Exam 1 Material Flashcards
(397 cards)
1
Q
Order molecular bonds strongest to weakest
A
Covalent - ionic - hydrogen - Van der Waals
2
Q
What is unique about covalent bonds?
A
Longest duration of action; irreversible drug binding
3
Q
What molecular bonds are the most prominent in drug/receptor alignment?
A
Van der Waals and ionic bonds
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
5
Q
Define agonist
A
A drug that activates a receptor by binding to that receptor
6
Q
What happens when an agonist is bound to the receptor?
A
The effect of the drug is produced
7
Q
Define antagonist
A
A drug that binds to the receptor WITHOUT activating the receptor; can block the action of agonists
8
Q
Competitive antagonists
A
Present when increasing concentrations of the antagonist progressively inhibit the response of the agonist-dose response relationship
9
Q
Noncompetitive antagonism
A
After administration of antagonist, even high concentrations of agonist cannot completely overcome the antagonism
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
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
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
13
Q
Define pharmacokinetics
A
Describes what body does to the drug
14
Q
Define pharmacodynamics
A
The drugs effect on the body; what the body’s response to drug
15
Q
What are the 4 principles of pharmacokinetics
A
Absorption, metabolism, distribution and excretion/elimination
16
Q
What can affect pharmacokinetics
A
Genetic metabolism differences
interactions with other drugs
liver/kidney disease
17
Q
Define metabolism
A
Coverts pharmacologically active, lipid soluble drugs into water soluble drugs
18
Q
What are the four pathways of metabolism
A
Oxidation, reduction, hydrolysis, and conjugation
19
Q
What are the phase I reactions?
A
Oxidation, reduction and hydrolysis, also demethylation
20
Q
How are receptors classified?
A
By location; cell membrane lipid bilayer, intracellular etc
21
Q
Define enzyme inhibition
A
Some drugs work by inhibiting enzymes that are involved in certain chemical reactions in the body
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
23
Q
Ficks Law of diffusion
A
Movement of particles from high to low concentration is directly proportional to the particles concentration gradient
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
25
What effects absorption
-pH, solubility of drug, presence of other substances, route of admin
26
Define distribution
Once drug is absorbed, spread throughout the body, how medication is influenced by the physical and chemical properties of the body
27
Define metabolism
How the body uses different enzymes to break down the medication
28
Define excretion/elimination
How the body eliminates and removes medications through various routes (ex: liver, kidneys, lungs, skin)
29
What is bioavailability ( f )
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
30
What are some factors that can effect bioavailability?
Route of admin, physical and chemical proprieties of the medication, presence of food or other substances with PO medications
31
What are some routes of admin that bypass the first pass effect
IV, inhaled anesthetics, sublingual, some transdermal
32
Describe PO absorption route
Absorbed in stomach, goes to liver, goes to venous system,, right heart, lungs, left heart then to arterial system
33
What are components of the “central compartment?”
Brain, kidney, liver, heart, lungs
34
What is the equation for plasma concentration
[plasma concentration]=mass of drug/ volume
35
What are enantiomers?
Mirror images but can’t be superimposed
36
Explain metabolism
Converts pharmacologically active lipid soluble drugs into water soluble pharmacologically inactive metabolites
37
Define and give examples of intracellular proteins
Intracellular proteins are fat or water soluble, they can readily diffuse across the cell membrane lipid bilayer
Ex: caffeine, insulin, steroids
38
Explain and give examples of drugs that don’t interact with proteins
These drugs work by changing the pH of the environment
Ex: antacids
39
What is volume of distribution (Vd)
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
40
Vdcc
Volume of distribution in central compartment (vessel rich groups)
41
Vdss
Volume of distribution steady state;
Drug is being administered at the same rate that it is being eliminated
42
Why do we care about plasma drug concentration
Because we assume that it’s proportional to the target tissue concentration
Exceptions: local topical drugs, inhaler, eye drops
43
Which organ would most likely affect drug metabolism if became dysfunctions? Which part of the cell is metabolism occurring
Liver; smooth endo plastic reticulum
44
What isFirst pass metabolism
Metabolism of a drug before it reaches systemic circulation
45
2 routes of drug admin that would be subjected to first pass?
Rectal, PO
46
2 routes of drug admin that would not be subjected to first pass
IV, sublingual, IM
47
What are three outcomes of metabolism
Active to inactive ex: most drugs
Non toxic to toxic ex Tylenol
Inactive to active ex codiene to morphine
48
Why do we need metabolism
To make drugs more water soluble for excretion
49
Name 2 sets of chemical reactions that metabolize drugs; give example of enzyme type used during
Phase 1: (Modification) -hydrolysis, reduction, oxidation —-enzyme CYP450 (oxidases)
Phase 2: conjugation—-glucuronic, glutathione, sulfonic acid, acetylation (transferases)
50
What is the difference between phase 1 and phase 2 reactions
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)
51
Name common phase 1 and phase 2 enzymes
Phase 1: cyp450, cyp3a4 or cyp2d6
Phase 2: glucaronate( UGT) gluthiaonine(GST), sulfate(SULT), acetate (NAT)
52
First order kinetics 3 things
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
53
Zero order kinetics 3 things
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
54
What are three examples that saturate liver enzymes and reach zero order kinetics quickly?
Aspirin, phenytoin, alcohol (ETOH)
55
Define clearance
The volume of blood that gets eliminated of drug per unit time
56
If you have low Vd what does that do to your 1/2 life
Decreases the 1/2 life
57
What is GFR
The flow rate of drug that is being filtered
58
Definition of steady state
The rate of infusion is equal to the rate of elimination
59
How much time does it take to reach steady state?
About 4.5 half lives
60
What do we do if we need to achieve the therapeutic concentration rapidly?
Give a loading dose; essentially an IV bolus
61
How to calculate the maintenance dose?
CL* desired plasma concentration/bioavailability
62
Therapeutic window
Dosage range between minimum effective concentration and minimum toxic concentration
63
What do you do if there is a narrow therapeutic window?
Give more doses over shorter interval to minimize peaks and troughs
64
Why is continuous infusion beneficial?
You don’t have the fluctuations between minimum toxic concentration and minimum effective concentrations, you remain steady in therapeutic window
65
Define potency
The amount of drug it takes to elicit an effect; high potency= smaller dose
66
Define efficacy
A measure of drug effectiveness once it occupies the receptor; measure of the ability for a drug to produce a physiological or clinical effect
67
ED50
The dose required to produce a specific desired effect in 50% of individuals receiving the drug
68
LD50
The dose of a drug required to produce death in 50% of patients receiving the drug
69
EC50
the concentration of a drug that produces 50% of maximal response
70
What are the 4 surgical wound classifications
Clean, clean-contaminated, contaminated, dirty/infected
71
Clean surgical wound classification
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
72
Clean-contaminated
An incision through which the respiratory, alimentary, or urinary tract
73
Contaminated
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
74
Dirty/infected
An incision in which the viscera are perforated or when acute inflammation with pus is encountered during the operation
75
Patient risk factors for SSI (8)
-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
76
Hospital factors for SSI
-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
77
When should a patient stop smoking before a procedure and why?
4-8 weeks; descreases infection risk 50%
78
Why is maintaining normothermia important?
Hypothermia-> vasoconstriction, decreased wound oxygen tension
Decrease in the ability of the tissue to recruit leukocytes to area of infection
79
What temp should you maintain perioperative? And why?
At least 36 * C
Reduces risk of SSI by 64%
80
What is the ideal BS perioperative?
Below 200 and above 80
Hypoglycemia leads to increased mortality
81
What are the most important performance measures for anesthesia?
-ABX within 30 min of incision
-correct abx for procedure
-blood sugar control 80-less than 200
-normothermia (36*C) perioperative period
82
What are the most prescribed prophylaxis abx for surgery
Beta lactams
83
Beta lactams
2 examples and MOA
What bacteria does it target?
Ex: PCN, cephalosporins
MOA: inhibit peptidoglycan synthesis in bacterial cell wall;
Target: gram + and gram -
84
What does PCN treat and what surgeries is it used for?
Treats pneumococcal, streptococcal, and meningococcal infections
Used in dental surgery, tonsil/adenoids, GU/GI surgery
85
How is PCN administered and excreted?
Given IM with poorly soluble salts to prolong duration of action
Rapidly renal excretion
86
Why would you use ampicillin? (4)
-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
87
What does ampicillin cover?
Everything PCN covers + haemophilus flu, e.coli
88
What is the adverse reaction to ampicillin?
Bright red Skin rash, usually 7-10 days after start of therapy
Usually caused by protein impurities in commercial prep of drug
89
What are most often prescribed in surgical abx prophylaxis?
Cephalosporins
90
How do cephalosporins work?
Bactericidal; inhibit bacterial cell wall synthesis with low risk of cell toxicity
91
All cephalosporins can penetrate ___ and ___?
Joints and cross placenta
92
Risk of cephalosporins?
Thrombophlebitis and >3rd gen are expensive
Cutaneous reactions; often delayed maculopapular rashes and/or fevers
93
What are the 4 kinds of beta lactams?
Penicillins, cephalosporins, carbapenems, and monobactams
94
What are carbapenems and ertapenem used to treat?
Klebsiella PNA, nose mouth GI normal flora, VAP,
Last line for MDR pathogens
95
What has the broadest spectrum of activity and greatest potency against gram + and gram -?
Carbapenems and ertapenem
96
What is a type A drug reaction?
Side effect; diarrhea, nausea, etc
97
Type B type I
-IgE mediated
-Can be mild (urticaria) to severe (cardiovascular collapse)
- onset-2hrs
98
Type B type II
-antibody dependent cytotoxicity
-hemolytic anemia, thrombocytopenia
-happens weeks after exposure
99
Type B type III
-Immune complex, serum sickness
-weeks after exposure
100
Type B type IV
- Tcell mediated
-rash, Stevens Johnson Syndrome
-happens 48hrs to weeks after exposure
101
What’s is Stevens Johnson Syndrome and how is it treated?
-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
102
Loading dose=
Vd*desired plasma concentration/ bioavailability
103
Drug with high Vd >than TBW is called? And give example
Lipophilic
Ex: propofol
104
Drug with Vd < TBW is called? Give example
Hydrophilic
Ex: rocuronium
105
How does Vd affect loading dose?
High Vd= larger loading dose
Low Vd = smaller loading dose
106
What is the equation for Vd
Vd= amount of drug/desired plasma concern
107
How much water does TBW contain?
42 L
108
Clearance is directly proportional to? (3)
-blood flow to clearing organ
-extraction ratio
-drug dosage
109
Clearance is inversely proportional to (2)
-half life
-drug concentration in central compartment
110
Steady state is achieved after how many half-lives?
5
111
Define half-life
Time it takes for 50% of the drug to be eliminated from the body
112
Define half-time
Time it takes for 50% of the drug to be removed from the plasma during the elimination phase
113
How many half times does it take to clear the dose from the plasma?
5
114
What is context sensitive half time?
The time required for the plasma concentration to decline by 50% after the infusion rate is stopped
115
What is the “context” in the context sensitive half-time?
Duration of the infusion (time)
116
Which opioid has a similar context-sensitive half-time regardless of infusion duration?
Remifentanil
117
I’m which circumstance is a drug MORE likely to pass through a lipid membrane?
- 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
118
Define ionization
The process where a molecule gains a positive or negative charge; this affects a molecules ability to diffuse through lipid membranes
119
A weak acid will ____ a proton to water?
Donate
120
A weak base will ____ a proton from water?
Accept
121
What is ionization dependent on?
-pH of the solution
-the pKa of the drug
122
What is pKa? What does high or low pKa mean?
A constant value; tells us how much a molecule wants to behave like an acid
-low pKa= amazing acid
-high pKa= terrible acid
123
Weak bases in a acidic solution?
Weak bases in a basic solution?
-more ionized and water soluble in acidic solution
-more non-ionized and lipid soluble in a basic solution
124
Weak acids in acidic solution?
Weak acids in basic solution?
-more non-ionized and lipid soluble in acidic solution
-more ionized and water soluble in basic solution
125
The ionization fraction predominates if:
-the molecule is a weak base and the pH of the solution is the pKa of the drug (an acid is added to a basic solution)
126
The non-ionized fraction predominates if:
-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)
127
What does pKa tell you?
A drugs pKa = the pH where 50% of the drug is ionized and the other 50% of the drug is non-ionized
128
Which circumstance creates the STRONGEST gradient for the passage of local anesthetic from the mother to the fetus?
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
129
What happens when lidocaine enters the fetal circulation?
A more acidic environment increases lidocaines ionized fraction
130
How does uncontrolled maternal pain affect local anesthetic concentration in the fetus
Pain causes the mothers minute ventilation to increase (resp alkalosis) and this increases lidocaine transfer across the placenta.
131
What conditions can decrease protein concentrations?
-liver disease, renal disease, old age, malnutrition and pregnancy
132
What happens when a drug is bound to a plasma protein?
It cannot bind to receptor; only when drug is released from the protein is it able to affect the body
133
Name 3 plasma proteins
Albumin, alpha 1 acid glycoprotein, beta-globulin
134
Which plasma proteins bind to acidic drugs? Which to basic drugs?
-acidic: albumin
-basic: alpha- 1acid glycoprotein and beta-globulin
135
Vd is ____ related to the degree of plasma binding
Inversely
136
Highly protein bound drugs typically slower rate of ____and ____
Metabolism and elimination
137
How to calculate percent change
Percent change = (new value- old value)/old value x 100%
138
Metabolism depends on 2 factors:
-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
139
What is the purpose of metabolism?
Change a lipid-soluble pharmacologically active compound into a water soluble pharmacologically inactive compound
140
Describe enterohepatic circulation and give two examples of drugs that use it
Some conjugated compounds are excreted into the bile, reactivated in the intestine, and then reabsorbed into the systemic circulation
Ex: diazepam and warfarin
141
What are the three phases of metabolism
Modification, conjugation and elimination
142
What happens to a drug during conjugation
Phase 2 adds on an endogenous, highly polar, water soluble substrate to the drug molecule
143
Name 3 drugs that undergo perfusion dependent hepatic elimination
Fentanyl, lidocaine, and propofol
144
Name 2 drugs that undergo capacity-dependent hepatic elimination
Diazepam and rocuronium
145
What is extraction ratio
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
146
Hepatic clearance is the product of(2)
Liver blood flow- how much drug is delivered to the liver
Hepatic extraction ratio- how much drug is removed by the liver
147
Perfusion dependent elimination
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
148
Capacity dependent hepatic elimination
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
149
What p450 enzyme is most important
CYP3A4
Metabolized nearly 50% of drugs we administer
150
What is an enzyme inducer?
They stimulate the synthesis of additional enzymes which increases drug clearance
Ex: alcohol, tobacco, phenytoin
151
What is an enzyme inhibitor?
These compete for binding sites in the enzymes and reduces drug clearance
Ex: SSRIs, omeprazole, grapefruit juice
152
Cefazolin dose, redose, special considerations
2g
3g >120 kg
Redose q4hrs
T1/2 1.2-2.2 hrs
Most common first line abx surgical prophylaxis; inexpensive
153
Clindamycin dose; redose
600-900mg IV x1
Can be redose q6hr
Used for SSI prevention in PCN hypersensitivity
Half-life: 2-4 hrs
154
Efficacy
Measure of the intrinsic ability of a drug to elicit a given clinical effect
155
Potency
The dose required to achieve a given clinical effect
156
Individual variability
When administered the same dose, different patients may have different clinical effects
157
ED 50 and ED 90 are measures of?
Potency
158
What does a steep slope on the dose response curve imply?
It implies that most of the receptors must be occupied before we observe the clinical response
159
How is potency represented on the dose response curve?
Represented on the x axis
Left shift =more potent
Right shift = less potent
160
How do you calculate therapeutic index?
TI= TD50/ED50
Therapeutic index= toxic dose 50/effective dose 50
161
What is chirality?
The tetrahedral bonding of carbon to 4 different atoms
162
Examples of drugs that have R and S enantiomers
Ketamine, isoflurane, morphine
163
What antibiotics are safe for pregnancy?
PCN and Cephalosporins
164
What are elderly considerations for absorption, metabolism, distribution and excretion
Oral absorption- decreased gastric acidity, reduced GI motility
Distribution- increased total body fat, decreased albumin
Metabolism- decreased hepatic blood flow
Excretion- decreased GFR
165
What is the first agent to treat MRSA?
Vancomycin
166
Aminoglycosides: MOA, examples, target bacteria
Targets gram neg
Ex: gentamycin, kanamycin
-mycin, except vancomycin
MOA: inhibit protein synthesis by targeting ribosomal unit 30s
167
Glycopeptides: MOA, target bacteria, examples
Ex: vancomycin
MOA: inhibit peptidoglycan synthesis in bacterial cell walls
Targets gram +
168
Cephalosporins example, target bacteria and MOA
Ex: 1st gen cefazolin, 2 cefoxitin 3 ceftriaxone 4 cefepime
MOA: inhibit peptidoglycan synthesis in bacterial cell wall
Target gram + and gram -
169
PCN example, MOA, target bacteria
Ex: PCN G, ampicillin, methacillin
MOA: inhibits cell wall synthesis beta lactam ring
1st gen targets gram +
2nd gen targets gram -
170
Quinolones/ fluoroquinolones MOA, target bacteria and examples
MOA: inhibits DNA replication (toposomerase II-IV)
Targets gram + and gram -
Ex: ciprofloxacin and levofloxacin
171
Macrolides MOA, example and target bacteria
Ex: Erythromycin, clindamycin, azithromycin
Targets gram +
MOA: target bacterial ribosomal subunit 50s
-thromycin
172
Sulfonamides MOA, target bacteria, examples
MOA: inhibits folate synthesis in bacteria
Examples: sulfamethizole
Targets gram + and gram -
173
Cefoxitin dose, and redose
Dose: 2g
Half-life: 0.7-1.1
Redose: 2 hrs
174
Metronidazole dose, half life and redose
Dose: 500mg/100ml over 1hr
Half-life: 6-8 hrs; 9-15hrs
Redosing: repeat q8hr if indicated
175
Metronidazole target bacteria and used for?
Bactericidal against ANAEROBIC GRAM NEG and cdiff
Used for colorectal surgeries or any bowel perf
176
Vancomycin dosing, half life and redose
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
Azithromycin dose half-life indications
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
Pipercillin-tazobactam, dose, redose, and class
Class: PCN and beta-lactamase inhibitor
Dose: 3.375g
Redose: 2hrs
179
Gentamycin class, dose, and redose?
Class: aminoglycoside
Dose: 5mg/kg
redose: n/a
180
Ceftriaxone dose and redose
Dose: 2g
Redose: n/a
3rd gen cephalosporin
181
What is the MH hotline number
1-800-644-9737
182
What affects a drugs Vd?
Molecular size, ionization, protein binding
Pregnancy and burns
183
Which drug class has anti-inflammatory effects
Macrolides/lincosamides
184
What drugs do we avoid with myasthenia gravis
Macrolides, aminoglycosides, quinolones
185
adverse effects of aminoglycosides
-mycin drugs
-ototoxicity, nephrotoxicity, muscle weakness with NMB, destruction of cochlear sensory hairs (dose dependent)
186
what adverse effects of quinolones?
GI disturbance, tendon ruptures, weakness in Myasthenia Gravis pts
187
what abx are used for urology cases?
fluoroquinolones or cefazolin
if betalactam allergy use clindamycin or vanc+aminoglycoside (gentamycin)
188
what abx used in colorectal surgery?
cefazolin + metronidazole
or
cefotetan
if betalactam allergy
clindamycin + aminoglycoside (gentamycin)
gentamycin + metronidazole
189
what parts of NMJ are affected by aminoglycosides?
nerve terminal, axon, ACh release, muscle membrane, and cholinergic receptors
190
what is big risk of Erythromycin?
prolong cardiac repolarization- torsades
can cause toxicity/cardiac death
191
what are some benefits of Erythromycin
-increases lower esophageal sphincter tone (lowers aspiration risk)
-increases gastric emptying
192
what abx is used as alternative in surgery for patients with allergy to cephalosporins?
clindamycin
193
Why do we choose 1st gen cephalosporins for sx prophylaxis?
-wide therapeutic index (gram - and gram +)
-low incidence of side effects/adverse rxns
-affordable
194
What is epi IM and IV dose for anaphylaxis?
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
Anaphylaxis management
-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
all cephalosporins can ____ and _____?
penetrate joints and cross placenta
197
what abx penetrates pleura, ascitic and synovial fluid?
gentamycin
198
how do you overcome effect of aminoglycosides at the NMJ?
IV calcium
199
clindamycin can cause ___ when used with succinylcholine or NMB?
prolonged neuromuscular blockade
200
what antiseptic targets gram + and gram - bacteria?
CHG
201
what antiseptic/disinfectant is most important for disinfectant of the skin?
iodine; kills bacteria, viruses and spores
202
how many mg of ryanodex vs dantrolene in vial
ryanodex 250mg in vial
dantrolene 20mg per vial
203
What is MH
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
What two classes of drugs trigger MH?
Halogenated anesthetics
Depolarizing neuromuscular blockers (succinylcholine)
205
What three co-existing diseases are definitively associated with MH?
1. King-Denborough syndrome
2. Central core disease
3. Multiminicore disease
206
What are the consequences of increased intracellular calcium in the myocyte?
-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
What conditions are risk of MH not increased with?
-Becker muscular dystrophy
-neuroleptic malignant syndrome
-myotonia congenita
-myotonic dystrophy
-osteogenesis imperfecta
208
What are risk factors of Mh and how often is incidence?
1. Geography- Wisconsin, Nebraska, west Va, Michigan higher risk
2. Male
3. Youth
1:5,000 to 1:50,000
209
What is the primary intracellular ion affected by MH?
Disordered calcium
210
Is duchenne muscular dystrophy a risk factor for MH?
No
211
The earliest signs of MH are? (3)
Tachycardia, increased EtCO2, masseter spasm
212
What are the late signs of MH?
Hyperthermia, cola colored urine (rhabdomyolysis), and DIC
213
What is the gold standard for diagnosing MH?
Caffeine-halothane contracture test (CHCT)
High sensitivity
Low specificity
214
What is trismus?
A tight jaw that can still be opened; normal response to succinylcholine
215
What is masseter muscle rigidity?
A tight jaw that CANNOT be opened; not normal response to succinylcholine
216
What drugs are contraindicated in MH management?
Ca channel blockers; life threatening hyperkalemia can result when ca channel blocker co administered with dantrolene
217
How to treat MH
-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
Dantrolene MOA
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
What is MIC?
the minimal inhibitory concentration- tissue concentration to prevent bacterial growth
220
what are the three phases of multi-compartment model?
-rapid distribution
-slow distributiom
-terminal phase
221
which channels are activated by neuromuscular blocking agents?
ligand-gated channels
222
what protein receptors do Haloperidol, morphine, losartan and plavix use?
G- coupled protein receptors
223
What is an example of covalent bound drug?
warfarin
224
define the lock and key theory
a cell receptor has a specific binding site that is shaped to fit a specific signaling molecule
225
name 4 meds that have selective agonism?
albuterol, phenylephrine, dobutamine, esmolol
226
what is Cmx and Tmax
Cmax- peak plasma concentration ( depends on rate and extent of absorption)
Tmax- time when Cmax occurs( depends on rate only)
227
What phase 1 processes are cyp450 involved in?
Oxidation, reduction and hydrolysis
228
What a drugs taken up by first pass pulmonary effect
-basic lipophilic amines
-lidocaine, propranolol and fentanyl
229
Describe route of excretion in kidneys?
-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
Oxidation
Removes a electron from a compound
231
Reduction
Adds electrons to a compound
232
Hydrolysis
Adds water to a compound to split it apart (usually an ester)
233
Where are CYP450 enzymes located
Smooth endo plastic reticulum of hepatocyte
234
In regards to the variables on the dose-response curve what does the ED50 measure?
Potency
235
What can result from giving Duchenne & Becker muscular dystrophy succinylcholine?
Rhabdo and hyperkalemia
236
what is an example of G coupled protein receptors
muscarinic receptors, Ach receptors
seconds
237
What are examples of ligated channel receptors
nicotinic ach recptors, neuromuscular blocking agents
miliseconds
238
which organs have highest to lowest perfusion?
Kidneys --> Liver--> Heart--> brain--> bone--> fat
239
what drug class increases effect of oral anticoagulants and thiazide drugs?
sulfonamides
240
What MH grade would judge the likelihood of true MH
20 and higher
241
What conditions can mimic MH?
-contrast dye
-diabetic coma
-drug toxicity/overdose
-heat stroke
-anesthesia machine malfunction with increased CO2
-thyroid storm
-intracranial free bleed
-pheochromocytoma
-sepsis
242
what diseases have increased risk of RYR1 abnormalities?
exertional rhabdomyolysis
severe statin induced myopathy
native american myopathy,
243
gold standard testing for MH
Caffeine-halothane contracture test
80% specificity
high sensitivity
244
most common cause of death with MH
Vfib
245
which anesthesia gases trigger MH
halothane
enflurane
isoflurane
sevoflurane
desflurane
246
side effects of Dantrolene
nausea, diarrhea, blurred vision, muscle weakness
247
what class of drug is dantrolene considered
muscle relaxant
248
What anesthetic agents have bronchodilating properties
Volatile anesthetics and ketamine
249
Albuterol class and MOA
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
Albuterol indications and dose
Indications: preferred B2 agonist for treatments of acute bronchi spasm due to asthma; wheezing and airflow obstruction
Dose: nebulizer 2.5 mg
251
Albuterol duration and side effects
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
Albuterol anesthesia considerations
Have pt continue medication up to surgery, including day of
253
Albuterol MOA
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
Why do we use albuterol?
-strong B2 selectivity
- short onset time
-average duration of action
255
Describe pathway of airflow
Nose/mouth -> pharynx > larynx > trachea > bronchi > bronchioles > alveoli
256
What autonomic nervous system effects respiratory system
-Parasympathetic innervation via vagus nerve
-muscarinic 3 (M3) receptor stimulation = bronchoconstriction
-PNS regulates airway construction/dilation as well as microvasculature of airway
257
How do beta agonists work?
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
Where is nitric oxide produced?
In the endothelial cells (inner linings of blood vessels)
259
How does nitric oxide work?
-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
Define chronic bronchitis
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
Define emphysema
Presence of permanent enlargement of airspace’s distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis
262
Salmetrol class and indications
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
Salmeterol duration and side effects
Duration: >12 hrs
SE: headache, HTN, edema, dizziness anxiety
264
Salmeterol MOA
-same as SABA
-Has side chain that binds to B2 receptor and prolongs activation
265
Salmeterol anesthesia considerations
-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
The lower airway is more ____
Muscular
267
Where are M3 and B2 adrenergic receptors located?
Lower airway
268
Inhaled and nebulized medications are targeting which area of lungs?
12-16th generation/locations of bronchiole tree
269
Name 3 things that increase ionized Ca and what’s that result in?
Cytokines (CysLT1)
Histamines (H1)
M3
Causes bronchoconstriction/contraction
270
B2 and PDE work by ____ and _____which causes _____
Increasing cAMP and decreasing ionized calcium which causes relaxation
271
How do inhaled cortiocosteroid work?
Prevent destabilization of mast cells; prevent mast cell degranulation
272
Management steps for asthma
1. SABA
2. Inhaled corticosteroids
3. LABA
273
Inhaled anesthesia and formoterol (and all LABA) cause increased risk of _____
Prolonged QT and increase risk of cardiac arrhythmias
274
Theophylline class and MOA
Class: methylxanthines
MOA: inhibits PDE which increases cAMP, reduces iCa and causes bronchodilation;
releases endogenous catecholamimes;
inhibits adenosine receptor
275
Side effects >20mcg/mL and >30mch/mL plasma levels for theophylline
>20: N/v, diarrhea, headache, disrupted sleep
>30: seizures, tachydysrhythmias, CHF
276
Theophylline anesthesia considerations
-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
When used with COPD what is a risk of using inhaled corticosteroids?
Increased risk of serious PNA
278
Inhaled corticosteroids drugs and MOA?
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
Side effects of inhaled corticosteroids
Dysphonia- hoarse voice
Myopathy of laryngeal muscles
Oropharyngeal candidiasis
Possible adrenal suppression
280
Inhaled corticosteroids indications
Asthmatic obstruction
281
Inhaled corticosteroids anesthesia considerations
Inhaled and systemic corticosteroids should be continued during the perioperative period
282
Why would we use systemic corticosteroids
Treat asthma and COPD exacerbations that are not responsive to B2 adrenergic agonists
283
Side effects of systemic corticosteroids
HTN,
hyperglycemia,
adrenal suppression
Increased infections
Cataracts
Dermal thinning
Psychosis
284
Why are inhaled corticosteroids less effective in COPD patients
Their disease inflammation is resistant to the action of inhaled corticosteroids
285
If a patient is on systemic corticosteroids steroid >2 weeks what is an anesthesia consideration
They are at risk for adrenal suppression and may need Intraoperative supplementation of IV corticosteroids
286
What are Inhaled corticosteroids dosing based off of
Patients age
1-2 puffs 1-2x day
287
How do anticholinergic medications work?
They work by blocking the actions of ACh
288
Name short acting, long acting and systemic anticholinergics
Short: ipratropium
Long: tiotropium
Systemic: atropine and glycopyrrolate
289
Which autonomic nervous system involved with bronchoconstriction/dilation?
PNS
290
What are M1 and M3 receptors responsible for
Bronchoconstriction and mucus production
291
Inhaled cholinergic antagonist MOA
They reduce smooth muscle tone by blocking ACh from binding to M3 receptors
292
Side effects of inhaled cholinergic antagonists
Dry mouth, urinary retention, pupil dilation
293
What resp drug class is used for exacerbations but not maintenance therapy?
Inhaled anticholinergic (cholinergic antagonists)
294
Ipratropium class and MOA
Class: anticholinergic, antimuscarinic
MOA: similar to atropine except a quaternary amine so DOES NOT CROSS BBB; almost complete protection against bronchospasm
295
Ipratropium dose, onset, DOA
Dose: 200unit/inh 2 puffs 4x day
Onset: immediate
Duration: 5-6 hrs
*effects in 30-90 min lasting 4 hrs; not rescue*
296
Ipratropium side effects and anesthesia considerations
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
What is a risk of anticholinergics?
Increased CNS effects
298
Atropine class and dose and considerations
Class: anticholinergic
Dose 0.5-1mg 30-60 min preop for secretions repeat 4-6 hrs max 3mg
Consider: tachyarrhythmias most common
299
Glycopyrrolate class dose considerations
Anticholinergic
4mcg 30-60 min preop for secretions
SE: flushing, twchyarrhymthmias, heart block, headache, vomiting, dry mouth, constipation, urinary retention
300
Scopolamine considerations
-decreases airway resistance and increases dead space by 1/3
-similar effects as glycopyrrolate but has CNS effects
301
Leukotriene modifiers drugs and MOA
Drugs: montelukast
MOA: inhibits 5 lipoxygenase enzyme (decreases leukotrine synthesis)
decreases -->
bronchospasm,
vasoconstriction
eosinophil recruitment promoted by leukotrienes
302
Leukotriene modifiers indications and side effects
Indication: COPD
SE: negligible
303
Leukotriene modifiers anesthesia considerations
- montelukast and zafirlukast NOT used in the treatment of acute bronchospasm
-continue up to surgery and immediately after
304
What meds do betalactamase and penicillinase not effect?
Methicillin
Oxacillin
Dicloxacillin
305
Which abx can cause neurotoxicity and hyperkalemia in CKD pts?
PCN
306
Where are ligand gated channels located
Lipid bilayer of the cell
307
What anesthesia drugs do we avoid in asthma and copd patients
Succs, atracurium, morphine, merperidine
Release histamines
308
In asthma and copd pts, if you need to use a beta blocker which one and why
Esmolol bc it’s B1 selective
309
What is the multicompartment model
-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
IM Epi dosing adults
.2-.5 mg
311
what is the incidence of MH in children? adults? what is the mortality rate for MH?
1 in 40,000 in children
1 in 250,000 in adults
mortality rate is 10%
312
what are the 11 clinical manifestations of MH
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
what is the earliest sign of MH
increased end tidal CO2, out of proportion to minute ventilation
314
Can masseter spasm be an early sign of MH? will masseter spasm be the first sign of MH
Masseter spasm is an early sign, though generally not the first
315
what response is considered evidence of MH in children?
masseter muscle rigidity after admin of succs, especially children undergoing strabismus surgery
316
how fast may temp increase during an episode of MH?
1-2 degrees C every 5 min
317
8 initial actions for initial managment of MH
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
a patient has just experienced masseter muscle rigidity from succ. what lab value may confirm the diagnosis of MH?
elevated creatine phosphokinase (CPK >20,000)
319
a child has received sevo and succs and mouth cannot be opened. what action should be taken?
possible MH, discontinue the trigger and begin MH treatment
320
How and where does dantrolene work?
-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
dose and how long should you give dantrolene in management of MH
-2.5mg/kg q 5 min until episode is terminated
-max dose is 10-20mg/kg
322
how much dantrolene is found in each vial? how must it be prepared?
-contains 20mg of dantrolene and 3g mannitol
-mix with 60ml warmed sterile water
-keep warm bc of the mannitol
323
you have successfully treated acute episode of MH. dantrolene should be re-administered at what intervals and how long?
-continue therapy for 24 hrs
-1mg/kg q 4-6 hrs as a bolus or 0.25 mg/kg/hr continuous infusion
324
list 4 ways to actively cool pt in acute MH episode?
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
at what body temp should cooling pt in MH be stopped and why?
38*C
to prevent deleterious effects of hypothermia
326
once the initial episode of MH is controlled, the patient will remain at risk for what 5 complications?
1. reoccurence
2. DIC
3. myoglobinuric renal failure
4. skeletal muscle weakness
5. electrolyte abnormalities
327
a patient in MH crisis has pvcs. what is the antiarrhythmic drug of choice?
amiodarone
328
a woman in labor identified as susceptible to MH. What anesthesia technique are acceptable?
-prophylactic dantrolene not recommended, prepare the anesthesia workstation
329
what 6 steps do you take when family hx of MH? are non depolarizing muscle relaxants safe?
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
5. arterial and central venous monitoring is recommending in MH susceptible pts
6. observe pt closely in postoperative period
330
what syndrome can mimic MH
neuroleptic malignant syndrome-presents as hypermetabolic episode with hyperthermia, ANS instability, muscle rigidity and rhabdomyolysis
331
pts treated with what drugs are susceptible to neuroleptic malignant syndrome?
antipsychotic agents
-phenothiazines, haloperidol, etc
-antipsychotic drugs reflect dopamine depletion in the CNS
332
stepwise managment of COPD medications
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
early asthma body response
-IgE response causes mast cells to degranualte, releasing large # of inflammatory mediators
-vasodilation
-increase capillary permeability
-mucosal edema
-bronchospasm
-tenacious mucous secretion
334
late asthma response
-air trapping
-hyperinflation distal to obstruction
-increase work of breathing
-hypoxemia
335
clinical manifestations of asthma
-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
what medications can reduce histamine release?
presynaptic H2 receptor agonists
AVOID H2 antagonists like famotidine and ranitidine- allow H1 stimulation which leads to bronchospasm
337
MOA anticholinergics
blocks M3 receptor which decreases IP3 which leads to decreased ionized Ca
338
Bacteriostatic vs Bactericidal
Static: inhibits bacteria from reproducing but doesn’t otherwise kill them
Cidal: actively kills bacteria
339
What enzyme does the beta lactam ring inhibit
Transpeptidase
340
Name some beta lactamase inhibitors
Clavulanic acid, tazobactam, Silva tan
Augmentin (amox-clav)
Zosyn (piperacillin tazobactam)
341
What is the most common side effect of antibiotic prophylaxis?
Pseudomembranous colitis
342
How often should cefazolin be re-dosed in OR?
Every 4 hrs
343
Key side effect for PCN
Allergic rxn
344
Key side effect gentamycin
-ototoxicity
-nephrotoxicity
-skeletal muscle weakness
345
Key side effect clindamycin
-skeletal muscle weakness
-allergic rxn
346
Key side effect for doxycycline
-hepatotoxicity
-nephrotoxicity
347
Key side effect of metronidazole
-peripheral neuropathy
-alcohol intolerance
348
Key side effect of vancomycin
-hypotension
-red man syndrome
-SJS
349
Epinephrine treats anaphylaxis in what 3 ways?
1. Prevents degranulation
2. Provides CV support
3. Dilates the airways
350
What’s the most common cause of drug mediated anaphylaxis in the perioperative period
Succinylcholine
351
A patient with asthma experiences bronchospasm immediately following tracheal intubation. This is MOST likely the result of:
Vagal stimulation result of direct PNS stimulation
352
What is the greatest risk factor for developing asthma
Atopy- condition of being hyper allergic
353
Anesthetic management for asthma
-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
What is the most common ABG finding in a patient with asthma?
Respiratory alkalosis, hypocarbia
355
How does Intraoperative bronchospasm present
-Wheezing
-Decreased breath sounds
-Increased peak inspiratory pressure(decreased dynamic compliance)
- increased alpha angle on etCO2 waveform
356
How do you treat intraop bronchospasm?
-100% fiO2
-deepen anesthetic
-SABA
-inhaled ipratropium
-epi 1mcg/kg IV
-hydrocortisone 2-4mg/kg IV
-aminophylline
-helium oxygen gas mixture
357
T/F: all halogenated anesthetics dilate the lower airways?
True
358
T/F: you should select a volatile agent with high blood:gas solubility
False
359
T/F: tuning on NO can produce a pneumothorax
True
360
Staph, streptococcal, enterococcal, and endocarditis treated with what abx?
IV vancomycin
361
How would the presence of a competitive antagonist alter the dose response curve of a drug?
Shift the curve to the right with no change to efficacy or slope
Right shift caused by competition for same receptors
362
How does the presence of a noncompetitive antagonist alter the dose response curve?
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
LD50/ED50
Therapeutic index or margin of safety
Larger therapeutic index greater margin of safety
364
Define tachyphylaxis
Fairly rapid acute development of resistance to the effects of a drug
365
Diffusion of a drug across a membrane is proportional to the concentration gradient. Diffusion is also dependent on what 3 other factors?
1. Solubility of drug in lipid
2. Thickness of the membrane
3. Molecular weight
366
The degree of protein binding of a drug in the blood is dependent on what primary factor?
Total amount of protein in the blood
The amount of drug bound to protein will change when plasma protein levels change
367
Besides blood flow, what two other factors determine the IV anesthetic going into and out of the tissue compartment?
-ionization
-lipid solubility
368
Which cell types can cause bronchoconstriction
Mast cells- they degranulate and release histamine
369
What is the initial symptom of an asthma attack
Decrease in expiratory flow
370
What is the most common physical sign of an asthma attack?
Wheezing, cough and dyspnea may be present
371
What is the universal ABG finding during an asthma attack?
Hypoxemia
Hypocarbia and alkalosis are typical, CO2 retention is a late finding
372
What two types of drugs should be avoided in patients with asthma?
-b2 blocking actions like propranolol and labetalol
-histamine releasing such as astracurium, morphine, succs, merperidine
373
What two properties does a substance need to diffuse through the lipid bilayer?
Small (low molecular weight)(H2O/CO2)
Lipid soluble
374
Explain M3 pathway
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
What can cause airway inflammation?
Basophils
Mast cells
Eosinophils
PMNs
M1 macrophages
M2 macrophages
376
What inhaled anesthetic reduces coughing?
Sevoflurane
377
DuoNeb dosing
Ipatropium 0.5mg/ albuterol 2.5
Q4-6hrs
378
Albuterol nebulized and MDI dose
Neb 2.5mg/3mL q4-8 hrs
MDI 90mcg/puff 2 inhales q 4-6 or prn
379
What anesthetic drug is not chiral?
Sevoflurane
380
What is bioavailability of subq drugs?
75-100-%
381
Where do 80% of nosocomial infections come from?
Urinary tract
Respiratory system
Bloodstream
382
How does hypothermia affect abx
Causes vasoconstriction so abx don’t circulate to tissues, increased risk of infection
383
What are fluoroquinolones used to treat?
GI/GU infections
384
Ryanodine activation by DHP results in?
Release of calcium stores from sarcoplastic reticulum
385
What are 3rd gen cephalosporins used for?
Penetrate CSF to treat meningitis
386
What is the bioavailability of IM drugs?
75-100%
387
What are ABG or mixed venous s/s MH
Arterial hypoxemia
Hypercarbia (PaCO2 100-200 mmHg)
Acidosis (mixed resp and metabolic)
Central venous O2 desat
388
Bioavailability of PO drugs?
5-<100%, first pass significant
389
What normally resolves MH hyperkalemia?
Normothermia, <39*C
390
What fraction of MH crisis happens during the first anesthetic?
2/3
391
What are S/S of rhabdo
Hyperkalemia
Myoglobinuria
392
How do you maintain urine output in MH
Hydration
Mannitol 0.25g/kg
Furosemide 1mg/kg IV
393
What is dose of bicarb for MH treatment?
1-2mEq/kg IV
394
What is bioavailability of rectal drugs
30-<100%
395
Apart from ryanodine receptors what 3 abnormalities can also cause MH
Fatty acid
Phosphatidylinositol
Abnormal Na channels
396
Apart from ryanodine receptors what 3 abnormalities can also cause MH
Fatty acid
Phosphatidylinositol
Abnormal Na channels
397
Ways that antibiotics interfere with bacteria ribosome 30s
Inhibit protein synthesis
Premature termination of protein synthesis
Ribosomal stalling
Cellular stress
