Comprehensive Review Flashcards
1
Q
What adverse effects are associated with the use of aminoglycosides?
A
a. Nephrotoxicity-
b. Ototoxicity
c. Neurotoxicity-
2
Q
With Nephrotoxicity with aminoglycosides there is
A
decreased creatinine clearance, casts in urine (chunks of glomerulus), decreased specific gravity, oliguria, proteinuria
3
Q
With ototoxicity with aminoglycosides there is
A
directly r/t duration > 10 days & concurrent administration of ototoxic drugs
4
Q
With neurotoxicity with aminoglycosides there is
A
skeletal muscle weakness, inhibits pre-junctional release of Ach & decreased postsynaptic sensitivity to Ach- potentiates NMB. *Caution with Parkinson & Myasthenia
Gravis, IV Ca+ can counteract
5
Q
Examples of Aminoglycosides are
A
Amikacin, Gentamicin, Neomycin Streptomycin, &
Tobramycin
6
Q
What is common adverse reaction associated with the use of Tetracyclines? (Doxycycline, Minocycline, Demeclomycin)
A
a. Photosensitivity
b. Vestibular symptoms with MINOCYCLINE
c. Deposition in teeth in pediatrics (stains teeth permanently)
7
Q
Vestibular symptoms associated with
A
minocycline
8
Q
What is the recommended time of administration of cefazolin (1st Gen) for prevention of post-op
infections?
A
a. Give pre-op in OR before induction, no sooner than 1 hour prior to procedure
b. Infuse over 3-5 min
c. <120 kg = 2 g IV, >120 kg = 3 g IV
9
Q
What is the percentage of cross reactivity between penicillins and cephalosporins?
A
a. Approximately 5%
10
Q
What may result if vancomycin is infused too fast?
A
a. Red Neck or Redman Syndrome
b. Clinical signs/symptoms- Histamine release (Non-Immune mediated *Barash) & hypotension
11
Q
What can prevent red neck redman syndrome with vanco
A
*Give over 60 minutes to reduce this phenomenon
12
Q
What NMB can Vancomycin potentiate?
A
a. Succinylcholine
13
Q
Adverse reactions of Vancomycin?
A
a. Nephrotoxicity
b. Ototoxicity (would be at a disadvantage if we added this with an aminoglycoside)
c. Allergic Reactions
14
Q
What antibiotics are classified as beta-lactams?
A
PCN, Cephalosporins, Imipenem/ Cilastin, Meropenem, Aztreonam is a monobactam, Carbapenems
15
Q
Which antibiotics are associated with prolongation of neuromuscular blockade?
A
Aminoglycosides, Polymyxin B
16
Q
What antibiotics are associated with prolongation of the QTc interval?
A
Macrolides (Erythromycin, Clarithromycin, Azithromycin), Vorconazole (antifungal)
17
Q
- What antibiotic can be used if patient has an allergy to penicillin and cephalosporin?
A
a. Aztreonam (only gram -)
18
Q
What are some adverse reactions of Cephalosporins?
BPHRH
A
a. Bleeding (prolonged PT)
b. Hypersensitivity
c. Pseudomembranous colitis
d. Renal Impairment
e. Hepatic Impairment with Cefoperazone
19
Q
What is an adverse reaction of Chloramphenicol?
A
a. Aplastic Anemia
20
Q
Use of Chloremphenical is
A
Use is limited to Typhoid Fever & Salmonellosis (if alternatives are less effective)
21
Q
Define zero order kinetics.
A
A fixed/constant amount of drug is eliminated/unit of time
22
Q
Define Hoffman degradation.
A
Spontaneous degradation via temperature & pH (Acidosis & Cold prolongs)
23
Q
- What drugs undergo zero order kinetics?
A
a. ETOH, ASA, phenytoin, heparin, warfarin, acetaminophen
24
Q
Define first order kinetics?
A
a. A percentage (%) or fraction of drug is eliminated/unit of time
25
Define half-life.
a. Time it takes for plasma concentration to fall by half
26
How are clearance, VD and half-life related?
Half-life is directly related to Vd and inversely related to clearance
27
Large volume of distribution =
long half-life
28
Increase in clearance =
Decrease in half-life
29
What opioids are most effective for the treatment of post-op shivering?
a. Meperidine (via Kappa), butorphanol (Stadol),
30
Clonidine as far as shivering
effective than meperidine
31
Which narcotic agonist have the shortest effect site equilibration time?
a. Alfentanil (1.4 min), Remifentanil (1.1)
32
What are common adverse effects associated with the use of narcotics?
Respiratory depression, N/V, urinary retention, pruritus
33
Can exacerbate CO2 narcosis
Opiods
34
Which opioid agent can blunt the adrenal response to stress?
Fentanyl
35
25. How are opioid receptors classified?
a. Mu1 (supraspinal & spinal)-
c. Delta (supraspinal & spinal)- antidepressant effects, physical dependence, vent depression,
constipation (minimal), urinary retention, modulates Mu receptor activity. Agonist- enkephalins,
no delta selective agents. Antagonists- naloxone.
d. Kappa (supraspinal & spinal)- analgesia, sedation, dysphoria, low abuse potential, miosis,
diuresis.
produces analgesia, euphoria, decreased abuse potential, miosis, urinary retention, hypothermia. Agonists- endorphins, morphine, synthetic opioids. Antagonistnaloxone
36
Mu2 (spinal only)-
analgesia, hypoventilation, physical dependence physical dependence. Agonists- endorphins, morphine, synthetic opioids.
37
Constipation (marked),
Mu 2
38
Dysphoria and Diuresis with
Kappa
39
Mu 2 agonists
Endorphins, morphine, synthetic opioids.
40
OPIOID AGONIST-ANTAGONISTS principally work here. A
Kappa
41
Agonists-
Dynorphins (inhibit NT release via type N Ca++ channel causing analgesia, decreased resp. depression, may cause diuresis & dysphoria, increased intensity antagonist- naloxone.
42
Painful simulation may be resistant to analgesic effects of
kappa receptors,
43
Low abuse potential which receptors
Kappa
44
Constipation (minimal)
Delta
45
Antidepressant effects,
Delta (supraspinal & spinal)-
46
Physical dependence
Mu2
47
Which induction agent is associated with increases in ICP?
Ketamine
48
Which induction agent can blunt the adrenal response to stress?
Etomidate
49
Caution in adrenal insufficiency patient’s
Etomidate
50
Which induction agents possess analgesic properties?
Ketamine
51
29. What is the mechanisms of action of:
Etomidate-
e.
binds GABA, enhances affinity of GABA receptor
52
What is the mechanisms of action of Propofol?-
activates GABA, increases Cl ions- hyperpolarizes cell, functional inhibition, decreases rate of GABA dissociation
53
What is the mechanisms of action of Dexmedetomidine-
Central alpha-2 agonist (Can cause bradycardia and hypotension)
54
What is the mechanisms of action of Ketamine
Non-competitive NMDA antagonist, weak GABA actions?, interacts with mu, delta, kappa receptors, muscarinic antagonist, K and Ca channels
55
What is the mechanisms of action of benzo
Benzodiazepines- different from barbs- enhance affinity of GABA receptor for GABA, by binding/
56
The benzos increase the
frequency of GABA-mediated ion channel opening and increase Cl permeability and thus cause cellular hyperpolarization and inhibition of neuronal firing
57
Barbiturates-
Binds to GABA-A receptor at barb binding site and increases GABA mediated Cl influx- hyperpolarizes
cell membrane
58
Decreases dissociation of GABA, increases duration of GABA activation,
Barbiturates
59
Depresses RAS, depresses SNS transmission, decreases sensitivity of Ach receptors.
Barbiturates
60
Can cause bradycardia and hypotension
Dexmedetomidine
61
What induction agent has most stable cardiovascular profile?
Etomidate
62
What induction agent increase BP, and cardiac output?
Ketamine
63
Explain the physiological response to the release of thromboxane and prostacyclin?
a. TXA2- platelet aggregation and vasoconstriction
b. Prostacyclin- inhibits platelet aggregation & vasodilates
c. these 2 work in a balance, if one is opposed, then the other can exert it’s intrinsic properties
64
What agent can be used to prevent ductus arteriosus closure (Keeps the PDA patent/open)?
a. Alprostadil (Prostin VR, Muse, PGE1)
b. Alprostadil can also give men boners (tx erectile dysfunction if the old lady isn’t doing it for us
anymore…)
65
Where can we see the use of Alprostadial?
a. Neonatal congenital heart defects
i. Cyanotic PPTT: Pulmonary atresia, pulmonary stenosis, tricuspid atresia, Tetralogy Of Fallot
ii. Acyanotic: Coarctation of aorta, hypoplastic LV (CH)
66
What agent can be used to close ductus arteriosis?
Indomethacin
67
36. What effects will each prostaglandin have on SVR?
| Prostacyclin (PGI2) Epoprostenal *Flolan – *
Decrease SVR, Increase PVR, Decrease Platelet
| Aggregation
68
Epoprostenal *Flolan Treatment of
Primary Pulmonary HTN
69
What effects will each prostaglandin have on SVR? Alprostadil (PGE1)
Decrease SVR, Increases PVR, Decreases Platelet Aggregation, & Increase Uterine Tone *Keeps PFO open
70
What effects will each prostaglandin have on SVR? Iloporost (Nebulizer) –
Decrease SVR, Decrease PVR, Decrease Platelet Aggregation
71
Prostaglandins use as a nebulizer
Iloporost
72
What effects will each prostaglandin have on SVR? Thromboxane (TXA2)
Thromboxane (TXA2) – Increase SVR, Increases PVR, & Increases Platelet aggregation
73
What effects will each prostaglandin have on SVR? Dinoprost (PGF2)
Increase or Decrease SVR, Increase PVR, Increase Uterine Tone
74
Increases Uterine Tone ONLY
Dinoprostone (PGE2) –
75
3 agents used Increase uterine tone
Alprostadil
Dinoprost
Dinoprotone
76
What prostaglandin can be used to treat refractory post-partum bleeding? What is the dose?
Carboprost (Hemabate) a PGF-2α that produces uterine contractions? Dose = 250 mcg IM, repeat 1.5-3.5 min intervals
77
Carboprost Risks of this agent-
vomiting, diarrhea, hyperthermia
78
What are some characteristics of Prostaglandins?
a. Acidic lipids with great pharmacologic activities
b. Act as local hormones
c. Synthesized from arachidonic acid, dihydrolinoleic acid, & eicosapentaenoic acid
79
What causes the release of Arachidonic Acid?
Phospholipase C and A2
80
What drugs can we give to inhibit Phospholipase production inhibiting the Arachidonic acid pathway?
Corticosteroids
81
What is the half-time of Thromboxane A2?
30 seconds (shorter)
82
What is the half- time of Prostacyclin?
3 minutes (longer)
83
What component of prostaglandin synthesis has Several 1000x MORE POTENT bronchial smoothmuscle vasoconstriction than Histamine?
a. Leukotrienes *Therefore it is important to not give asthmatic patients high dose of aspirin or NSAIDs because you can push the phospholipase pathway down the lipoxygenase path producing more leukotrienes
84
All opioids antagonists
Narcan
85
What can NSAIDs do to the kidneys?
a. Inhibit cyclooxygenase, interfering with renal prostaglandins
b. Catecholamine induced renal vasoconstriction
86
What agents are used for cervical ripening prior to labor induction?
a. Dinoprostone; Cervidil, Prostin E2, Prepidil
b. Can be used during weeks 12-28 to evacuate the uterus after missed abortion or intrauterine fetal
death
87
What enzymes play a role in each step of prostaglandin synthesis?
a. Phospholipase A2 → Arachidonic Acid
i. Cyclooxygenase → Endoperoxides→
1. Thromboxane Synthetase→ Thromboxane (vasoconstriction & platelet agg.)
2. Prostacyclin Synthetase→ Prostacyclin (vasodilator & inhibits platelet agg.)
ii. Lipoxygenase → 5-hydroxyarachidonic acid→ Leukotrienes (1000x more potent
bronchoconstriction than Histamine)
88
4What is the mechanism of action of:Cromolyn:
Inhibits antigen-induced release of histamine and other autocoids (leukotrienes from
pulmonary mast cells, and other tissue mast cells). basophils.
89
Does Cromolyn prevent release of histamine form
NO
90
Does Cromolyn relax bronchial or vascular smooth muscle
No
91
What is the mechanism of action of antihistamines?
competitive antagonists- occupy receptors on effector cell membranes
92
Which H2 antagonist is associated with greatest risk of CYP-450 enzyme inhibition? What can it lead to ?
a. Cimetidine
b. Increases plasma concentration of Propranolol, Diazepam, & Lidocaine (all have hepatic extraction ratios & depend on microenzyme metabolism)
93
What are physiologic responses to histamine release?
| H1 receptor physiologic response-
Smooth muscle contraction in GI and Pulmonary, induces NO release which stimulates guanylate cyclase to cause vasodilation, increase capillary permeability,
hypotension, tachycardia, flushing, headache, release of prostacyclin
94
H2 receptor physiologic response
stimulation of gastric H+ secretion
95
Increase myocardial contractility and HR
H2 receptor
96
H3 receptor physiologic response-
inhibition of synthesis and release of histamine (Antagonism of H2 attenuates H3 function)
97
Antagonism of H2
attenuates H3 function
98
What is the result of blocking H2 receptor alone, followed by the administration of a histamine releasing drug?
An increase in release of histamine
99
How do first generation antihistamines differ? What are examples of first and second generation antihistamines?
1st generation- more sedation, may also block muscarinic, serotonin, or alpha adrenergic (
diphenhydramine, promethazine
100
What are examples of second generation antihistamines?
2nd generation- less sedation (fexofenadine, loratadine, cetirizine)
101
Which generation antihistamine may also block muscarinic, serotonin, or alpha adrenergic?
1st
102
Examples of first generation antihistamines are
Diphenhydramine
| Promethazine
103
Examples of 2nd generation antihistamines are
fexofenadine, loratadine, cetirizine)
104
52. Compare the potency of ketorolac to narcotics?
30 mg ketorolac IM = 10 mg morphine =100mg meperidine
105
What dose of aspirin is required to inhibit the cox-1 enzyme?
75-325mg
106
What is the recommended dose of ketorolac?
30 mg
107
What is the recommended dose of ketorolac in a 65 y.o patient?
Do not exceed 30 mg in elderly for loading dose and don’t exceed 15 mg for maintenance
108
What is the recommended dose of IV acetaminophen?
a. <50kg: 12.5mg/kg q 4 hours OR 15 mg/kg q 6h Pediatrics
| b. >50kg: 650 mg q 4 hours OR 1 gram q6h
109
Infusion time for IV acetaminophen (Ofirmev)?
Over 15 minutes
110
What coagulation test can be used to monitor aspirin?
a. Bleeding time? prothrombin time? Platelet function?
111
What is the mechanism of action of corticosteroids?
Block phospholipase A2 from producing arachidonic acid
112
What are adverse reactions from NSAIDs?
a. Most common: Dyspepsia, Renal adverse effects, Peptic ulcer less common
b. Other: skin rxn, CNS effects, postop bleeding
c. Rare: blood dyscrasias, uticaria, erythema multiform, pneumonitis, aseptic meningitis
113
PUD may be a side effect of ______And it is ____common
NSAIDS, less
114
Most common side effect of NSAIDS
Dyspepsia
115
What are the clinical properties of acetaminophen?
a. Mild/moderate analgesic, antipyretic, low gastric irritation & platelet aggregation
b. NO ANTI-INFLAMMATORY PROPERTIES!!!!
116
What are clinical effects of aspirin?
Analgesic, antipyretic, platelet inhibition (for the life of the platelet ~ 7 days)
117
How long should aspirin be held prior to elective surgery?
7-10 days
118
What agents can be used to treat an acute gout attack?
Colchicine
119
Does Tylenol have anti-inflammatory effects?
NO
120
What are physiological effects of high and low dose aspirin?
a. High dose: anti-inflammatory dose 2.5-5.4 g/day
| b. Low dose: MI prophylaxis 75-325 mg/day, analgesic/antipyretic 325-650 mg q 4-6 hours
121
What patients are at highest risk from aspirin associated bronchospasms? What is the cause of this reaction?
a. Asthma pts- increases availability of arachidonic acid for production of leukotrienes
122
Define the role of NSAIDs for the treatment of post-operative pain.
Decreases postop pain,and requirements (20-50%), not used as sole treatment,
should be combined with short-acting opioids or LA, less N/V than with opioids alone
123
What are the maximum recommended doses With Epi and Without for:
Etidocaine- 400 mg, 300mg (Not used for spinals)
124
What are the maximum recommended doses With Epi and Without for:. Bupivacaine-
225 mg, 175 mg
125
For Bupivacaine, Intervals must be
> 3 hours & Max dose in 24 hrs = 400 mg
126
For Bupivacine, OB continuous epidurals:
if 0.5% solution plain (no epi) limit dose to 320 mg
127
What are the maximum recommended doses With Epi and Without for:
Lidocaine- 7 mg/kg (500mg total), 4.5 mg/kg (300mg total)
128
What are the maximum recommended doses With Epi and Without for
Chloroprocaine – 14 mg/kg (1000 mg total), 11 mg/kg (800 mg total)
129
What are the maximum recommended doses With Epi and Without for: Procaine
Procaine (Novocaine) – Max 1000 mg
130
What is the maximum recommended dose of prilocaine (EMLA)?
a. Max 600 mg
| b. O-toludine = Methemoglobin
131
Which local anesthetic best demonstrates a differential block?
bupivacaine
132
What will result when bicarbonate is added to a local anesthetic solution?
a. Speeds onset
| b. Can form a precipitate, so need to use right away
133
What effect will adding bicarbonate to LA have this have on onset of action?
LA will become mostly non-ionized with higher pH of surrounding solution
134
What concentration of bupivacaine is not recommended by the FDA in OB?
0.75% = known to have CV toxicity and arrest
135
Which local anesthetic has greatest cardiac toxicity?
Bupivicaine
136
This LA is not used for spinal
Etidocaine
137
What are signs/symptoms of CNS toxicity?
Circumoral numbness, lightheadedness, tinnitus, visual disturbances, slurring of speech, muscle twitching, unconsciousness, grand mal seizures, coma, apnea
138
76. What is the order of nerve blockade by local anesthetics? What are the clinical signs of the order of
nerve blockade by local anesthetics?
a. 1st:
c. 3
d. 4th: A-beta (sensory/proprioception, touch, pressure)
e. 5th: A-alpha (motor, skeletal muscle, proprioception)
```
B fibers, C fibers and
A delta fibers
A gamma
A beta
A alpha
```
139
B fibers
preganglionic autonomic
140
A-delta
fast pain & temp
141
C fibers
slow pain, temp, touch and
142
Slow pain, temp, touch which fiber
C fibers
143
Postganglionic autonomics, which fiber
C fibers
144
A-gamma action
muscle tone, motor, reflexes
145
A-beta
sensory/proprioception, touch, pressure
146
A-alpha
motor, skeletal muscle, proprioception
147
First fibers blocked
B fibers
148
What was the first Local anesthetics
Cocaine
149
What is a metabolite of ester local anesthetics?
a. Paraaminobenzoic acid (PABA)
150
What is the primary determinant of the potency,of local anesthetics?
lipid solubility
151
What is the primary determinant of onset of LA?
IONIZATION
152
What is the primary determinant of duration of action of LA ?
Protein binding
153
What should be done at the first sign of suspected CNS local anesthetic toxicity?
a. Restlessness, vertigo, tinnitus, & difficulty focusing occur initially
154
Primary concern with CNS toxicity with LA
seizures- maintain airway and oxygenate patient
155
Non-CNS LA toxicity- can have patient
hyperventilate
156
Which local anesthetic is recommended for an emergency C-section?
Chloroprocaine (ester LA, least toxicity known to man, good for epidural, but NOT for spinal d/t NO plasma esterases in CSF to metabolize so it depends highly on redistribution for metabolism)
157
What is the mechanism of action of local anesthetics?
Block fast Na channels (greater affinity for open or inactive
158
2 states of Na channel LA work on
Open or Inactive
159
What local anesthetic can cause methemoglobinemia?
Prilocaine, Benzocaine, Cetacaine, Lidocaine
160
What are causes of increase in the minimal blocking concentration for local anesthetics?
Increase nerve fiber diameter, increase myelination, greater distance b/w nodes of Ranvier
161
What is the diameter of each nerve fiber A-alpha:
15-20 microns (largest)
162
What is the diameter of each nerve fiber. A-beta:
5-12 microns
163
What is the diameter of each nerve fiber. A-gamma:
3-6
164
What is the diameter of each nerve fiber A-delta:
1-4 (pain)
165
What is the diameter of each nerve B fibers:
<3
166
What is the diameter of each nerve fiber C fibers
0.3-1.3 (smallest) (pain)
167
How many nodes of Ranvier must be blocked to inhibit nerve conduction?
2-3
168
How are local anesthetics metabolized?Amides
Liver
169
How are local anesthetics metabolized?Esters
Plasma cholinesterases
170
What local anesthetics are classified as amides?
they all contain 2 "i" Prilocaine>etidocaine>lidocaine>mepivicaine>bupivacaine
171
What local anesthetics are classified as esters?
They all contain 1 "i"
| Chloroprocaine>procaine>tetracaine>Cocaine
172
How does cocaine differ from other ester local anesthetics?
Vasoconstrictor, metabolized by liver & plasma esterases.
173
Only ester metabolized by the liver is
Cocaine
174
Cocaine and neurotransmitter
Also is a sympathomimetic increasing post-synaptic NE and; Dopamine
175
Which local anesthetic can be used to treat recalcitrant (resistant) seizure activity?
Lidocaine
176
What is recommended treatment for local anesthetic cardiac toxicity?
Intralipid therapy 20%
177
Which local anesthetic will NOT cause vasodilatation?
Cocaine & Mepivacaine
178
Why is epinephrine added to local anesthetic solutions? What are PROS of epinephrine use?
Decreases absorption of LA & prolongs the effects, decreases systemic toxicity, permits higher doses of LA
179
Cons of EPI use with LA
Tachycardia, do not use with patient who are tachycardic?
180
Know potencies of the local anesthetics.O:Water P/C
The higher the oil:water p.c., the more potent
181
Potency of LA
Bupivacaine=tetracaine>ropivacaine>etidocaine>lidocaine=mepivacaine>chloroprocaine (B=
TREL=MC)
182
Onset of absorption, for most to least (ITIC PEBSS)
IV>tracheal>intercostal>caudal>paracervical (pudendal block)>epidural>Brachial Plexus>SubArachnoid/Sciatic/Femoral>SQ (ITIC PEBSS)
183
What is the selectivity in cardiac toxicity of LA?
a. Bupivacaine > Etidocaine > Lidocaine
184
FIRST SIGN of LA toxicity
Circumoral numbness (mouth, lip, tongue)
185
What are the 3 characteristics segments of Local anesthetics?
```
Aromatic ring (lipophillic)
Intermediate Carbon group (ester or amide)
Tertiary amine (hydrophillic)
```
186
What clotting factor is deficient in patients with: Hemophilia A-
Factor VIII deficiency
187
What clotting factor is deficient in patients with:
Hemophilia B- Factor IX deficiency (Christmas factor)
188
98. What laboratory test are abnormal in a patient with:
| a. Hemophilia A-
normal PT, abnormal aPTT, the specific factor assay for factor VIII will reveal
the appropriate defect. Should undergo test for vWB
189
What laboratory test are abnormal in a patient with Hemophilia B-
normal PT, abnormal aPTT, specific assay for factor IX
190
What laboratory test are abnormal in a patient with Hemophilia Bm-
both PT & aPTT prolonged
191
How should a patient with inhibitors for factor VIII or factor IX be managed prior to elective surgery?
Reduce inhibitor levels with immunosuppressant therapy (cyclophosphamide), gamma-globulin, plasmapheresis, or by tolerance with high dose or frequent administration of factors
192
What products are recommended for the prevention of bleeding in a patient with Von Willibrand’s
disease?
Cryoprecipitate, Humate-P, Koate-HS and Koate HP have been reported to achieve clinical
hemostasis prior to surgery and can be used in place of cryoprecipitate
193
Goals of therapy for VWD are to
improve factor VIII levels, and improve bleeding time
194
What is the recommended treatment for mild bleeding associated with VWB disease?
Desmopressin 0.3-0.4 mcg/kg, infuse over 15 minutes may be given to treat mild bleeding episodes
195
What are most common adverse effects associated with desmopressin?
Facial flushing (most common)
196
DDAVP can cause
platelet aggregation and severe thrombocytopenia
197
DDAVP Used in type
IIb vWB
198
Less Frequent SE of DDAVP:
Mild H/A, increase HR, decrease BP (you wouldn’t think), water retention which may lead to severe hyponatremia, increase plasminogen activator
199
What agent can be given to inhibit the potential fibrinolysis from DDAVP?
Aminocarproic acid
200
What is goal concentration of factor VIIIX prior to surgery?
Desired factor VIII levels 1 hour prior to surgery 100%, then 50% until wound healing begins, then 30% until complete would healing
201
What is goal concentration of factor IX prior to surgery?
Half-life of factor IX is 24 hours, with normal hemostasis occurring when plasma levels area about 10-25%
202
What are signs/ symptoms of Class I hemorrhage?
| Class I
loss of up to 15% of total blood volume. Causes vasoconstriction and mild tachycardia.
203
What are signs/ symptoms of Class II hemorrhage?
| Class II
loss of 15-30% of blood volume, produces tachycardia, decreased pulse pressure,anxiety, restlessness
204
Class I and II hemorrhages, How should these patients be managed?
IV crystalloid therapy
205
What are the signs/symptoms of Class III hemorrhage?
| Class III-
loss of 30-40%. Produces hypovolemia, marked tachycardia, systolic hypotension, AMS.
206
What are the signs/symptoms of Class IV hemorrhage?Class IV
more than 40% of total blood volume is life threatening and accompanied by marked tachycardia and very narrow pulse pressure, and low urine output. Mental status markedly depressed.
207
Class III and IV hemorrhages, How should these patients be managed?
In young, healthy patient, up to 30-40% of blood volume usually can be treated adequately with
crystalloid therapy
208
What are the indications for the administration of platelets?
d. Determination of whether pts with intermediate (50,000-100,000) require therapy should be
based on risk of bleeding
Transfusion of one platelet concentrate will increase the platelet count by approximately 5,000- 10,000 in an average adult.
209
Usual therapeutic dose is (for platelet)
1 platelet concentrate per 10kg body weight
210
Prophylactic platelet transfusion
is rarely indicated in surgical platelet with thrombocytopenia d/t decreased platelet production when platelet count is >100,000 and is usually indicated when <50,000.
211
What are the indications for administration of packed RBCs?Transfusion is rarely indicated when
Hgb concentration is >10g/dL
212
Transfusion is Almost always indicated when it
is less than 6g/dL, especially when anemia is acute
213
Transfusion 1 unit whole PRBCs increases
Hct 3% or Hgb 1g/dL, in a 70 kg non-bleeding adult
214
What are the indications for the administration of FFP?
a. Urgent reversal of warfarin therapy
| b. Microvascular bleeding with elevated PT or PTT (>1.5 times normal)
215
What is the most common inheritable coagulopathy?
Von Willebrand Disease
216
VWD Results in
abnormal platelet function & defective for plasma clotting
217
What is VWD, needed for
factor VIII complex, stimulates VIII production
218
113. When should we not use DDAVP, in what type of Von Willebrand Disease?
Type 2B
219
Can ause platelet aggregation & severe thrombocytopenia
DDAVAP
220
Never use DDAVP in the beginning of presumed Von Willebrand Disease for this reason why?
because different sub-types exist and require different treatment modalities
221
Relative clinical potency and BUPIVACAINE Oil/ water partition
8;30
222
Relative clinical potency and Tetracaine Oil/ water
8; 80
223
Relative clinical potency and Lidocaine Oil/ water partition
2;4
224
Relative clinical potency and Mepivacaine; Oil/ water partition
2; 1
225
Relative clinical potency and chloroprocaine; Oil/ water partition
1;1
226
Lidocaine primary metabolite is
Monoethylglyceinexylidide (use to assess hepatic functions to predict morbidity and mortality)
227
Prilocaine hepatic derived metabolite
O-Toluidine
228
Define minimum blocking concentration (Cm)
The lowest concentration of drugs needed for blocking impulse propagation. think of it like MAC for local anesthetics
229
A patient is known to be allergic to penicillin.This patient may be allergic to what other an,bio,cs?
Cephalosporins (Cross-reac,vity 5%) among beta-lactams
230
Is there cross-sensitivity among ester local anesthetics? •
There is cross reactivity among ester LA. Due to common metabolite para-aminobenzoic
acid.
231
Between ester and amide anesthetics?
No
