase I of clinical trials

A

First stage of drug testing in humans; determines whether humans and animals show significantly different responses; 25-50 ppl; if drug induces toxicity, sick volunteers are used; generally not blind; absorption, half life and metabolism are studied; usually in patient

270
Q

What is phase II of clinical trials

A

100-200 patients that have the target disease to determine efficacy; typically single blind; include placebo, established drug for positive control and investigational agent; efficacy, dosing, and toxicity are reported; often in clinical centers; drug failure typically occurs here

271
Q

What is phase III of clinical trials

A

Conducted after preliminary studies; further establishes drug safety and efficacy by including 300-3000 patients with the target disease; crossover and double blind techniques used; carried out in similar settings to how the drug will be used; most expensive

272
Q

What is phase IV of clinical trials

A

After approval to marker the new drug; new drugs with side effects that occur with incidence of 1 in 1,000, this is essential; no fixed duration

273
Q

What kind of xenobiotics can be excreted by the kidneys

A

Polar and small compounds

274
Q

What is biotransformation

A

Chemical modification of lipophilic, unionized or large compounds to terminate their actions

275
Q

What is an example of biotransformation that activates a compound

A

L-dopa to dopamine

276
Q

What is an example of a drug that undergoes extensive first pass biotransformation

A

Morphine *need to give IV

277
Q

Can phase II Reactions proceed phase I

A

Yes

278
Q

Describe the features of phase I Reactions

A

Catabolic; converts to more polar metabolite by adding or removing functional group; oxidation, reduction, hydrolysis, hydroxylation, epoxidation, dealkylation, deamination, desulfurization, dechlorination; Carried out by mixed function oxidases (MFOs) or monooxygenases (located in ER membrane of liver)

279
Q

Describe the features of phase II reactions

A

Anabolic; occurs at faster rate

280
Q

How does CYP450 work

A

Uses O2, H+ derived from NADPH to carry out oxidation

281
Q

What does a defect in pseudocholinesterase cause

A

Metabolize succinylcholine slower than normal

282
Q

What is slower acetylator phenotype

A

Have decrease in N-acetyltransferase which causes isoniazid, hydralazine, caffeine and other amines to be metabolized at slower rates leading to toxicity (hepatitis)

283
Q

What are cyp inducers

A

Phenytoin (Anti convulsants), ethanol, armonatic hydrocarbons benzopyrene (Tobacco smoke), rifampin, phenobarbital (anesthesia)

284
Q

What does grapefruit juice inhibit

A

CYP3A4

285
Q

What is the effect of administering allopurinol with mercaptopurine

A

Allopurinol will inhibit metabolism of mercaptopurine which extends its action (enhances toxic effect)

286
Q

What are the changes related to aging that affect pharmacokinetics

A

Body water, lean body mass, body fat, serum albumin, kidney weight, hepatic blood flow

287
Q

What drugs are flow-limited

A

Rate of elimination depends on rate of blood flow; therefore will be affected with cardiac dz; examples are morphine, lidocaine, beta blockers, verapamil

288
Q

The wider the therapeutic window the _________ the drug

A

Safer

289
Q

How are GPCR responses desensitized

A

GRK phosphorylates the GPCR and arrestin binds to it; cannot bind ligand

290
Q

What does a small alpha mean

A

Small unbound portion of drug

291
Q

What is the impact of an inducer on pro drugs

A

Faster onset but a shorter duration

292
Q

How is the rate of elimination related to the blood concentration in a first order drug

A

Rate of elimination is proportional to the amount of drug in the blood; fraction lost doesn’t change (ie: lose 50% every time)

293
Q

What would be the difference between an IV push and IV drip

A

IV push has sharp increase in drug concentration, drip does not because controlled

294
Q

What units is the Vd in

A

L/kg

295
Q

What is clearance measured in

A

L/hr

296
Q

For a first order drug, what happens to the steady state if you double the dose you give your patient

A

The steady state will double

297
Q

What is potency

A

The amount of drug required to produce an effect *ED50; determines clinical dose

298
Q

What is efficacy

A

Maximum effect

299
Q

What is the relationship between clearance and half life

A

Inversely proportional

300
Q

What does G6PD do

A

Converts NADP to NADPH which then reduces glutathione; if deficient do not give antimalarial, aspirin, nitrofurantoin, NSAIDs, quinidine, or sulfa drugs

301
Q

Does norepi have effects on beta 2

A

No

302
Q

What are the effects of clonidine

A

When given IV: vasoconstriction b/c occurs post synaptically

Orally: vasodilation and Bradycardia (decrease release of NE)

303
Q

What are the side effects of AChE inhibitor poisoning

A

Salivation, lacrimation, urination, defecation, GI pain and gas, emesis

304
Q

How do you treat organophosphate poisoning

A

Atropine and pralidoxime (pulls organophosphate out of AChE - used for nicotinic effects)

305
Q

What is glycopyrrolate

A

MAChR antagonist; used after surgery to reverse paralysis

306
Q

What is oxybutynin used for

A

Urinary disorders

307
Q

What are ipatropium and tiotropium used for

A

COPD; inhaled *charged

308
Q

What is varenicline used for

A

Smoking cessation; partial agonist to nAChR

309
Q

What effect do anti-histamines have on the cholinergic system

A

MAChR antagonist

310
Q

Can physostigmine cross the BBB

A

Yes

311
Q

What cholinergic drug is used for Parkinson’s

A

Benzotropine

312
Q

What two drugs make up lomotil

A

Diphenoxylate (opiate) and atropine

313
Q

If you don’t have dobutamine, what combination of drugs can you give for a similar affect

A

NE and phentolamine

Neuro II (3 decks)

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