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Prodigy > Week 2 Prodigy > Flashcards

Week 2 Prodigy Flashcards

1
Q

What receptors do anticholinergics bind to?

A

(reversible binding) with muscarinic cholinergic

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2
Q

What do anticholinergic drugs do?

A

prevent ACh from binding to the receptor

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3
Q

The 3 anticholinergic drugs in use in anesthesia?

A

atropine, glycopyrollate, and scopolamine

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4
Q

How do anticholinergics affect airway resistance?

A

cause bronchodilation which reduces airway resistance but increase dead space–> effect pronounced in those with COPD and asthma

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5
Q

Does atropine or glyco increase hr in fetus?

A

atropine can cross placenta, but there is no significant change in fetal hr after its admin or glyco’s admin

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6
Q

The anticholinergic safest in glaucoma pts and the anticholinergic least safe in glaucoma pt?

A

safest: glyco bc little to no mydriatic effect; least safe: scop bc causes largest mydriatic effect; atropine 0.4-1 mg IV is considered safe when admin w anticholinesterase drug bc little to no change in pupil size noted

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7
Q

Which anticholinergic drug has greatest sedative effect?

A

scop, atropine causes slight sedation, and glyco none

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8
Q

How do anticholinergics compare with their antisisalogue effects?

A

scop>glyco>atropine

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9
Q

How do anticholinergics compare with tendency to increase hr?

A

atropine>glyco>scop

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10
Q

Can anticholinergics be given orally?

A

no bc not absorbed w enough predictability

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11
Q

How does onset of increased hr of glyco compare w that of atropine?

A

atropine increases hr w/in a min, glyco takes about 2 to 3 minutes

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12
Q

How do anticholinergics affect gastric function?

A

decreases gastric secretions, decreases peristalsis and motility, prolongs gastric emptying time, reduces LES tone

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13
Q

What is ipratropium?

A

inhaled anticholinergic. it’s a derivative of atropine that has limited systemic absorption from resp tract. Used in COPD for bronchodilation w no change in hr or IOP

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14
Q

How do anticholinergics effect gastric pH?

A

increase gastric pH and have been used in treatment of PUD. none are selective for this and large doses are required to affect gastric pH. this results in high incidence of side effects

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15
Q

Indications for transdermal scop?

A

nausea w hx of motion sickness, should be give 4 hours prior to stimulus, doesn’t have sedative, cycloplegic, or tachy side effects of parenteral

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16
Q

Besides tachycardia, what other effects do anticholinergics have on EKG?

A

shorten PR interval

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17
Q

How does effect of atropine on hr change in infants, adults, vs elderly?

A

vagal tone enhanced in young adults so increase in hr is most evident in this population, in infants and elderly even large doses of atropine may not have much effect on hr

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18
Q

What is the treatment for central anticholinergic syndrome?

A

the anticholinesterase physostigmine at 15-60 mcg/kg IV treats postop delirium too and CAS. it’s a lipid sol tertiary amine that crosses the BBB

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19
Q

Why aren’t neostigmine, edrophonium, and pyrodostigmine appropriate treatments for CAS?

A

they do not cross the BBB readily

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20
Q

What anticholinergic has been used in treatment for hiccups?

A

atropine 0.5 mg IV after LMA

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21
Q

What drugs can potentially predispose pts to CAS?

A

tricyclic antidepressants (amitriptilline), antipsycotics, and antihistamines bc they have antimuscarinic characteristics which can potentiate anticholinergics and predispose pt to CAS

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22
Q

What is central anticholinergic syndrome?

A

scop and atropine can cross BBB and block muscarinic cholinergic receptors in CNS, causing restlessness, hallucinations, somnolence, and unconsciousness

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23
Q

What is the chemical origin of barbs?

A

derived from barbituric acid which is formed from condensation of urea and malonic acid

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24
Q

What chemically defines theobarbiturates? Whats an example?

A

thiobarbs replace O2 at the 2nd carbon atom w a sulfur atom. thiopental is an example

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25
Q

What chemically defines the methylated oxybarbs? What is an example?

A

they retain the O2 at the 2nd carbon atom, but have a methyl group at the 1st carbon atom. methohexital is an ex

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26
Q

Are barbs weak acids or bases?

A

weak acids and are prepared as sodium salts

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27
Q

To which receptor do barbs bind to and exert effects and where is this receptor located?

A

GABA-A receptor found in neurons of CNS

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28
Q

What chemically defines the oxybarbs? What are some examples?

A

oxybarbs are known as true barbs and have an O2 at the 2nd carbon atom, ex are pentobarb, methohexital, secobarbital, phenobarb

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29
Q

How do barbs affect cerebral blood flow and metabolism?

A

they reduce cerebral metabolic rate and CBF by increasing cerebrovascular resistance

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30
Q

How do barbs produce an inverse steal phenomenon in the brain?

A

they produce cerebral vasoconstriction only in normal tissue resulting in preferential blood flow to ischemic areas while simultaneously reducing total CBF (Robin Hood Effect)

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31
Q

What is the pKa of thiopental?

A

7.6

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32
Q

Does thiopental provide analgesia?

A

no, low doses may produce hyperalgesia

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33
Q

Can thiopental be reconstituted with LR? Why or why not?

A

no, they must be reconstituted with sterile water or sterile saline bc even though they’re weak acids, they’re prepared w anhydrous sodium carbonate which makes the powder alkaline. if LR or any other acidic solution is used then thiopental will precipitate out of the solution

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34
Q

Can thiopental cross the placental barrier?

A

yes, it’s extremely lipid sol and can cross the BBB and placenta

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35
Q

What accounts for the short duration of action of thiopental? What part does metabolism play?

A

short duration is d/t rapid redistribution away from brain and into systemic circulation, metabolism does not play a significant role in the duration of action of a single dose of thiopental

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36
Q

Why does thiopental not undergo a significant elimination via the kidneys?

A

only 1% of thiopental is eliminated unchanged by the kidneys, primary reason is bc thiopental is 80% protein bound and protein drug complex is not easily filtered at glomerulus

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37
Q

What are the cardiac effects of an induction dose of thiopental? why does this happen?

A

produces dose dep decreases in SV, CO, and arterial BP, this is d/t increased venous capacitance and myocardial depression

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38
Q

How would pt pH affect clinical action of thiopental? why?

A

it’s an acidic compound and the more acidic a pt becomes, the more nonionized the drug becomes. therefore, more of the drug is in the lipid sol state that can cross the BBB and exert clinical effect. acidosis increases clinical effect of thiopental, alkalosis decreases the effect

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39
Q

To what degree is thiopental protein bound?

A

80%

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40
Q

How long can reconstituted thiopental sit at room temp and still be used for injection?

A

stabile and sterile at room temp for 6 days

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41
Q

What are side effects of methohexital admin?

A

spontaneous muscle movement, myoclonus, hiccoughs, seizures

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42
Q

How long is reconstituted methohexital stable?

A

6 weeks

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43
Q

How do the distribution kinetics and metabolism of thiopental and methohexital compare?

A

they’re quite similar, hepatic extraction ratio for methohexital is 3 times that of thiopental

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44
Q

Where in the brain do benzos work?

A

sedative effects work on the cortex of the brain, amnesia mediated by receptors in forebrain and hippocampus, anxiolytic exerted in amygdala, hippocampus, and limbic system

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45
Q

How do benzodiazepines exert their action on GABA receptors?

A

Specific benzodiazepine receptor sites exist on a protein complex that contains binding sites for benzodiazepines, GABA, ethanol, barbiturates, and a chloride channel. When these receptor sites are occupied by one of the drugs listed above, the GABA receptor increases the frequency of chloride channel opening which results in hyperpolarization of the postsynaptic membrane and inhibition of neuronal transmission.

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46
Q

What are the dose-dependent CNS depressant effects of benzodiazepines?

A

sedation, amnesia, hypnosis, anxiolysis, anticonvulsant in dose dep fashion

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47
Q

How do benzodiazepines affect CMRO2 and cerebral blood flow?

A

they decrease both in manner similar to propofol and thiopental

48
Q

How are benzodiazepines metabolized?

A

hepatic oxidation and glucuronide conjugation

49
Q

How is the metabolism of benzodiazepines affected by hepatic disease?

A

They undergo oxidation, which is impaired in the presence of hepatic disease.

50
Q

How do benzodiazepines affect upper airway reflexes?

A

decrease the swallowing reflex and the upper airway reflexes

51
Q

How do diazepam, lorazepam, and midazolam compare with respect to duration of action?

A

Diazepam is long-lasting with an elimination half-life of 36-50 hours, lorazepam is of intermediate duration with an elimination half-life of 10-22 hours, and midazolam is short-acting with an elimination half-life of about 2 hours

52
Q

How do the formulations of midazolam, lorazepam, and diazepam differ? How does this affect pain on injection?

A

Lorazepam and diazepam are not water soluble. They are formulated in propylene glycol which can cause pain on injection. Midazolam is water-soluble and formulated in an aqueous solution that causes minimal pain on injection

53
Q

What is the typical IV or IM premedication dose of midazolam? What is the typical PO premedication dose of midazolam?

A

IV or IM midazolam is 0.02-0.04 mg/kg; 0.4 to 0.8 mg/kg for the PO dose

54
Q

How does midazolam affect cerebral autoregulation?

A

preserves the ability of the blood vessels to vasoconstrict in response to a decrease in blood flow. Despite a decrease in cerebral perfusion pressure, the intracranial pressure would be relatively unaffected

55
Q

Can midazolam be used to prevent seizures?

A

yes

56
Q

How is the duration of action of diazepam affected by aging? Renal disease? Hepatic disease?

A

prolonged in the elderly and in patients with hepatic or renal disease and doses should be decreased

57
Q

How does diazepam affect minute ventilation?

A

decreases

58
Q

How does diazepam affect minute ventilation?

A

decreases the slope of the CO2 response curve

59
Q

What is the only benzodiazepine antagonist available in the United States?

A

flumazenil

60
Q

How does flumazenil reverse the effects of benzodiazepines?

A

It is structurally similar to the benzodiazepines, but a phenyl group is replaced with a carbonyl group which makes the drug essentially inert, but still able to bind with the benzodiazepine receptor. It acts as a competitive antagonist

61
Q

How is flumazenil metabolized?

A

rapidly metabolized in liver and excreted in urine

62
Q

What is the elimination half-life of flumazenil and what is the significance of this?

A

half-life of about 1 hour, so it is possible that re-sedation can occur with benzodiazepines that half a longer half-life than this

63
Q

How does flumazenil affect intracranial hemodynamics?

A

does not affect CMRO2 or cerebral blood flow. There is evidence that it can increase intracranial pressure when administered in head-injured patients

64
Q

What are the cardiovascular effects of flumazenil?

A

none, no stress response either

65
Q

What is the typical dose of flumazenil and how long would you expect its effects to last?

A

1-3 mg will reverse the effects of benzodiazepines for about 45-90 minutes

66
Q

You can measure the amt of oxygen carried in the blood if you have what 3 values?

A

hg level, PaO2, and O2 sat

67
Q

How do you calculate bound O2?

A

hg x 1.34 x 0.97

68
Q

Hemoglobin carries how many mL of O2 per g of hg at 100% sat?

A

1.34

69
Q

How do you calculate the amt of O2 dissolved in the blood?

A

multiply PaO2 by 0.003

70
Q

What is Bernoulli’s Principle?

A

flow of a gas or fluid through a tube increases if the diameter of the tube narrows, at same time, there is a drop in pressure in the area of the constriction

71
Q

What’s the Venturi Effect?

A

utilizes the Bernoulli principle to entrain gas into a tube, If you place an opening in the tube at the point where the diameter narrows and the pressure drops, the decreased pressure will act as a vacuum and draw in gas through the opening

72
Q

What is the Coanda Effect?

A

describes the predisposition for a fluid or gas to follow a curved path at the bifurcation point of a tube. As the cross-sectional area of the tubes increases, the velocity of the gas or fluid decreases and the pressure increases. The tube in which the pressure increases last tends to receive a greater distribution of the gas or fluid

73
Q

What is the stimulus for the bainbridge reflex?

A

atrial dilation from increased venous return (to prevent congestion in the atria and venous circulation)

74
Q

What % can the heart rate increase to accomodate increased venous return?

A

75

75
Q

What 2 factors contribute to the heart being able to increase its heart rate 75% to maintain forward flow?

A

direct effect of stretching of the sinus node and stretch receptors in atria (Bain Bridge Reflex)

76
Q

Stretch receptors in atria transmit afferent signals to?

A

medulla

77
Q

Medulla receptors to stretch receptors in atria by which fibers that increase hr and contractility?

A

vagal and sympathetic

78
Q

EBL of premi, neonate, infant, adult male, and adult female?

A

premi: 95 mL/kg, full term neonate: 85 mL/kg, infant: 80 mL/kg, adult male: 75 mL/kg; adult female: 65 mL/kg

79
Q

Where do sympathetic postganglionic neurons originate?

A

one of the peripheral sympathetic ganglia or one of the sympathetic chain ganglia

80
Q

Parasympathetic nerve fibers from cranial nerve IX innervate what gland?

A

parotid gland

81
Q

Parasympathetic fibers from cranial nerve VII serve what areas?

A

nasal, submandibular, and lacrimal glands

82
Q

Parasympathetic nerve fibers located within cranial nerve III innervate what two areas?

A

ciliary muscle of the eye and the pupillary sphincter

83
Q

Parasympathetic nerves are supplied via the vagus nerves to what areas of the body?

A

Esophagus, heart, lungs, entire small intestine, stomach, liver, gallbladder, proximal half of the colon, pancreas, upper portions of the ureters, and the kidneys

84
Q

Where do parasympathetic nerve fibers exit the central nervous system?

A

cranial nerves 3, 7, 9 and 10 and the 2nd and 3rd sacral spinal nerves.

85
Q

At what point do preganglionic sympathetic fibers exit spinal nerves?

A

Immediately following the spinal nerve’s exit from the spinal canal

86
Q

Where are the cell bodies of sympathetic preganglionic neurons found?

A

intermediolateral horn of the spinal cord

87
Q

How do sympathetic nerves differ from skeletal motor nerves?

A

Skeletal motor nerves are comprised of a single neuron, whereas sympathetic pathways are composed of two neurons which are termed a preganglionic neuron and postganglionic neuron

88
Q

Between what spinal cord segments do sympathetic nerve fibers originate?

A

T-1 and L-2

89
Q

Approximately 75% of all parasympathetic nerve fibers can be found in what cranial nerve?

A

X (vagus)

90
Q

Does the parasympathetic nervous system contain both preganglionic and postganglionic neurons? 2. How do they differ from the sympathetic pathways?

A
  1. Yes. 2. Most preganglionic parasympathetic fibers travel uninterrupted the entire way to the effector organ.
91
Q

Why does autonomic hyperreflexia occur?

A

Stimulation of the anterolateral column of the spinal cord below the level of the lesion results in an increase in sympathetic activity. Normally, these impulses are counteracted by inhibitory impulses from higher centers of the nervous system. Because of the spinal cord injury, however, the inhibitory impulses are blocked, resulting in unimpeded sympathetic outflow

92
Q

In what patient population does autonomic hyperreflexia occur?

A

patients who have experienced spinal shock and appears in conjunction with the return of spinal reflexes

93
Q

What are the hallmark cardiovascular symptoms of autonomic hyperreflexia?

A

Severe hypertension and reflex bradycardia. It may also be accompanied by blurred vision, loss of consciousness, seizures, cardiac dysrhythmias, and pulmonary edema

94
Q

What factors can trigger autonomic hyperreflexia?

A

cutaneous or visceral stimulation

95
Q

How is the incidence of autonomic hyperreflexia related to the level of the spinal cord injury?

A

About 85% of patients with an injury above T6 will suffer from autonomic hyperreflexia, but it is unlikely to occur at all in patients with a lesion below T10

96
Q

What are methods of preventing autonomic hyperreflexia?

A

prevent the triggering event from initiating the reflex by deep general anesthesia, neuraxial anesthesia, or regional anesthesia

97
Q

Will an epidural prevent autonomic hyperreflexia from occurring in a laboring parturient with a T6 injury?

A

Epidural anesthesia has been reported to be effective in preventing autonomic hyperreflexia from occurring due to uterine contractions, but, because epidurals may spare the sacral segments, spinal anesthesia is more protective

98
Q

What is the treatment for autonomic hyperreflexia if it occurs?

A

Vasodilators with a short half-life (such as sodium nitroprusside) should be available to treat the sudden onset of systemic hypertension

99
Q

During anesthesia, when is autonomic hyperreflexia most likely to occur?

A

initiation of surgical stimulation at the beginning of the case, especially if the patient is not under a deep enough anesthetic, and at the end of the case as the effects of the anesthetic are wearing off

100
Q

What symptoms may be seen in a patient who is awake and experiences autonomic hyperreflexia?

A

Severe headache and blurred vision may occur due to severe hypertension and nasal stuffiness may occur due to reflexive cutaneous vasodilation

101
Q

What is reflexive cutaneous vasodilation and how does it relate to autonomic hyperreflexia?

A

When a patient experiences autonomic hyperreflexia, a reflex dilation of the tissues ABOVE the level of the spinal cord injury will occur to help offset the sudden increase in blood pressure. Patients may experience nasal stuffiness as a result of this effect

102
Q

Define status asthmaticus

A

life-endangering bronchospasm that is unresponsive to treatment

103
Q

What are the two components to the treatment of asthma?

A
  1. Treatments that aim to “control” the airway so that acute airway narrowing is less frequent. This treatment includes theophylline, systemic and inhaled corticosteroids, and antileukotrienes. 2. Treatments that aim to “relieve” or rescue acute bronchospasm, such as beta-adrenergic agonists and anticholinergic drugs
104
Q

What are the three main characteristics of asthma?

A

reversible expiratory airflow obstruction, airway hyperreactivity, and chronic inflammation of the airways

105
Q

Describe the treatment for status asthmaticus

A

Inhaled or nebulized Beta-2 agonists are given repeatedly every 15-20 minutes, supplemental O2 is given to help maintain an oxygen saturation greater than 90%, and IV corticosteroids are administered. Due to the time it takes for corticosteroid effects to be seen, they should be initiated early in the treatment of status asthmaticus

106
Q

Name three beta-2 selective sympathomimetic agents that can be administered as inhaled aerosols

A

Metaproterenol, terbutaline, and albuterol

107
Q

How does aminophylline treat bronchospasm?

A

Aminophylline is a phosphodiesterase inhibitor that inhibits the breakdown of cyclic AMP, increases diaphragmatic contractility, and causes bronchodilation

108
Q

What is the difference between extrinsic and intrinsic asthma?

A

Intrinsic asthma is caused by factors such as placement of an endotracheal tube, inhalation of irritants, exposure to cold, and exercise. Extrinsic asthma is due to triggers that activate the immune system such as inhaling allergens that stimulate the release of IgE antibodies

109
Q

What are the two most common arterial blood gas findings in the asthmatic patient?

A

Respiratory alkalosis and hypocarbia

110
Q

The degree of expiratory airflow obstruction can be directly measured by what two pulmonary function tests?

A

The maximum mid-expiratory flow rate (FEF 25%-75%), and the forced expiratory volume in 1 second (FEV1). Patients necessitating hospitalization and treatment of asthma typically present with maximum mid-expiratory flow rates of 20% or less than normal and a FEV1 of less than 35% of normal

111
Q

What is the primary goal of the preoperative evaluation in regards to the asthmatic patient?

A

To design an anesthetic that attenuates or prevents expiratory airflow obstruction

112
Q

What undesirable effects can result from administering anticholinergic medications to an asthmatic patient?

A

Airway secretions can become more viscous, thus making their removal more difficult

113
Q

What are some treatments for intraoperative bronchospasms due to asthma?

A

Beta-2 agonist therapy, increasing the depth of anesthetic with a volatile agent, corticosteroid administration

114
Q

Why would a regional anesthetic be more desirable than a general anesthetic in an asthmatic patient undergoing surgery?

A

Manipulation of a hyperreactive airway is avoided, thus avoiding bronchoconstriction

115
Q

Reasons for deep extubation in asthmatic pt?

A

decreases the risk for bronchospasm because airway reflexes are suppressed

116
Q

What factors are associated with an increased risk for perioperative complications due to asthma?

A

Excessive production of sputum, a prior history of asthmatic complications during the perioperative peroid, continuous or frequent corticosteriod use, recent ER visit or hospitalization due to asthma, coexisting cardiovascular disease

117
Q

During induction of general anesthesia in the operating room, a patient with a history of cardiac disease exhibits what appears to be bronchospasm. What are your best treatment options in this case?

A

Selective beta-2 sympathomimetic agents such as albuterol, terbutaline, and metaproterenol would be the most appropriate choices for patients with cardiac disease because of the limited effect they would have on cardiac tissue compared to other non-selective agents

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