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Advanced Pharm > Exam 1 Material > Flashcards

Exam 1 Material Flashcards

1
Q

Order molecular bonds strongest to weakest

A

Covalent - ionic - hydrogen - Van der Waals

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2
Q

What is unique about covalent bonds?

A

Longest duration of action; irreversible drug binding

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3
Q

What molecular bonds are the most prominent in drug/receptor alignment?

A

Van der Waals and ionic bonds

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4
Q

Define stereochemistry

A

Study of spatial arrangement of atoms in molecules and the effects the arrangement has on the chemical and physical properties of the molecule

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5
Q

Define agonist

A

A drug that activates a receptor by binding to that receptor

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6
Q

What happens when an agonist is bound to the receptor?

A

The effect of the drug is produced

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7
Q

Define antagonist

A

A drug that binds to the receptor WITHOUT activating the receptor; can block the action of agonists

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8
Q

Competitive antagonists

A

Present when increasing concentrations of the antagonist progressively inhibit the response of the agonist-dose response relationship

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9
Q

Noncompetitive antagonism

A

After administration of antagonist, even high concentrations of agonist cannot completely overcome the antagonism

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10
Q

Partial agonist

A

Drug that binds to a receptor where it activates the receptor, but not as much as a full agonist; cannot cause full effect

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11
Q

Agonist-antagonist

A

When a partial agonist is administered with a full agonist, it decreases the effect of the full agonist;

Ex: butorphanol given with fentanyl partially reverses the fentanyl

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12
Q

Inverse agonist

A

Bind at the same site as the agonist but produce the opposite effect of the agonist; “turn off” the constitutive activity of the receptor

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13
Q

Define pharmacokinetics

A

Describes what body does to the drug

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14
Q

Define pharmacodynamics

A

The drugs effect on the body; what the body’s response to drug

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15
Q

What are the 4 principles of pharmacokinetics

A

Absorption, metabolism, distribution and excretion/elimination

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16
Q

What can affect pharmacokinetics

A

Genetic metabolism differences
interactions with other drugs
liver/kidney disease

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17
Q

Define metabolism

A

Coverts pharmacologically active, lipid soluble drugs into water soluble drugs

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18
Q

What are the four pathways of metabolism

A

Oxidation, reduction, hydrolysis, and conjugation

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19
Q

What are the phase I reactions?

A

Oxidation, reduction and hydrolysis, also demethylation

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20
Q

How are receptors classified?

A

By location; cell membrane lipid bilayer, intracellular etc

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21
Q

Define enzyme inhibition

A

Some drugs work by inhibiting enzymes that are involved in certain chemical reactions in the body

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22
Q

How does the phospholipid bilayer work

A

Works by preventing or allowing solutes to freely move or restrict movement into and out of the cell

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23
Q

Ficks Law of diffusion

A

Movement of particles from high to low concentration is directly proportional to the particles concentration gradient

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24
Q

Non-ionized drugs take home points

A

-lipid soluble (easily cross the phospholipid bilayer)
- diffuse across BBB, GI tract, placenta, hepatocytes
-usually pharmacologically active

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25
Q

What effects absorption

A

-pH, solubility of drug, presence of other substances, route of admin

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26
Q

Define distribution

A

Once drug is absorbed, spread throughout the body, how medication is influenced by the physical and chemical properties of the body

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27
Q

Define metabolism

A

How the body uses different enzymes to break down the medication

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28
Q

Define excretion/elimination

A

How the body eliminates and removes medications through various routes (ex: liver, kidneys, lungs, skin)

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29
Q

What is bioavailability ( f )

A

The amount of drug or medication that reaches the target site in the body after it’s been administered; medication that is left after first pass effect

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30
Q

What are some factors that can effect bioavailability?

A

Route of admin, physical and chemical proprieties of the medication, presence of food or other substances with PO medications

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31
Q

What are some routes of admin that bypass the first pass effect

A

IV, inhaled anesthetics, sublingual, some transdermal

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32
Q

Describe PO absorption route

A

Absorbed in stomach, goes to liver, goes to venous system,, right heart, lungs, left heart then to arterial system

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33
Q

What are components of the “central compartment?”

A

Brain, kidney, liver, heart, lungs

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34
Q

What is the equation for plasma concentration

A

[plasma concentration]=mass of drug/ volume

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35
Q

What are enantiomers?

A

Mirror images but can’t be superimposed

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36
Q

Explain metabolism

A

Converts pharmacologically active lipid soluble drugs into water soluble pharmacologically inactive metabolites

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37
Q

Define and give examples of intracellular proteins

A

Intracellular proteins are fat or water soluble, they can readily diffuse across the cell membrane lipid bilayer

Ex: caffeine, insulin, steroids

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38
Q

Explain and give examples of drugs that don’t interact with proteins

A

These drugs work by changing the pH of the environment

Ex: antacids

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39
Q

What is volume of distribution (Vd)

A

The relationship between a drugs plasma concentration following a specific dose; the theoretical measure of how the drug distributed throughout the body

Vd= amount of drug in body/ plasma concentration

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40
Q

Vdcc

A

Volume of distribution in central compartment (vessel rich groups)

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41
Q

Vdss

A

Volume of distribution steady state;
Drug is being administered at the same rate that it is being eliminated

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42
Q

Why do we care about plasma drug concentration

A

Because we assume that it’s proportional to the target tissue concentration
Exceptions: local topical drugs, inhaler, eye drops

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43
Q

Which organ would most likely affect drug metabolism if became dysfunctions? Which part of the cell is metabolism occurring

A

Liver; smooth endo plastic reticulum

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44
Q

What isFirst pass metabolism

A

Metabolism of a drug before it reaches systemic circulation

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45
Q

2 routes of drug admin that would be subjected to first pass?

A

Rectal, PO

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46
Q

2 routes of drug admin that would not be subjected to first pass

A

IV, sublingual, IM

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47
Q

What are three outcomes of metabolism

A

Active to inactive ex: most drugs
Non toxic to toxic ex Tylenol
Inactive to active ex codiene to morphine

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48
Q

Why do we need metabolism

A

To make drugs more water soluble for excretion

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49
Q

Name 2 sets of chemical reactions that metabolize drugs; give example of enzyme type used during

A

Phase 1: (Modification) -hydrolysis, reduction, oxidation —-enzyme CYP450 (oxidases)

Phase 2: conjugation—-glucuronic, glutathione, sulfonic acid, acetylation (transferases)

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50
Q

What is the difference between phase 1 and phase 2 reactions

A

Phase 1 uses oxidases to introduce a polar group to the drug (oxidation, reduction or hydrolysis)
Phase 2 uses transferases to attach a small polar molecule to drug to make it more water soluble ( via conjugation)

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51
Q

Name common phase 1 and phase 2 enzymes

A

Phase 1: cyp450, cyp3a4 or cyp2d6

Phase 2: glucaronate( UGT) gluthiaonine(GST), sulfate(SULT), acetate (NAT)

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52
Q

First order kinetics 3 things

A
  1. Increase of plasma drug concentration leads to increase of rate of drug metabolism
  2. Rate of metabolism is proportional to drug concentration
  3. Half life is constant
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53
Q

Zero order kinetics 3 things

A
  1. Increase of plasma drug concentration; no increase of rate of drug metabolism
  2. Rate of metabolism is independent of drug concentration
  3. Rate of metabolism is constant; Vmax is reached
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54
Q

What are three examples that saturate liver enzymes and reach zero order kinetics quickly?

A

Aspirin, phenytoin, alcohol (ETOH)

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55
Q

Define clearance

A

The volume of blood that gets eliminated of drug per unit time

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56
Q

If you have low Vd what does that do to your 1/2 life

A

Decreases the 1/2 life

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57
Q

What is GFR

A

The flow rate of drug that is being filtered

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58
Q

Definition of steady state

A

The rate of infusion is equal to the rate of elimination

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59
Q

How much time does it take to reach steady state?

A

About 4.5 half lives

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60
Q

What do we do if we need to achieve the therapeutic concentration rapidly?

A

Give a loading dose; essentially an IV bolus

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61
Q

How to calculate the maintenance dose?

A

CL* desired plasma concentration/bioavailability

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62
Q

Therapeutic window

A

Dosage range between minimum effective concentration and minimum toxic concentration

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63
Q

What do you do if there is a narrow therapeutic window?

A

Give more doses over shorter interval to minimize peaks and troughs

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64
Q

Why is continuous infusion beneficial?

A

You don’t have the fluctuations between minimum toxic concentration and minimum effective concentrations, you remain steady in therapeutic window

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65
Q

Define potency

A

The amount of drug it takes to elicit an effect; high potency= smaller dose

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66
Q

Define efficacy

A

A measure of drug effectiveness once it occupies the receptor; measure of the ability for a drug to produce a physiological or clinical effect

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67
Q

ED50

A

The dose required to produce a specific desired effect in 50% of individuals receiving the drug

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68
Q

LD50

A

The dose of a drug required to produce death in 50% of patients receiving the drug

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69
Q

EC50

A

the concentration of a drug that produces 50% of maximal response

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70
Q

What are the 4 surgical wound classifications

A

Clean, clean-contaminated, contaminated, dirty/infected

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71
Q

Clean surgical wound classification

A

An incision in which no inflammation is encountered in a surgical procedure, without break in sterile field, during which the resp/alimentary/GU tracts not entered

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72
Q

Clean-contaminated

A

An incision through which the respiratory, alimentary, or urinary tract

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73
Q

Contaminated

A

An incision during an operation where there is a major break in sterile technique or gross spillage from the GI tract or an incision in which acute nonpurulent inflammation is encountered

Open traumatic wounds that are more than 12-24 hrs old

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74
Q

Dirty/infected

A

An incision in which the viscera are perforated or when acute inflammation with pus is encountered during the operation

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75
Q

Patient risk factors for SSI (8)

A

-extreme of age; <5 and >65
-poor nutritional status
-obesity
-DM, perioperative glycemic control
-PVD
-tobacco use, substance abuse
-coexisting infections
- altered immune response
-recent surgery, 3 or more comirbidities, massive transfusion

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76
Q

Hospital factors for SSI

A

-corticosteroid therapy
-skin prep (scrub and razor)
-length of preoperative hospitalization
-surgical experience and technique
-duration of procedure
-hospital sterilization of instruments
-maintenance of perioperative normothermia

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77
Q

When should a patient stop smoking before a procedure and why?

A

4-8 weeks; descreases infection risk 50%

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78
Q

Why is maintaining normothermia important?

A

Hypothermia-> vasoconstriction, decreased wound oxygen tension

Decrease in the ability of the tissue to recruit leukocytes to area of infection

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79
Q

What temp should you maintain perioperative? And why?

A

At least 36 * C

Reduces risk of SSI by 64%

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80
Q

What is the ideal BS perioperative?

A

Below 200 and above 80

Hypoglycemia leads to increased mortality

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81
Q

What are the most important performance measures for anesthesia?

A

-ABX within 30 min of incision
-correct abx for procedure
-blood sugar control 80-less than 200
-normothermia (36*C) perioperative period

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82
Q

What are the most prescribed prophylaxis abx for surgery

A

Beta lactams

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83
Q

Beta lactams
2 examples and MOA
What bacteria does it target?

A

Ex: PCN, cephalosporins

MOA: inhibit peptidoglycan synthesis in bacterial cell wall;

Target: gram + and gram -

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84
Q

What does PCN treat and what surgeries is it used for?

A

Treats pneumococcal, streptococcal, and meningococcal infections

Used in dental surgery, tonsil/adenoids, GU/GI surgery

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85
Q

How is PCN administered and excreted?

A

Given IM with poorly soluble salts to prolong duration of action

Rapidly renal excretion

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86
Q

Why would you use ampicillin? (4)

A

-absorbed well orally
-slightly broader coverage than PCN
-effective to some bacteria PCN resistant
-stable at higher pH; effective in urinary tract, GI tract, and stomach

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87
Q

What does ampicillin cover?

A

Everything PCN covers + haemophilus flu, e.coli

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88
Q

What is the adverse reaction to ampicillin?

A

Bright red Skin rash, usually 7-10 days after start of therapy

Usually caused by protein impurities in commercial prep of drug

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89
Q

What are most often prescribed in surgical abx prophylaxis?

A

Cephalosporins

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90
Q

How do cephalosporins work?

A

Bactericidal; inhibit bacterial cell wall synthesis with low risk of cell toxicity

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91
Q

All cephalosporins can penetrate ___ and ___?

A

Joints and cross placenta

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92
Q

Risk of cephalosporins?

A

Thrombophlebitis and >3rd gen are expensive

Cutaneous reactions; often delayed maculopapular rashes and/or fevers

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93
Q

What are the 4 kinds of beta lactams?

A

Penicillins, cephalosporins, carbapenems, and monobactams

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94
Q

What are carbapenems and ertapenem used to treat?

A

Klebsiella PNA, nose mouth GI normal flora, VAP,

Last line for MDR pathogens

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95
Q

What has the broadest spectrum of activity and greatest potency against gram + and gram -?

A

Carbapenems and ertapenem

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96
Q

What is a type A drug reaction?

A

Side effect; diarrhea, nausea, etc

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97
Q

Type B type I

A

-IgE mediated
-Can be mild (urticaria) to severe (cardiovascular collapse)
- onset-2hrs

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98
Q

Type B type II

A

-antibody dependent cytotoxicity
-hemolytic anemia, thrombocytopenia
-happens weeks after exposure

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99
Q

Type B type III

A

-Immune complex, serum sickness
-weeks after exposure

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100
Q

Type B type IV

A
  • Tcell mediated
    -rash, Stevens Johnson Syndrome
    -happens 48hrs to weeks after exposure
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101
Q

What’s is Stevens Johnson Syndrome and how is it treated?

A

-rare serious skin disorder, mostly caused by abx rxn (all classes), starts with flu like symptoms, followed by painful rash that spreads and blisters, top layer of skin dies, sheds, heals
-can take 48hrs to weeks after exposure
-treatment is supportive care

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102
Q

Loading dose=

A

Vd*desired plasma concentration/ bioavailability

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103
Q

Drug with high Vd >than TBW is called? And give example

A

Lipophilic
Ex: propofol

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104
Q

Drug with Vd < TBW is called? Give example

A

Hydrophilic
Ex: rocuronium

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105
Q

How does Vd affect loading dose?

A

High Vd= larger loading dose
Low Vd = smaller loading dose

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106
Q

What is the equation for Vd

A

Vd= amount of drug/desired plasma concern

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107
Q

How much water does TBW contain?

A

42 L

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108
Q

Clearance is directly proportional to? (3)

A

-blood flow to clearing organ
-extraction ratio
-drug dosage

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109
Q

Clearance is inversely proportional to (2)

A

-half life
-drug concentration in central compartment

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110
Q

Steady state is achieved after how many half-lives?

A

5

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111
Q

Define half-life

A

Time it takes for 50% of the drug to be eliminated from the body

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112
Q

Define half-time

A

Time it takes for 50% of the drug to be removed from the plasma during the elimination phase

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113
Q

How many half times does it take to clear the dose from the plasma?

A

5

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114
Q

What is context sensitive half time?

A

The time required for the plasma concentration to decline by 50% after the infusion rate is stopped

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115
Q

What is the “context” in the context sensitive half-time?

A

Duration of the infusion (time)

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116
Q

Which opioid has a similar context-sensitive half-time regardless of infusion duration?

A

Remifentanil

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117
Q

I’m which circumstance is a drug MORE likely to pass through a lipid membrane?

A
  • a weak BASE where the pH of the solution is > the pKa of the drug

-a weak ACID where the pH of the solution is < the pKa of the drug

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118
Q

Define ionization

A

The process where a molecule gains a positive or negative charge; this affects a molecules ability to diffuse through lipid membranes

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119
Q

A weak acid will ____ a proton to water?

A

Donate

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120
Q

A weak base will ____ a proton from water?

A

Accept

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121
Q

What is ionization dependent on?

A

-pH of the solution
-the pKa of the drug

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122
Q

What is pKa? What does high or low pKa mean?

A

A constant value; tells us how much a molecule wants to behave like an acid

-low pKa= amazing acid
-high pKa= terrible acid

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123
Q

Weak bases in a acidic solution?
Weak bases in a basic solution?

A

-more ionized and water soluble in acidic solution
-more non-ionized and lipid soluble in a basic solution

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124
Q

Weak acids in acidic solution?
Weak acids in basic solution?

A

-more non-ionized and lipid soluble in acidic solution
-more ionized and water soluble in basic solution

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125
Q

The ionization fraction predominates if:

A

-the molecule is a weak base and the pH of the solution is <pKa of the drug (a base is added to an acidic solution)

-the molecule is a weak acid and the pH of the solution is >the pKa of the drug (an acid is added to a basic solution)

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126
Q

The non-ionized fraction predominates if:

A

-the molecule is a weak base and the pH of the solution is >the pKa of the drug (base is added to a basic solution)

-a molecule is a weak acid and the pH of the solution is < the pKa of the drug (an acid is added to an acidic solution)

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127
Q

What does pKa tell you?

A

A drugs pKa = the pH where 50% of the drug is ionized and the other 50% of the drug is non-ionized

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128
Q

Which circumstance creates the STRONGEST gradient for the passage of local anesthetic from the mother to the fetus?

A

Maternal alkalosis and fetal acidosis

Maternal alkalosis: increases the non-ionized fraction in the maternal circulation; more local anesthetic is available to diffuse across the placenta

Fetal acidosis: increases the ionized fraction inside the fetus. This prevent the local anesthetic from crossing the placenta (back to the mother) thus trapping it inside the fetus

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129
Q

What happens when lidocaine enters the fetal circulation?

A

A more acidic environment increases lidocaines ionized fraction

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130
Q

How does uncontrolled maternal pain affect local anesthetic concentration in the fetus

A

Pain causes the mothers minute ventilation to increase (resp alkalosis) and this increases lidocaine transfer across the placenta.

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131
Q

What conditions can decrease protein concentrations?

A

-liver disease, renal disease, old age, malnutrition and pregnancy

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132
Q

What happens when a drug is bound to a plasma protein?

A

It cannot bind to receptor; only when drug is released from the protein is it able to affect the body

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133
Q

Name 3 plasma proteins

A

Albumin, alpha 1 acid glycoprotein, beta-globulin

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134
Q

Which plasma proteins bind to acidic drugs? Which to basic drugs?

A

-acidic: albumin

-basic: alpha- 1acid glycoprotein and beta-globulin

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135
Q

Vd is ____ related to the degree of plasma binding

A

Inversely

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136
Q

Highly protein bound drugs typically slower rate of ____and ____

A

Metabolism and elimination

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137
Q

How to calculate percent change

A

Percent change = (new value- old value)/old value x 100%

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138
Q

Metabolism depends on 2 factors:

A

-the concentration of drug at the site of metabolism; influenced by blood flow to the site of metabolism

-the intrinsic rate of the metabolic process; influenced by genetics and enzyme activity

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139
Q

What is the purpose of metabolism?

A

Change a lipid-soluble pharmacologically active compound into a water soluble pharmacologically inactive compound

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140
Q

Describe enterohepatic circulation and give two examples of drugs that use it

A

Some conjugated compounds are excreted into the bile, reactivated in the intestine, and then reabsorbed into the systemic circulation

Ex: diazepam and warfarin

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141
Q

What are the three phases of metabolism

A

Modification, conjugation and elimination

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142
Q

What happens to a drug during conjugation

A

Phase 2 adds on an endogenous, highly polar, water soluble substrate to the drug molecule

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143
Q

Name 3 drugs that undergo perfusion dependent hepatic elimination

A

Fentanyl, lidocaine, and propofol

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144
Q

Name 2 drugs that undergo capacity-dependent hepatic elimination

A

Diazepam and rocuronium

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145
Q

What is extraction ratio

A

A measure of how much drug is delivered to the clearing organ vs how much drug is removed by that organ

ER 1.0= 100% of the drug delivered to the clearing organ is removed

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146
Q

Hepatic clearance is the product of(2)

A

Liver blood flow- how much drug is delivered to the liver

Hepatic extraction ratio- how much drug is removed by the liver

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147
Q

Perfusion dependent elimination

A

A drug with high hepatic extraction ratio (>0.7) clearance is dependent on liver blood flow; blood flow exceeds enzymatic activity so alterations to enzyme activity has little effect

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148
Q

Capacity dependent hepatic elimination

A

Drug has low hepatic extraction ratio (<0.3) the clearance is dependent on the ability of the liver to extract the drug from the blood; changes in hepatic enzyme activity or protein binding have profound impact on clearance

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149
Q

What p450 enzyme is most important

A

CYP3A4
Metabolized nearly 50% of drugs we administer

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150
Q

What is an enzyme inducer?

A

They stimulate the synthesis of additional enzymes which increases drug clearance
Ex: alcohol, tobacco, phenytoin

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151
Q

What is an enzyme inhibitor?

A

These compete for binding sites in the enzymes and reduces drug clearance

Ex: SSRIs, omeprazole, grapefruit juice

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152
Q

Cefazolin dose, redose, special considerations

A

2g
3g >120 kg
Redose q4hrs
T1/2 1.2-2.2 hrs

Most common first line abx surgical prophylaxis; inexpensive

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153
Q

Clindamycin dose; redose

A

600-900mg IV x1
Can be redose q6hr
Used for SSI prevention in PCN hypersensitivity
Half-life: 2-4 hrs

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154
Q

Efficacy

A

Measure of the intrinsic ability of a drug to elicit a given clinical effect

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155
Q

Potency

A

The dose required to achieve a given clinical effect

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156
Q

Individual variability

A

When administered the same dose, different patients may have different clinical effects

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157
Q

ED 50 and ED 90 are measures of?

A

Potency

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158
Q

What does a steep slope on the dose response curve imply?

A

It implies that most of the receptors must be occupied before we observe the clinical response

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159
Q

How is potency represented on the dose response curve?

A

Represented on the x axis
Left shift =more potent
Right shift = less potent

160
Q

How do you calculate therapeutic index?

A

TI= TD50/ED50

Therapeutic index= toxic dose 50/effective dose 50

161
Q

What is chirality?

A

The tetrahedral bonding of carbon to 4 different atoms

162
Q

Examples of drugs that have R and S enantiomers

A

Ketamine, isoflurane, morphine

163
Q

What antibiotics are safe for pregnancy?

A

PCN and Cephalosporins

164
Q

What are elderly considerations for absorption, metabolism, distribution and excretion

A

Oral absorption- decreased gastric acidity, reduced GI motility

Distribution- increased total body fat, decreased albumin

Metabolism- decreased hepatic blood flow

Excretion- decreased GFR

165
Q

What is the first agent to treat MRSA?

A

Vancomycin

166
Q

Aminoglycosides: MOA, examples, target bacteria

A

Targets gram neg

Ex: gentamycin, kanamycin

-mycin, except vancomycin

MOA: inhibit protein synthesis by targeting ribosomal unit 30s

167
Q

Glycopeptides: MOA, target bacteria, examples

A

Ex: vancomycin
MOA: inhibit peptidoglycan synthesis in bacterial cell walls
Targets gram +

168
Q

Cephalosporins example, target bacteria and MOA

A

Ex: 1st gen cefazolin, 2 cefoxitin 3 ceftriaxone 4 cefepime

MOA: inhibit peptidoglycan synthesis in bacterial cell wall

Target gram + and gram -

169
Q

PCN example, MOA, target bacteria

A

Ex: PCN G, ampicillin, methacillin
MOA: inhibits cell wall synthesis beta lactam ring

1st gen targets gram +
2nd gen targets gram -

170
Q

Quinolones/ fluoroquinolones MOA, target bacteria and examples

A

MOA: inhibits DNA replication (toposomerase II-IV)

Targets gram + and gram -

Ex: ciprofloxacin and levofloxacin

171
Q

Macrolides MOA, example and target bacteria

A

Ex: Erythromycin, clindamycin, azithromycin
Targets gram +
MOA: target bacterial ribosomal subunit 50s
-thromycin

172
Q

Sulfonamides MOA, target bacteria, examples

A

MOA: inhibits folate synthesis in bacteria

Examples: sulfamethizole

Targets gram + and gram -

173
Q

Cefoxitin dose, and redose

A

Dose: 2g
Half-life: 0.7-1.1
Redose: 2 hrs

174
Q

Metronidazole dose, half life and redose

A

Dose: 500mg/100ml over 1hr
Half-life: 6-8 hrs; 9-15hrs
Redosing: repeat q8hr if indicated

175
Q

Metronidazole target bacteria and used for?

A

Bactericidal against ANAEROBIC GRAM NEG and cdiff

Used for colorectal surgeries or any bowel perf

176
Q

Vancomycin dosing, half life and redose

A

Dose: 15 mg/kg; round to nearest 250mg

Half-life: 4-8hrs 8-12hr half life

Redose:n/a

1-2 g loading dose

177
Q

Azithromycin dose half-life indications

A

Dose: 500mg IV very slow infusion or 500mg daily PO 7-10 day therapy

Extremely long half-life 68hrs

Indications: bacterial exacerbation of COPD, bacterial sinusitis, community acquired PNA

178
Q

Pipercillin-tazobactam, dose, redose, and class

A

Class: PCN and beta-lactamase inhibitor
Dose: 3.375g

Redose: 2hrs

179
Q

Gentamycin class, dose, and redose?

A

Class: aminoglycoside

Dose: 5mg/kg

redose: n/a

180
Q

Ceftriaxone dose and redose

A

Dose: 2g

Redose: n/a

3rd gen cephalosporin

181
Q

What is the MH hotline number

A

1-800-644-9737

182
Q

What affects a drugs Vd?

A

Molecular size, ionization, protein binding

Pregnancy and burns

183
Q

Which drug class has anti-inflammatory effects

A

Macrolides/lincosamides

184
Q

What drugs do we avoid with myasthenia gravis

A

Macrolides, aminoglycosides, quinolones

185
Q

adverse effects of aminoglycosides

A

-mycin drugs
-ototoxicity, nephrotoxicity, muscle weakness with NMB, destruction of cochlear sensory hairs (dose dependent)

186
Q

what adverse effects of quinolones?

A

GI disturbance, tendon ruptures, weakness in Myasthenia Gravis pts

187
Q

what abx are used for urology cases?

A

fluoroquinolones or cefazolin
if betalactam allergy use clindamycin or vanc+aminoglycoside (gentamycin)

188
Q

what abx used in colorectal surgery?

A

cefazolin + metronidazole
or
cefotetan

if betalactam allergy
clindamycin + aminoglycoside (gentamycin)
gentamycin + metronidazole

189
Q

what parts of NMJ are affected by aminoglycosides?

A

nerve terminal, axon, ACh release, muscle membrane, and cholinergic receptors

190
Q

what is big risk of Erythromycin?

A

prolong cardiac repolarization- torsades
can cause toxicity/cardiac death

191
Q

what are some benefits of Erythromycin

A

-increases lower esophageal sphincter tone (lowers aspiration risk)
-increases gastric emptying

192
Q

what abx is used as alternative in surgery for patients with allergy to cephalosporins?

A

clindamycin

193
Q

Why do we choose 1st gen cephalosporins for sx prophylaxis?

A

-wide therapeutic index (gram - and gram +)
-low incidence of side effects/adverse rxns
-affordable

194
Q

What is epi IM and IV dose for anaphylaxis?

A

IM dose 0.5mg for 1:1000 5-15 min between doses

IV dose 50-100mcg slow IV push for 1:10,000 concentration

195
Q

Anaphylaxis management

A

-remove cause
-call for help
-IM/IV epi
-place pt supine unless airway swelling (then upright leaning forward); pregnant pt on left side
-supplement O2
-volume resuscitate

196
Q

all cephalosporins can ____ and _____?

A

penetrate joints and cross placenta

197
Q

what abx penetrates pleura, ascitic and synovial fluid?

A

gentamycin

198
Q

how do you overcome effect of aminoglycosides at the NMJ?

A

IV calcium

199
Q

clindamycin can cause ___ when used with succinylcholine or NMB?

A

prolonged neuromuscular blockade

200
Q

what antiseptic targets gram + and gram - bacteria?

A

CHG

201
Q

what antiseptic/disinfectant is most important for disinfectant of the skin?

A

iodine; kills bacteria, viruses and spores

202
Q

how many mg of ryanodex vs dantrolene in vial

A

ryanodex 250mg in vial
dantrolene 20mg per vial

203
Q

What is MH

A

An inherited disease of skeletal muscle that’s characterized by disordered calcium homeostasis

Exposure to halogenated anesthetics or succinylcholine activates the defective ryanodine RYR1; this stimulates sarcoplasmic reticulum to release way too much calcium into cell

204
Q

What two classes of drugs trigger MH?

A

Halogenated anesthetics

Depolarizing neuromuscular blockers (succinylcholine)

205
Q

What three co-existing diseases are definitively associated with MH?

A
  1. King-Denborough syndrome
  2. Central core disease
  3. Multiminicore disease
206
Q

What are the consequences of increased intracellular calcium in the myocyte?

A

-rigidity from sustained contraction
-accelerated metabolic rate/rapid depletion of atp
-increased O2 consumption
- increased CO2 and heat production
-mixed resp and lactic acidosis
-sarcolemma breaks down
-k+ and myoglobin leak into the systemic circulation

207
Q

What conditions are risk of MH not increased with?

A

-Becker muscular dystrophy
-neuroleptic malignant syndrome
-myotonia congenita
-myotonic dystrophy
-osteogenesis imperfecta

208
Q

What are risk factors of Mh and how often is incidence?

A
  1. Geography- Wisconsin, Nebraska, west Va, Michigan higher risk
  2. Male
  3. Youth

1:5,000 to 1:50,000

209
Q

What is the primary intracellular ion affected by MH?

A

Disordered calcium

210
Q

Is duchenne muscular dystrophy a risk factor for MH?

A

No

211
Q

The earliest signs of MH are? (3)

A

Tachycardia, increased EtCO2, masseter spasm

212
Q

What are the late signs of MH?

A

Hyperthermia, cola colored urine (rhabdomyolysis), and DIC

213
Q

What is the gold standard for diagnosing MH?

A

Caffeine-halothane contracture test (CHCT)

High sensitivity
Low specificity

214
Q

What is trismus?

A

A tight jaw that can still be opened; normal response to succinylcholine

215
Q

What is masseter muscle rigidity?

A

A tight jaw that CANNOT be opened; not normal response to succinylcholine

216
Q

What drugs are contraindicated in MH management?

A

Ca channel blockers; life threatening hyperkalemia can result when ca channel blocker co administered with dantrolene

217
Q

How to treat MH

A

-discontinue triggering agent, continue with TIVA
-call for help/notify surgeon to terminate surgery
-hyperventilate with 100% O2 at minimum FGF of 10L/min
-apply charcoal filters to inspiratory and expiratory port
-Administer dantrolene 2.5mg/kg IV q 5-10min
-cool pt
-treat acidosis and electrolyte disturbances
- maintain urine output 2ml/kg/hr

218
Q

Dantrolene MOA

A
  1. Reduces calcium release from the RyR1 receptor in skeletal muscle myocyte
  2. Prevents Ca entry into the myocyte, which reduces the stimulus for calcium induced calcium release
219
Q

What is MIC?

A

the minimal inhibitory concentration- tissue concentration to prevent bacterial growth

220
Q

what are the three phases of multi-compartment model?

A

-rapid distribution
-slow distributiom
-terminal phase

221
Q

which channels are activated by neuromuscular blocking agents?

A

ligand-gated channels

222
Q

what protein receptors do Haloperidol, morphine, losartan and plavix use?

A

G- coupled protein receptors

223
Q

What is an example of covalent bound drug?

A

warfarin

224
Q

define the lock and key theory

A

a cell receptor has a specific binding site that is shaped to fit a specific signaling molecule

225
Q

name 4 meds that have selective agonism?

A

albuterol, phenylephrine, dobutamine, esmolol

226
Q

what is Cmx and Tmax

A

Cmax- peak plasma concentration ( depends on rate and extent of absorption)
Tmax- time when Cmax occurs( depends on rate only)

227
Q

What phase 1 processes are cyp450 involved in?

A

Oxidation, reduction and hydrolysis

228
Q

What a drugs taken up by first pass pulmonary effect

A

-basic lipophilic amines
-lidocaine, propranolol and fentanyl

229
Q

Describe route of excretion in kidneys?

A

-glomerular filtration: passive filtration removes unbound drug from plasma (GFR is key)
-tubular secretion- active transport of acid and basic drugs (proximal tubule)
-tubular reabsorption- passive or active uptake of drug from urine into plasma (proximal and distal region of nephron)

230
Q

Oxidation

A

Removes a electron from a compound

231
Q

Reduction

A

Adds electrons to a compound

232
Q

Hydrolysis

A

Adds water to a compound to split it apart (usually an ester)

233
Q

Where are CYP450 enzymes located

A

Smooth endo plastic reticulum of hepatocyte

234
Q

In regards to the variables on the dose-response curve what does the ED50 measure?

A

Potency

235
Q

What can result from giving Duchenne & Becker muscular dystrophy succinylcholine?

A

Rhabdo and hyperkalemia

236
Q

what is an example of G coupled protein receptors

A

muscarinic receptors, Ach receptors

seconds

237
Q

What are examples of ligated channel receptors

A

nicotinic ach recptors, neuromuscular blocking agents

miliseconds

238
Q

which organs have highest to lowest perfusion?

A

Kidneys –> Liver–> Heart–> brain–> bone–> fat

239
Q

what drug class increases effect of oral anticoagulants and thiazide drugs?

A

sulfonamides

240
Q

What MH grade would judge the likelihood of true MH

A

20 and higher

241
Q

What conditions can mimic MH?

A

-contrast dye
-diabetic coma
-drug toxicity/overdose
-heat stroke
-anesthesia machine malfunction with increased CO2
-thyroid storm
-intracranial free bleed
-pheochromocytoma
-sepsis

242
Q

what diseases have increased risk of RYR1 abnormalities?

A

exertional rhabdomyolysis
severe statin induced myopathy
native american myopathy,

243
Q

gold standard testing for MH

A

Caffeine-halothane contracture test

80% specificity
high sensitivity

244
Q

most common cause of death with MH

A

Vfib

245
Q

which anesthesia gases trigger MH

A

halothane
enflurane
isoflurane
sevoflurane
desflurane

246
Q

side effects of Dantrolene

A

nausea, diarrhea, blurred vision, muscle weakness

247
Q

what class of drug is dantrolene considered

A

muscle relaxant

248
Q

What anesthetic agents have bronchodilating properties

A

Volatile anesthetics and ketamine

249
Q

Albuterol class and MOA

A

Class: short acting B2 adrenergic agonist

MOA: B2 stimulation increases cAMP and decreases ionized Ca which causes bronchiole smooth muscle dilation; also stabilizes mast cell membranes to decrease mediator release

250
Q

Albuterol indications and dose

A

Indications: preferred B2 agonist for treatments of acute bronchi spasm due to asthma; wheezing and airflow obstruction

Dose: nebulizer 2.5 mg

251
Q

Albuterol duration and side effects

A

Duration: 4-8 hrs ; effects of albuterol and volatile agents on bronchomotor tone are additive

SE: excitement, nervousness, tremors, bronchospasm, exacerbation of asthma, pharyngitis, rhinitis, upper resp infection

252
Q

Albuterol anesthesia considerations

A

Have pt continue medication up to surgery, including day of

253
Q

Albuterol MOA

A

Binds to B2 adrenergic agonist located on the plasma membrane if smooth muscles, epithelial, endothelial leading to increase cAMP and decreases release of calcium which leads to smooth muscle relaxation

254
Q

Why do we use albuterol?

A

-strong B2 selectivity
- short onset time
-average duration of action

255
Q

Describe pathway of airflow

A

Nose/mouth -> pharynx > larynx > trachea > bronchi > bronchioles > alveoli

256
Q

What autonomic nervous system effects respiratory system

A

-Parasympathetic innervation via vagus nerve
-muscarinic 3 (M3) receptor stimulation = bronchoconstriction
-PNS regulates airway construction/dilation as well as microvasculature of airway

257
Q

How do beta agonists work?

A

Stimulate G proteins which converts ATP to cAMP which reduces intracellular calcium release in the pulmonary vasculature which causes vasodilation in the pulmonary smooth muscle

258
Q

Where is nitric oxide produced?

A

In the endothelial cells (inner linings of blood vessels)

259
Q

How does nitric oxide work?

A

-noncholinergic PNS nerves release vasoactive intestinal peptide onto airway smooth muscle which increases NO production,

NO stimulates cGMP which fosters smooth muscle relaxation and bronchodilation

260
Q

Define chronic bronchitis

A

Chronic productive cough for 3 months in each of 2 successive years in a patient whom other causes of productive cough have been excluded

261
Q

Define emphysema

A

Presence of permanent enlargement of airspace’s distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis

262
Q

Salmetrol class and indications

A

Class: long acting B2 agonist

Indications: prescribed when rescue medications are used more the 2x per week for asthma and often in combo with steroids
Can be used prophylactically before exercise for exercise induced asthma

263
Q

Salmeterol duration and side effects

A

Duration: >12 hrs

SE: headache, HTN, edema, dizziness anxiety

264
Q

Salmeterol MOA

A

-same as SABA
-Has side chain that binds to B2 receptor and prolongs activation

265
Q

Salmeterol anesthesia considerations

A

-Have pt continue medication up to and including day of surgery, get back on as soon as appropriate
-pts have increased risk of bronchospasm/bronchiole reactivity with LABA
-not used as monotherapy

266
Q

The lower airway is more ____

A

Muscular

267
Q

Where are M3 and B2 adrenergic receptors located?

A

Lower airway

268
Q

Inhaled and nebulized medications are targeting which area of lungs?

A

12-16th generation/locations of bronchiole tree

269
Q

Name 3 things that increase ionized Ca and what’s that result in?

A

Cytokines (CysLT1)
Histamines (H1)
M3

Causes bronchoconstriction/contraction

270
Q

B2 and PDE work by ____ and _____which causes _____

A

Increasing cAMP and decreasing ionized calcium which causes relaxation

271
Q

How do inhaled cortiocosteroid work?

A

Prevent destabilization of mast cells; prevent mast cell degranulation

272
Q

Management steps for asthma

A
  1. SABA
  2. Inhaled corticosteroids
  3. LABA
273
Q

Inhaled anesthesia and formoterol (and all LABA) cause increased risk of _____

A

Prolonged QT and increase risk of cardiac arrhythmias

274
Q

Theophylline class and MOA

A

Class: methylxanthines

MOA: inhibits PDE which increases cAMP, reduces iCa and causes bronchodilation;
releases endogenous catecholamimes;
inhibits adenosine receptor

275
Q

Side effects >20mcg/mL and >30mch/mL plasma levels for theophylline

A

> 20: N/v, diarrhea, headache, disrupted sleep

> 30: seizures, tachydysrhythmias, CHF

276
Q

Theophylline anesthesia considerations

A

-Dc med the evening before surgery
-Get serum level before surgery; less than 20
-all pts need preventable measures in place to assess for seizures, tachydysrhythmias, CHf which can present under GA

277
Q

When used with COPD what is a risk of using inhaled corticosteroids?

A

Increased risk of serious PNA

278
Q

Inhaled corticosteroids drugs and MOA?

A

Drugs: beclomethasone, budesonide, flunisolide, fluticasone, triamcinolone

MOA: acts on bronchioles;
stimulates intracellular steroid receptors;
regulates inflammatory protein synthesis

-decrease airway inflammation
-decrease airway hyper responsiveness

279
Q

Side effects of inhaled corticosteroids

A

Dysphonia- hoarse voice
Myopathy of laryngeal muscles
Oropharyngeal candidiasis
Possible adrenal suppression

280
Q

Inhaled corticosteroids indications

A

Asthmatic obstruction

281
Q

Inhaled corticosteroids anesthesia considerations

A

Inhaled and systemic corticosteroids should be continued during the perioperative period

282
Q

Why would we use systemic corticosteroids

A

Treat asthma and COPD exacerbations that are not responsive to B2 adrenergic agonists

283
Q

Side effects of systemic corticosteroids

A

HTN,
hyperglycemia,
adrenal suppression
Increased infections
Cataracts
Dermal thinning
Psychosis

284
Q

Why are inhaled corticosteroids less effective in COPD patients

A

Their disease inflammation is resistant to the action of inhaled corticosteroids

285
Q

If a patient is on systemic corticosteroids steroid >2 weeks what is an anesthesia consideration

A

They are at risk for adrenal suppression and may need Intraoperative supplementation of IV corticosteroids

286
Q

What are Inhaled corticosteroids dosing based off of

A

Patients age
1-2 puffs 1-2x day

287
Q

How do anticholinergic medications work?

A

They work by blocking the actions of ACh

288
Q

Name short acting, long acting and systemic anticholinergics

A

Short: ipratropium
Long: tiotropium
Systemic: atropine and glycopyrrolate

289
Q

Which autonomic nervous system involved with bronchoconstriction/dilation?

A

PNS

290
Q

What are M1 and M3 receptors responsible for

A

Bronchoconstriction and mucus production

291
Q

Inhaled cholinergic antagonist MOA

A

They reduce smooth muscle tone by blocking ACh from binding to M3 receptors

292
Q

Side effects of inhaled cholinergic antagonists

A

Dry mouth, urinary retention, pupil dilation

293
Q

What resp drug class is used for exacerbations but not maintenance therapy?

A

Inhaled anticholinergic (cholinergic antagonists)

294
Q

Ipratropium class and MOA

A

Class: anticholinergic, antimuscarinic

MOA: similar to atropine except a quaternary amine so DOES NOT CROSS BBB; almost complete protection against bronchospasm

295
Q

Ipratropium dose, onset, DOA

A

Dose: 200unit/inh 2 puffs 4x day

Onset: immediate

Duration: 5-6 hrs

effects in 30-90 min lasting 4 hrs; not rescue

296
Q

Ipratropium side effects and anesthesia considerations

A

Side effects: headache, dizziness, GI xerostomia, nausea, UTI, dyspnea, flu like symptoms, upper resp tract infections

Considerations: do not d/c prior to surgery

297
Q

What is a risk of anticholinergics?

A

Increased CNS effects

298
Q

Atropine class and dose and considerations

A

Class: anticholinergic

Dose 0.5-1mg 30-60 min preop for secretions repeat 4-6 hrs max 3mg

Consider: tachyarrhythmias most common

299
Q

Glycopyrrolate class dose considerations

A

Anticholinergic

4mcg 30-60 min preop for secretions

SE: flushing, twchyarrhymthmias, heart block, headache, vomiting, dry mouth, constipation, urinary retention

300
Q

Scopolamine considerations

A

-decreases airway resistance and increases dead space by 1/3
-similar effects as glycopyrrolate but has CNS effects

301
Q

Leukotriene modifiers drugs and MOA

A

Drugs: montelukast

MOA: inhibits 5 lipoxygenase enzyme (decreases leukotrine synthesis)

decreases –>
bronchospasm,
vasoconstriction
eosinophil recruitment promoted by leukotrienes

302
Q

Leukotriene modifiers indications and side effects

A

Indication: COPD

SE: negligible

303
Q

Leukotriene modifiers anesthesia considerations

A
  • montelukast and zafirlukast NOT used in the treatment of acute bronchospasm
    -continue up to surgery and immediately after
304
Q

What meds do betalactamase and penicillinase not effect?

A

Methicillin
Oxacillin
Dicloxacillin

305
Q

Which abx can cause neurotoxicity and hyperkalemia in CKD pts?

A

PCN

306
Q

Where are ligand gated channels located

A

Lipid bilayer of the cell

307
Q

What anesthesia drugs do we avoid in asthma and copd patients

A

Succs, atracurium, morphine, merperidine

Release histamines

308
Q

In asthma and copd pts, if you need to use a beta blocker which one and why

A

Esmolol bc it’s B1 selective

309
Q

What is the multicompartment model

A

-rapid distribution: plasma, highly perfused tissues
-slow distribution: movement into low perfusion tissues and movement back into plasma
-terminal phase: more drug in tissues than in plasma, drug returns to plasma and is metabolized/ excreted

310
Q

IM Epi dosing adults

A

.2-.5 mg

311
Q

what is the incidence of MH in children? adults? what is the mortality rate for MH?

A

1 in 40,000 in children
1 in 250,000 in adults
mortality rate is 10%

312
Q

what are the 11 clinical manifestations of MH

A
  1. hypercarbia
  2. tachycardia
  3. tachypnea
  4. hyperthermia
    5 hypertension
    6 cardiac dysrhythmias
    7 metabolic acidosis
    8 hyperkalemia
    9 skeletal muscle rigidity
    10 myoglobinuria
    11 hypoxemia
313
Q

what is the earliest sign of MH

A

increased end tidal CO2, out of proportion to minute ventilation

314
Q

Can masseter spasm be an early sign of MH? will masseter spasm be the first sign of MH

A

Masseter spasm is an early sign, though generally not the first

315
Q

what response is considered evidence of MH in children?

A

masseter muscle rigidity after admin of succs, especially children undergoing strabismus surgery

316
Q

how fast may temp increase during an episode of MH?

A

1-2 degrees C every 5 min

317
Q

8 initial actions for initial managment of MH

A
  1. d/c inhaled anesthetics and succs
  2. hyperventilate with 100% O2
  3. admin dantrolene
  4. treat acidosis with Na bicarb 1-2mM/KG
  5. lower body temp to 38 degrees
    6 replace anesthetic circuit and canister
    7 monitor capnography and blood gas
    8 treat hyperkalemia and dysrhythmias
318
Q

a patient has just experienced masseter muscle rigidity from succ. what lab value may confirm the diagnosis of MH?

A

elevated creatine phosphokinase (CPK >20,000)

319
Q

a child has received sevo and succs and mouth cannot be opened. what action should be taken?

A

possible MH, discontinue the trigger and begin MH treatment

320
Q

How and where does dantrolene work?

A

-acts to decrease the calcium level in the skeletal muscle by decreasing the release of Ca from the sarcoplastic reticulum
-skeletal muscle relaxes when the supply of Ca to the contractile proteins is impaired

321
Q

dose and how long should you give dantrolene in management of MH

A

-2.5mg/kg q 5 min until episode is terminated
-max dose is 10-20mg/kg

322
Q

how much dantrolene is found in each vial? how must it be prepared?

A

-contains 20mg of dantrolene and 3g mannitol
-mix with 60ml warmed sterile water
-keep warm bc of the mannitol

323
Q

you have successfully treated acute episode of MH. dantrolene should be re-administered at what intervals and how long?

A

-continue therapy for 24 hrs
-1mg/kg q 4-6 hrs as a bolus or 0.25 mg/kg/hr continuous infusion

324
Q

list 4 ways to actively cool pt in acute MH episode?

A
  1. lavage (gastric, bladder, open cavities)
  2. admin cooled IV fluids
  3. ice packs (groin, axilla, neck, forced air blankets)
  4. cardiopulmonary bypass in severe cases
325
Q

at what body temp should cooling pt in MH be stopped and why?

A

38*C
to prevent deleterious effects of hypothermia

326
Q

once the initial episode of MH is controlled, the patient will remain at risk for what 5 complications?

A
  1. reoccurence
  2. DIC
  3. myoglobinuric renal failure
  4. skeletal muscle weakness
  5. electrolyte abnormalities
327
Q

a patient in MH crisis has pvcs. what is the antiarrhythmic drug of choice?

A

amiodarone

328
Q

a woman in labor identified as susceptible to MH. What anesthesia technique are acceptable?

A

-prophylactic dantrolene not recommended, prepare the anesthesia workstation

329
Q

what 6 steps do you take when family hx of MH? are non depolarizing muscle relaxants safe?

A
  1. anesthesia and premedication should be designed to produce low normal HR
  2. anesthesia machine is prepared by draining, removing or diasbling anesthetic vaporizors and cahnge tubing/ CO2 aborbent, flow O2 at 10ml for 10 min or longer
  3. measure etCO2
  4. core body temp (nasopharyngeal, rectal, esophageal)
  5. regional, local or major condection anesthetic should be used, TIVA followed by nitrous oxide, O2 and nondepolarizing relaxant with opioids
  6. arterial and central venous monitoring is recommending in MH susceptible pts
  7. observe pt closely in postoperative period
330
Q

what syndrome can mimic MH

A

neuroleptic malignant syndrome-presents as hypermetabolic episode with hyperthermia, ANS instability, muscle rigidity and rhabdomyolysis

331
Q

pts treated with what drugs are susceptible to neuroleptic malignant syndrome?

A

antipsychotic agents
-phenothiazines, haloperidol, etc
-antipsychotic drugs reflect dopamine depletion in the CNS

332
Q

stepwise managment of COPD medications

A
  1. reduce risk factors, add SABA
  2. add LABA and rehab
  3. Add inhaled glucocorticosteroids if repeated exacerbations
  4. add longterm O2; consider surgical/palliative treatment
333
Q

early asthma body response

A

-IgE response causes mast cells to degranualte, releasing large # of inflammatory mediators
-vasodilation
-increase capillary permeability
-mucosal edema
-bronchospasm
-tenacious mucous secretion

334
Q

late asthma response

A

-air trapping
-hyperinflation distal to obstruction
-increase work of breathing
-hypoxemia

335
Q

clinical manifestations of asthma

A

-asymptomatic between attacks
-chest constriction, expiratory wheezes, dyspnea, non productive cough, prolonged expiration, tachycardia, tachypnea
-pulsus paradoxus
-status asthmaticus (bronchospasm not reverse by usual measures, life threatening)
-ominous signs (silent chest and PaCO2 > 70mmHg

336
Q

what medications can reduce histamine release?

A

presynaptic H2 receptor agonists

AVOID H2 antagonists like famotidine and ranitidine- allow H1 stimulation which leads to bronchospasm

337
Q

MOA anticholinergics

A

blocks M3 receptor which decreases IP3 which leads to decreased ionized Ca

338
Q

Bacteriostatic vs Bactericidal

A

Static: inhibits bacteria from reproducing but doesn’t otherwise kill them

Cidal: actively kills bacteria

339
Q

What enzyme does the beta lactam ring inhibit

A

Transpeptidase

340
Q

Name some beta lactamase inhibitors

A

Clavulanic acid, tazobactam, Silva tan
Augmentin (amox-clav)
Zosyn (piperacillin tazobactam)

341
Q

What is the most common side effect of antibiotic prophylaxis?

A

Pseudomembranous colitis

342
Q

How often should cefazolin be re-dosed in OR?

A

Every 4 hrs

343
Q

Key side effect for PCN

A

Allergic rxn

344
Q

Key side effect gentamycin

A

-ototoxicity
-nephrotoxicity
-skeletal muscle weakness

345
Q

Key side effect clindamycin

A

-skeletal muscle weakness
-allergic rxn

346
Q

Key side effect for doxycycline

A

-hepatotoxicity
-nephrotoxicity

347
Q

Key side effect of metronidazole

A

-peripheral neuropathy
-alcohol intolerance

348
Q

Key side effect of vancomycin

A

-hypotension
-red man syndrome
-SJS

349
Q

Epinephrine treats anaphylaxis in what 3 ways?

A
  1. Prevents degranulation
  2. Provides CV support
  3. Dilates the airways
350
Q

What’s the most common cause of drug mediated anaphylaxis in the perioperative period

A

Succinylcholine

351
Q

A patient with asthma experiences bronchospasm immediately following tracheal intubation. This is MOST likely the result of:

A

Vagal stimulation result of direct PNS stimulation

352
Q

What is the greatest risk factor for developing asthma

A

Atopy- condition of being hyper allergic

353
Q

Anesthetic management for asthma

A

-suppress airway reflexes paramount!!
-avoid tracheal intubation if you can, regional, mask, lma
-deep extubation to avoid airway reactivity, lidocaine and opioids to reduce airway reactivity
-vent: limit inspiratory time, prolong expiratory time, tolerate moderate permissive hypercapnia
-heat moisture exchanger retains airway humidity and may benefit exercise induced asthma patients

354
Q

What is the most common ABG finding in a patient with asthma?

A

Respiratory alkalosis, hypocarbia

355
Q

How does Intraoperative bronchospasm present

A

-Wheezing
-Decreased breath sounds
-Increased peak inspiratory pressure(decreased dynamic compliance)
- increased alpha angle on etCO2 waveform

356
Q

How do you treat intraop bronchospasm?

A

-100% fiO2
-deepen anesthetic
-SABA
-inhaled ipratropium
-epi 1mcg/kg IV
-hydrocortisone 2-4mg/kg IV
-aminophylline
-helium oxygen gas mixture

357
Q

T/F: all halogenated anesthetics dilate the lower airways?

A

True

358
Q

T/F: you should select a volatile agent with high blood:gas solubility

A

False

359
Q

T/F: tuning on NO can produce a pneumothorax

A

True

360
Q

Staph, streptococcal, enterococcal, and endocarditis treated with what abx?

A

IV vancomycin

361
Q

How would the presence of a competitive antagonist alter the dose response curve of a drug?

A

Shift the curve to the right with no change to efficacy or slope

Right shift caused by competition for same receptors

362
Q

How does the presence of a noncompetitive antagonist alter the dose response curve?

A

Right and down with decrease in slope

This change occurs bc maximal effect cannot be achieved in the presence of a noncompetitive block, can’t be reversed by excess agonist

363
Q

LD50/ED50

A

Therapeutic index or margin of safety

Larger therapeutic index greater margin of safety

364
Q

Define tachyphylaxis

A

Fairly rapid acute development of resistance to the effects of a drug

365
Q

Diffusion of a drug across a membrane is proportional to the concentration gradient. Diffusion is also dependent on what 3 other factors?

A
  1. Solubility of drug in lipid
  2. Thickness of the membrane
  3. Molecular weight
366
Q

The degree of protein binding of a drug in the blood is dependent on what primary factor?

A

Total amount of protein in the blood

The amount of drug bound to protein will change when plasma protein levels change

367
Q

Besides blood flow, what two other factors determine the IV anesthetic going into and out of the tissue compartment?

A

-ionization
-lipid solubility

368
Q

Which cell types can cause bronchoconstriction

A

Mast cells- they degranulate and release histamine

369
Q

What is the initial symptom of an asthma attack

A

Decrease in expiratory flow

370
Q

What is the most common physical sign of an asthma attack?

A

Wheezing, cough and dyspnea may be present

371
Q

What is the universal ABG finding during an asthma attack?

A

Hypoxemia

Hypocarbia and alkalosis are typical, CO2 retention is a late finding

372
Q

What two types of drugs should be avoided in patients with asthma?

A

-b2 blocking actions like propranolol and labetalol
-histamine releasing such as astracurium, morphine, succs, merperidine

373
Q

What two properties does a substance need to diffuse through the lipid bilayer?

A

Small (low molecular weight)(H2O/CO2)
Lipid soluble

374
Q

Explain M3 pathway

A

Cholinergic endings release Ach —>activates M3 g couple protein receptor —>activates phospholipase C(PLC)—> activates inositol triphosphate (IP3)—> stimulates Ca release from sarcoplastic reticulum —> bronchoconstriction

375
Q

What can cause airway inflammation?

A

Basophils
Mast cells
Eosinophils
PMNs
M1 macrophages
M2 macrophages

376
Q

What inhaled anesthetic reduces coughing?

A

Sevoflurane

377
Q

DuoNeb dosing

A

Ipatropium 0.5mg/ albuterol 2.5

Q4-6hrs

378
Q

Albuterol nebulized and MDI dose

A

Neb 2.5mg/3mL q4-8 hrs

MDI 90mcg/puff 2 inhales q 4-6 or prn

379
Q

What anesthetic drug is not chiral?

A

Sevoflurane

380
Q

What is bioavailability of subq drugs?

A

75-100-%

381
Q

Where do 80% of nosocomial infections come from?

A

Urinary tract
Respiratory system
Bloodstream

382
Q

How does hypothermia affect abx

A

Causes vasoconstriction so abx don’t circulate to tissues, increased risk of infection

383
Q

What are fluoroquinolones used to treat?

A

GI/GU infections

384
Q

Ryanodine activation by DHP results in?

A

Release of calcium stores from sarcoplastic reticulum

385
Q

What are 3rd gen cephalosporins used for?

A

Penetrate CSF to treat meningitis

386
Q

What is the bioavailability of IM drugs?

A

75-100%

387
Q

What are ABG or mixed venous s/s MH

A

Arterial hypoxemia
Hypercarbia (PaCO2 100-200 mmHg)
Acidosis (mixed resp and metabolic)
Central venous O2 desat

388
Q

Bioavailability of PO drugs?

A

5-<100%, first pass significant

389
Q

What normally resolves MH hyperkalemia?

A

Normothermia, <39*C

390
Q

What fraction of MH crisis happens during the first anesthetic?

A

2/3

391
Q

What are S/S of rhabdo

A

Hyperkalemia
Myoglobinuria

392
Q

How do you maintain urine output in MH

A

Hydration
Mannitol 0.25g/kg
Furosemide 1mg/kg IV

393
Q

What is dose of bicarb for MH treatment?

A

1-2mEq/kg IV

394
Q

What is bioavailability of rectal drugs

A

30-<100%

395
Q

Apart from ryanodine receptors what 3 abnormalities can also cause MH

A

Fatty acid
Phosphatidylinositol
Abnormal Na channels

396
Q

Apart from ryanodine receptors what 3 abnormalities can also cause MH

A

Fatty acid
Phosphatidylinositol
Abnormal Na channels

397
Q

Ways that antibiotics interfere with bacteria ribosome 30s

A

Inhibit protein synthesis
Premature termination of protein synthesis
Ribosomal stalling
Cellular stress

Advanced Pharm (4 decks)

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