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Basic1 Flashcards

1
Q

Bioavalabilty

A

relative amount of a drug dose that reaches the systemic circulation unchanged and the rate at which this occurs

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2
Q

Drugs that easily pass through the lipid bilayer

A

small, nonpolar

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3
Q

Volume of distribution

A

Volume of tissue that the drug reaches

Vd=dose/concentration

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4
Q

Hepatic metabolism

A 
Phase 1 (oxidation, reduction, hydrolysis): by p450 this occurs hydroxylation, dealkylation, deamination, desulration, epoxidation, dehalogenation
Phase 2 (conjugation): conjoins hydrophobic drug molecules with polar moities to increase solubility and therefor renal clearance
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5
Q

Drugs with active metabolite

A

Morphine -> morphine 6-gluconoride (opioid)
Meperidine -> Normeperine (convulsant)
Atracuriun -> laudanosine (convulsant)
issues when pt is renally impaired

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6
Q

metabolism equations

A

Rate = Q (Cin - Cout)
Extration ratio =(Cin -Cout)/Cin
Clearance =Q X ER

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7
Q

Cockcroft-Gault equation (creatinine clearance)

A

Creatinine Clearance (ml/min) =[ (140-age) X weight] / 72 X serum creatinine

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8
Q

Tissue clearance

A

butylchilinesterase = Sux, mivacurium, 2 chroroprocaine, ester LA
nonspecific esters = remifentanil, atracurium
RBC esterases = esmolol

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9
Q

major plasma proteins for binding anesthetic drugs

A

albumin and alpha-1-acid glycoprotein

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10
Q

epidural opiods

A

must male their way out of the epidural space if they are to reach their site of action in the spinal cord’s dorsal horn

  • lipid soluble drugs (fentanyl, sufentanyl) reach lower peak concentrations in the CSF compard to hydrophilic (morphine)
  • lipiphylic drugs more easily transverse vascilar walls and therefor are cleared more rapidly
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11
Q

intrathecal opiods

A
  • lipophilic opioids tend to move out of the aqueous CSF primarily diffusing across the meninges into epidural fat
  • explains why morphine (hydrophylic) causes delayed respiratory depression (stays intrathecal and spreads up to brain)
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12
Q

Epidural LA

A
  • intrathecal bioavalabilty increases with lipiphilicity (opposite of opioids)
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13
Q

LA Spinals

A

1) baricity of solution (adds glucose to make hyperbaric)
2) position of patient
3) concentration of LA

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14
Q

Tolerance vs dependence

A

Tolerance: requiring increased dosages of a drug to achieve similar effects
dependence: compulsive need of an individual to use a drug to function normally

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15
Q

types of tolerance

A

1) dispositional (metabolic): repeated use of a drug reduces the amount of drug available at site
2) reduced responsiveness (pharmacodynamic): repeated use alters nerve cell functions
3) behavioral (context-specific): reduces its effect in the environment where it is typically administered but not in other environments.

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16
Q

tachyphylaxis

A

acute decrease in response to a drug following its administration

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17
Q

half life

A

half life = 0.693/ Ke

Ke = rate constant

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18
Q

Clearance equation

A

Clearance = Vd X Ke

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19
Q

Renal clearance

A

Renal Clearance = concentration of drug in urine X volume of urine / concentration of drug in plasma

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20
Q

Anaphylaxis vs anaphylactoid

A

anaphylaxis: severe allergic reaction mediated by an aintigen antibody reaction ( type I) IgE
Anaphylactoid resembles anaphylaxis but is not IgE mediated ( does not require prior sensitization)

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21
Q

most common cause of anaphylaxis

A

NDNMB

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22
Q

latex allergy risks

A

chronic exposure to latex, neural tube defects, frequent caths

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23
Q

MOA of inhaled gasses

A

proposed:
enhance inhibitory receptors (GABA and glycine)
dampen excitatory pathways (nicotinic and glutamate)

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24
Q

Rate of equilibirum in gasses

A

rate is directly related to alveolar gas concentration

high partition coefficient= high solubility= slow rate of induction

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25
Q

Cardiovascular effects of inhaled anesthetics

A
  • Map decreased by decreaseing SVR (except halothan which decreases CO and MAP with no change in SVR)
  • HR increases initially
  • abrupt changes in halothane can cause drastic increases in HR and BP
  • sensitize the myocardium to epinephrine, depress mycardial contractility
  • Sevo causes QT prolongation
  • Iso has coronary vasodilating properties
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26
Q

Pulmonary effects of inhaled anesthetics

A
  • Increase RR with decrease TV = same MV
  • blunt ventilatory stimulation caused by hypoxemia and hypercarbia
  • increases atelectasis and decrease FRC
  • bronchodilation
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27
Q

CNS effects of inhaled anesthetics

A
  • uncouple CBF and CMRO2. increase and decrease respectively
  • nitrous oxide increased CMRO2
  • depress the amplitude and increase the latency of somatosensory evoked potentials (SSEPs)
  • Sevo may be associated with epileptiform activity on the EEG at high concentration
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28
Q

Opioids MOA

A

work on mu, kappa and delta

  • G coupled receptors => cAMP
    1) inhibition of presynaptic Ca2+ influx
    2) increasing postsynaptic K+ efflux
    3) activation of the descending inhibitory pain pathway via inhibition of GABAergic receptors in brain stem
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29
Q

Bayes theorem

A

how the probability that a theory is true is affected by a new piece of evidence
- used to help develop preoperative testing algorithms by helping clinicians interpret testing results in light of the patient presentation and surgical procedure

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30
Q

ulnar nerve neuropathy

A

Postoperative ulnar nerve injury is the most common form of perioperative peripheral neuropathy. It occurs more commonly in males and very thin or obese patients. Ulnar neuropathy is typically transient but can persist and cause morbidity and disability. Nerve conduction studies are beneficial in evaluating both motor and sensory deficits.

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31
Q

most efficient way to decrease costs of OR

A

math OR scheduling with full time anesthesiology staffing

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32
Q

Latex allergy

A

Health care workers, children with spina bifida and urogenital syndromes, and people with allergies to banana, avocado, kiwi, pineapple, mango, and other tropical fruits have an increased risk for development of a latex allergy. Frequent cosmetic use may be related to antibodies against aminosteroid NMBDs (pancuronium, pipercurium, rocuronium, and vecuronium), but there is no increased association with a latex allergy.

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33
Q

Most influences how nitric oxide works in the body

A

site of production:

-due to very short half life

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34
Q

Drug abuse

A

Risk factors for substance abuse include access to substances of abuse, personal history of drug abuse, family history of drug abuse, younger age, psychologic disease, and a history of preadolescent sexual abuse.
NOT HIGH EXPECTATIONS- may be protective

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35
Q

POPE

A

mechanism of POPE is the large negative pressure developed by inspiration against an occluded airway, heralding an increased preload and afterload that increases pulmonary blood volumes and venous pressures, which leads to increased hydrostatic pressure and the formation of pulmonary edema

  • Two other factors involved are hypoxia and a hyperadrenergic response, both of which promote translocation of blood from the systemic to pulmonary circulation that also increases pulmonary pressures.
  • Tx: PPV
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36
Q

ABO incompatibility labs

A

INcreased: bilirubin (both), urine hemoglobin, INR, PT/PTT, fibrin degradation products, BUN, LDH, creatinine
Decreased: haptoglobin, fibrin, platelet count

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37
Q

upregulater acetylcholine nicotinic channels

A 
Causes of Nicotinic AChR Upregulation
 - Nerve Injuries
    o Stroke
    o Spinal cord injury
 - Burns (24 hours up to 1-2 years after burn injury)
 - Prolonged immobility (risk greatest after 16 days)
 - Prolonged exposure to neuromuscular blockers
 - Myopathies
    o Duchenne muscular dystrophy
 - Denervation Disorders
    o Multiple sclerosis
    o Guillain-Barré syndrome
    o Amyotrophic lateral sclerosis
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38
Q

Post MI treatment

A

Following a myocardial infarction lifestyle modification and control of systemic disease should occur. Medications to be initiated following a myocardial infarction should be beta-blocker, ACE-I, statin, and aspirin.

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39
Q

SSEP during ischemia

A

decreased amplitude and increased latency

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40
Q

etomidate

A
  • GABA agonist
  • minimal effects on cardiac function or vascular tone and does not cause histamine release
  • decreases cerebral metabolic oxygen demand, cerebral blood flow, and intracranial pressure (ICP), but maintains cerebral perfusion pressure
  • adrenal suppresion ; inhibits the adrenal enzyme 11-β hydroxylase, the downstream effects of which are inhibition of cortisol (and aldosterone) synthesis
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41
Q

methadone side effects

A

prolonged QT interval

- possible torsades de pointes

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42
Q

gas cylinder coloring

A

oxygen: green, carbon dioxide: gray, nitrous oxide: blue, nitrogen: black, air: yellow, helium: brown.

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43
Q

oxygen-hemoglobin dissociation curve

A

Hyperthermia, acidosis, high pCO2, and high levels of 2,3-DPG cause a shift to the right. Fetal hemoglobin shifts the curve to the left

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44
Q

Barbiturates

A

MOA: increase duration of cl- channels at GABA receptors, some NMDA action too

  • small nonionized form easily passes through BBB= quick, termination is by redistribution
  • cleared by liver (except phenobarbital = renal)
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45
Q

barbiturates CNS

A
  • methohexital can provoke involuntary muscle contractions and elicit seizure activity
  • overall decrease CMRO2,
  • decrease ICP
  • preserve autoregulation
  • minimal effects of SSEPs and MEPs
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46
Q

barbiturates cardio

A

decrease BP and increase HR

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47
Q

side effects of barbiturates

A

thiopental= garlic or onion taste
sulfur-containing thiobarbiturates evoke mast cell histamine release
intraarterial injection results in severe vasoconstriction

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48
Q

Clearance of propofol

A

metabolized in liver, but clearance exceeds liver metabolism suggesting extra-hepatic metabolism.

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49
Q

propofol and CNS

A

causes burst supression at intubation doses

decreases ICP, CMRO2, and CBF

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50
Q

Etomidate (2)

A
  • carboxylated imidazole
  • targets major inhibitory ion channels in the brain; the GABAa receptor
  • termination is due to redistribution for bolus
  • adrenocortical supression due to 11 beta hydroxylase
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51
Q

Ketamine

A
  • works as antagonists to NMDA in thalamus and limbic system
  • binds mu opioid receptors and provides analgesic effects at subanesthetic doses
  • raises ICP by increase in MAP and higher CPP
  • depresses myocardia and smooth muscle but also increases circulation catecholamines with net increase in BP, HR, CO and myocardial O2 consumption
  • increases secretions
  • clearance strongly related to liver blood flow
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52
Q

St John wart induces which enzyme

A

P450 3A4 and P450 2C9 enzymes.
St. John’s wort is a drug used to help treat anxiety and depression. St. John’s wort has mild sedative properties, which can affect anesthesia. St. John’s wort should be used with caution in patients taking MAO-Is or SSRIs. Additionally, St. John’s wort has been associated with delayed arousal from anesthesia, and some argue that MAC may be decreased in patients taking a St. John’s wort.

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53
Q

herbals that increase risk of bleeding

A

Ginger, garlic, ginkgo, and vitamin E

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54
Q

buprenorphine

A

-ceiling effect at higher doses

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55
Q

pipeline failure

A

Management of pipeline failure or gas crossover:

1) Disconnect the pipeline connection at the wall.
2) Open the emergency oxygen cylinder fully.
3) Ventilate by hand with the anesthesia breathing circuit.

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56
Q

hormones after acute stress (surgery)

A

1) Sympathoadrenomedullary axis: sympathetic nervous system activity, epinephrine secretion from the adrenal medulla
2) Hypothalamic-pituitary-adrenocortical (HPA) axis: corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH), cortisol
3) Counter-regulatory hormones: catecholamines, glucagon, growth hormone*, cortisol
4) Proinflammatory mediators: tumor necrosis factor–alpha (TNF-a), interleukin (IL)-1, and IL-6, IL-8, IFN-γ
5) Salt and water retention, sustain blood pressure: renin-angiotensin-aldosterone system, vasopressin#, catecholamines
* GH increases initially, followed by a decline on postoperative day 1.
# In response to surgical stress, vasopressin increases and remains elevated; in septic shock, an initial increase is followed by a decrease to extremely low concentrations
T3 is decreased

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57
Q

unilateral recurrent laryngeal nerve injury

A

ipsilateral vocal cord adduction

58
Q

paraspinal epidural approach

A

skin, subcutaneous tissue, and then the ligamentum flavum

59
Q

midline epidural approach

A

skin, subcutaneous tissue, supraspinous ligament, interspinous ligament, and then ligamentum flavum.

60
Q

decreased SVO2

A
  • Increased oxygen consumption (e.g. hyperthermia, shivering, or pain)
  • Decreased cardiac output (e.g. myocardial infarction or hypovolemia)
  • Decreased hemoglobin concentration
  • Decreased arterial oxygen saturation
61
Q

increased SVO2

A
  • Increasing the hemoglobin concentration via blood transfusions
  • Increased SaO2
  • Decreased VO2 (e.g. cyanide toxicity, sepsis, carbon monoxide poisoning, methemoglobinemia, hypothermia)
  • Increased CO (e.g. sepsis)
    A left to right intracardiac shunt, in addition to increasing cardiac output, also shifts oxygenated blood from the left side of the heart to mix with deoxygenated blood on the right side, thereby falsely elevating the SvO2.
62
Q

left sided IJ vs right

A

-increase risk for chylothorax , and small increase for carotid puncture

63
Q

carbon dioxide embolism

A

doesnt have significant improvement with cessation of nitrous

64
Q

substance abuse facts

A

1) 50% are < 35 years old
2) Residents are overrepresented
3) Many are Alpha Omega Alpha members
4) 33-50% are polydrug abusers
5) For 76-90%, opioids (e.g., fentanyl and sufentanil) are the abuse drug class of choice
6) 33% have a family history of addiction
7) 65% are associated with academic departments
- more common in academic settings
- no increased risk for anesthesia though more likely to report

65
Q

axillary nerve block

A

misses intercostobrachialis and possible musculocutaneous (innervation to the biceps muscle (elbow flexion)

66
Q

treatment of EPS in PACU

A

Treatment options for EPS or acute dystonic reactions from dopamine receptor antagonists include anticholinergics (preferred), benzodiazepines, beta-blockers, antihistamines, dopamine agonists, and alpha-adrenergic agonists. Commonly used anticholinergic agents are benztropine, diphenhydramine, and trihexyphenidyl

67
Q

K homeostasis

A
  • affected by aldosterone, cortisol and insulin
68
Q

methemoglobinemia

A

In a patient with methemoglobinemia, the only value that will significantly change on an ABG and pulse oximetry when supplemental oxygen is given will be the partial pressure of oxygen (PaO2).

69
Q

Cancer drug side effects

A

Bleomycin: pulmonary toxicity : dont use 100% O2
Cyclophosphamide: hemorraghic cystitis (prevented with mensa)
Methotrexate: myelosuppresion; leukovorin rescue
Vincristine: peripheral neuropathy
Doxurobicin: cardiomyopathy

70
Q

AKI

A
  • Increase in Serum Cr by ≥ 0.3 mg/dL (≥ 26.5 μmol/L) within 48 hours; or
  • Increase in Serum Cr to ≥ 1.5 times baseline, within the prior 7 days; or
  • Urine volume < 0.5 mL/kg/h for 6 hours
71
Q

TIme after MI before elective surgery

A

without intervention : 60
ballon angioplasty 14 days
BMS 30 days
DES 180 days

72
Q

dead space

A
  • increases in upright position
  • increased with neck extension
  • increases with PPV
  • increases with hypotension and PE
73
Q

Anterior spinal syndrome

A

there is loss of motor, temperature, and pain function

74
Q

angiotensin II

A

Angiotensin II results in increased inotropy, chronotropy, catecholamine release, catecholamine sensitivity, aldosterone levels, vasopressin levels, and cardiac remodeling through AT1 receptors. ACE inhibitors and ARBs help to prevent the remodeling that occurs secondary to angiotensin II and are beneficial in congestive heart failure.

75
Q

Fenoldopam

A

Fenoldopam is a selective dopamine-1 agonist that increases renal blood flow despite decreased systemic arterial blood pressure.

76
Q

PT (prothrombin time)

A

WEPT

Warfarin intrinsic PT

77
Q

LA elimination

A

Amides: degradated in lived by P450 microsomal enzymes
Esters: pseudocholinesterases => break down into PABA which can cause allergic reaction. Concern for ester toxicity is inreased in neonates and patients with atypical pseudocholinesterase levels

78
Q

LA block

A

work on the voltage gated sodium channels withing the nodes of ranvier
-lipid soluble unionized base (B) penetrates trhough the axonal membrane and the cationic (BH+) for binds to receptor
- block smaller nerves first, and mylinated better than unmylinated
-loss of sympatetic transmission, pain, temperature, touch, proprioception and then skeletal muscle tone
block the mantle before the core: proximal anesthesia before distal
- easier to bind to activated (open) and inactivated (closed) compared to reactivation (resting) state

79
Q

Classification of nerve fibers

A

B (mylinated) small: preganglionic autonomic
C (unmylinated) small : dull pain, temperature, touch
A (mylinated): Delta: pain temperature touch,
Gamma: Muscle tone
Beta: small motor, touch, pressure
Alpha: proprioception, large motor

80
Q

LA potency, Duration, Speed

A

potency: directly proportional to lipid solubility
duration: primarily directly proportional by protein binding, and also rate of vascular uptake at injection site
Speed: pKa; the closer the pKa to physiologic (7.4) (or the lower the pKa) the faster; poor penetration and delyaed onset in infected tissue due to acidic environment
- 2 chloroprociane has high pKa but due to high concentration has rapid onset

81
Q

LA additives

A

epinephrine: increase duration and decrease potential for systemic toxicity ( not for fingers, ears, penis, nose and toes)
- bicarb: increases concentration of the nonionized form (can cause precipitation)
- clonidine: prolongs and reduced requirement- hypotension, bradycardia and sedation
- opioids- neuraxial
- ketamine: prolong analgesia

82
Q

methemoglobineamia with LA

A

-prilocaine and benzocaine

83
Q

Transient Neurologic Symptoms with LA

A
  • due to transient direct neurotoxicity
  • severe pain in the lower back, buttocks, and lower extremities within 12-24 hours after uneventful spinal anesthesia
  • no sensory, motor or bowel and bladder dysfunction
  • risk factors: lidocaine use, high dose, lithotomy, ambulatory procedures
  • symptoms resolve in a week; treat with NSAIDS
84
Q

LA random facts

A

tetracaine: for long duration spinal anesthesia
cocaine: only LA that causes vasoconstrition; side effects of increased catecholamines
Chloroprocaine: impairs the action of subsequent bupiv epidural or opioids (concurrently or sequentially)
Mepivacaine: metabolism is prolonged in the fetus
Ropivicaine: less motor block (S- enantiomer of bupiv)
levobupiv: less toxicity risk than bupiv

85
Q

LAST symptoms

A

1) lightheadedness, dizzyness, periorbital numbness, metallic taste
2) visual and auditiory disturbances, tinnitus, diplopia, nystagmus
3) Excitatory symptoms: agitation, confusion, muscle twitches, tonic clonic seizures ( convulsive threshold of LA is inversely related to arterial PCO2)
4) depression symptoms: obtundation, LOC, coma, respiratory depression
5) Cardiovascular collapse: HTN, tachy, reentry dyshythrmias => hypotension and cardaic depression (most common fatal arrhythmia is refractory ventricular fibrillation)
- under GA cardiac symptoms may be first to show

86
Q

Cardio issues with LAST

A
  • conduction blockade at SA node creates favorable conditions for reentry dysrhythimas
  • negative inoptropic effects by decreasing calcium release from SR- decreases the excitation-contraction coupling
  • depress the baroreceptor reflex, decrease CO, and promote unopposed SNS activity
87
Q

Treatment of LAST

A
  • stop LA infusion
  • call for help
  • airway control - 100% O2 , increase RR (lowers PaO2 which helps with seizure threshold and plasma pH)
  • seizure control- benzos, sodium thiopental (not propofol due to cardiac depressant)
  • ACLS ( lower epinephrine dose to <1 mike/kg, avoid vasopressin, calcium channel blockers, beta blockers, procainamide and lidocaine)
  • Intralipid at 1.5ml/Kg (lean) bolus and infusin at 0.25 ml/kg/min. Can repeat bolus q 5 3X and cand ouble infusion if needed
  • If refractory prepare for cardiopulmonary bypass
  • monitor for 12 hours after resolution
88
Q

SCh side effects

A
  • bradycardia
  • MH
  • masseter muscle spasm
  • myalgias
  • increase IOP
  • hyperkalemiea
  • increase ICP
89
Q

Dibucaine #

A
  • DIbucaine is a LA that inhibits pseudocholinesterases
  • normal inhibits 80%
  • atypical inhibits 20%
  • heterozygous 40-60%
90
Q

Agents that potential muscle relaxants

A
  • volitile, LA, CCB, BB, antibiotics (aminoglycosides), magnesium, long term steroids, dantrolene
91
Q

disease that make you resistant/ sensitive to muscle blockers

A

myasthenia gravis- susceptible to depolarizing, resistant to non depolarizing
lamber- eaton, sensitive to both

92
Q

how to volatile gases prolong paralytics

A

Volatile anesthetics decrease the sensitivity of the postjunctional skeletal muscle cell membrane to depolarization

93
Q

Perioperative hyperglycemia

A

immunosuppression due to decreased white blood cell function, increased infections, stimulation of sympatho-adrenergic activity, osmotic diuresis causing volume depletion, reduced skin graft success, increased catabolism in burn patients, delayed wound healing, delayed gastric emptying, exacerbation of brain, spinal cord and renal damage by ischemia, and increased mortality.

94
Q

Cerebral blood flow

A

directly related to body temperature, PaCO2 (within normal physiologic ranges), and extremes of MAPs (< 50 or >150 mm Hg).
Cerebral blood flow is inversely related to PaO2 when less than 50 mm Hg.
Cerebral blood flow remains unchanged within the autoregulatory range of MAPs (50-150 mm Hg) and with PaO2 >50 mm Hg.

95
Q

Leukoreduction

A

Leukoreduction is a decrease or complete elimination of donor leukocytes in blood components. This can reduce the risk of febrile transfusion reactions and the risk of viral transmission (e.g. cytomegalovirus). It does not fully protect against bacterial infection and does not prevent graft-versus-host disease.

96
Q

Pain nerves

A

Type A Delta and Type C

97
Q

differential blockade

A

Sympathetic People Matter”: Sympathetics > Pain > Motor for neuraxial blockade levels.

98
Q

Hypercalcemia treatment

A

dilution (NS)

99
Q

TEG

A 
R = reaction time, zero to clot formation
Coagulation time (K) =measure speed of clot formation and strengthening
Maximum amplitude = strength of fully formed clot, 
alpha angle = speed of clot formation
MA value decreased -> platelets.
K value prolonged -> cryoprecipitate.
R value prolonged -> FFP.
Teardrop configuration -> antifibrinolytics.
100
Q

carotid body chemoreceptors

A

Carotid body chemoreceptors are primarily responsive to reductions in arterial partial pressure of oxygen (PaO2).

101
Q

Nicardipine

A
  • calcium channel blocker
  • coronary and peripheral arterial dialator
  • prolonged in liver disease
102
Q

milrinone

A

phosphodiesterase III (PDE3) inhibitor which increases inotropy.

103
Q

Suggamedex incompatible with

A

ondansetron, ranitidine, and verapamil

- kidney failure

104
Q

ASA

A
  • irrreversibly inhibits platelet function of thromboxane A2

- 10-14% of platelets created each day. Takes approximately 7 days for return to normal

105
Q

prolongation of Sch

A
  • pseudocholieserase deficiency
  • after neostigmine > pyridostigmine
  • large doses or repeat doses cause phase two block
  • echothiophate eye drops
106
Q

pulmonary metabolism

A

Angiotensin 1
bradykinin
norepinephrine

107
Q

CVP tracing

A

a wave: atrial contraction, absent in atrial fibrillation
c wave: TV bulging into RA during RV isovolumetric contraction
x descent: TV descends into RV with ventricular ejection and atrial relaxation
v wave: venous return to and systolic filling of the RA
y descent: atrial emptying into RV through open TV

108
Q

main types of pseudocholinesterase deficiency

A

A and K

109
Q

lowest density of gases given

A

helium

110
Q

Aprepitant

A

a neurokinin-1 antagonist

can be used as premedication to prevent PONV

111
Q

Steroid redosing for surgery

A

if patient on chronic steroids > 20 mg a day of prednisone for more than 3 weeks

112
Q

Calculate saturated vapor pressure (SVP)

A

SVP/total P = anesthetic vapor volume/ carrier volume +anesthetic volume
Therefore SVP = total P (anesthetic volume/ carrier anesthetic volume)

113
Q

estimate vapor output

A

Sevoflurane ~ 1/4
Enflurane ~ 1/3
Isoflurane ~ 1/2
Halothane~ 1/2

114
Q

NMDA receptor

A

Activation of the NMDA receptor increases intracellular calcium which in turn acts as a sort of second messenger for a variety of signaling pathways.
- both of the following two conditions must be met for the NMDA receptor to become activated:
1) Glutamate (and glycine) must be bound (ligand-gated) and
2) The cell must be depolarized (voltage-gated)
The receptor will not be active if only one of these conditions is met.

115
Q

Metoclopramide and SCh

A

metoclopramide can decrease pseudocholinesterase prolonging Sch

116
Q

Methadone

A

opioid analgesic with NMDA antagonistic properties

-good for nerve pain

117
Q

LA allergic reactions

A

ester = PABA
amides with epinephrine = metabisulfite
multiple dose amides = methylparaben

118
Q

alpha 2 stimulation vs lipolysis

A

inhibits

activated by beta 2 and 3, also women have increased function

119
Q

red vs black ecg

A

Lead II measures the voltage between the red (left leg) and white (right arm) electrodes. Lead III measures the voltage between the red and black (left arm) electrodes. Lead aVR (augmented vector right) measures the voltage between the white and a combination of the black and red electrodes.

120
Q

prolongtion of muscle relaxers by volatiles

A

desflurane > sevoflurane > isoflurane > halothane > TIVA (e.g. propofol)

121
Q

respiratory acidosis compensation

A

acute: 0.2 mmol/L of bicarb for each additional 1 mm Hg PaCO2
Chronic 0.4

122
Q

Tetnus

A

The tetanus toxin initially binds to peripheral nerve terminals and is transported within the axon and across synaptic junctions until it reaches the central nervous system. There it becomes rapidly fixed to gangliosides at the presynaptic inhibitory motor nerve endings and is taken up into the axon by endocytosis. The effect of the toxin is to block the release of inhibitory neurotransmitters glycine and gamma-aminobutyric acid (GABA) across the synaptic cleft, leading to generalized muscular spasms characteristic of tetanus. The toxin appears to act by selective cleavage of a protein component of synaptic vesicles, synaptobrevin II, and this prevents the release of neurotransmitters by the cells.

123
Q

Closing capacity

A

Closing capacity is the volume remaining in the lungs during expiration when alveoli BEGIN to close. Decreasing FRC relative to CC will lead to increased atelectasis and early alveolar closure.
-emptying of the apex and airway closure at the base of the lungs occurs during forced exhalation

124
Q

laryngospasm reflex

A
  • afferent = internal branch of SLR
  • efferent = RLN
    A mnemonic to differentiate the SLN branches is “SIME” for sensory = internal, motor = external.
125
Q

reverse Bainbridge reflex

A

decrease cardiac preload slows the heart down

126
Q

brainstem ischemia following intrathecal anesthesia

A
  • caused by severe hypotension

- causes apnea

127
Q

epidural spread

A
  • Volumes is greatest indicator
  • spread is greatest in old people
  • high blocks spread down, low blocks spread up
  • not effected by height, body composition and needle direction
128
Q

% of relapse in anesthesiologist residents

A

40%

129
Q

hypoxemia 2/2 to trendelengburg

A
  • endobrochial intubation
  • reduced compliances (chest wall and lung)
  • reduced TLC
  • NO INCREASED DEAD SPACE
130
Q

preop risk factors for AKI

A

Major independent preoperative risk factors for postoperative AKI following noncardiac surgery in patients with normal renal function include age ≥ 59, BMI ≥ 32, chronic liver disease, COPD requiring chronic bronchodilator use, peripheral vascular occlusive disease, high-risk surgery, and emergency surgery.

131
Q

anticholingergic/ cholinesterase inhibitor for reversal

A
  • glyco and neo (or pyrodostigmine)
  • atropine and edophonium
  • scop and neo or pyridostigmine
132
Q

smoking cessation

A
  • first 24-48 hours there is a R shift in ox/hemoglobin curve
  • Most benefits of smoking cessation occur after 2-3 months (reduced sputum production, improved ciliary function, improved closing volume, and increased FEF25-75%). However, a decrease in carboxyhemoglobin concentrations and the resultant rightward shift of the oxyhemoglobin dissociation curve occur in as little as 48 hours after smoking cessation.
133
Q

volatile anesthetic metabolism

A

Sevoflurane undergoes the most extensive metabolism (5-8%) followed by isoflurane (0.2%) then desflurane (< 0.2%).

134
Q

Spinal block levels

A

Sympathetic 1-2 above sensory 1-2 above motor

135
Q

LMA nerve damage

A

rare but;

lingual, recurrent laryngeal, and hypoglossal nerve palsies.

136
Q

elevations in peak and plateau

A

increase in elastic compliance would cause a raise in both

-increase in airway resistance just raises peak

137
Q

landmark for stellate ganglion block

A
  • chassignac tubercle

- transverse process of C6

138
Q

nerve block for awake fiberoptic intubation

A

glossopharyngeal, SLN, RLN

139
Q

bolus of precedex

A

decrease CO, decreases HR, increase BP

140
Q

neostigmine dose for reversal

A

no greater than .07mg/kg

-excessive dosing can cause weakness

141
Q

presevation of total hepatic blood flow with volatiles

A

sevoflurane > isoflurane > halothane

Basic (6 decks)

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