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Fall'20 Pharmacology III > Tocolytics > Flashcards

Tocolytics Flashcards

1
Q

Define Tocolytic Drug :

A

Any drug use to suppress premature labor

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2
Q

Most Common tocolytics

A

1) Beta agonist (Ritrodrine or Terbutaline ) but use has declined due to maternal side effects
2) Magnesium

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3
Q

Maternal (6)side effects of tocolytics: ( TRHAMM)

A
  1. Tachycardia
  2. Rarely Pulmonary edema
  3. Hyperglycemia + Hypokalemia
  4. Arrhythmia
  5. Myocardial Ischemia
  6. Mild hypotension
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4
Q

Why use caution when using ephedrine and /or Ketamine ?

A

🤰🤰

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5
Q

Premature labor is inhibited until ___________and ___________. What medication is given , and a minimum of _________hours is required.

A 
Until lung mature 
And
Sufficient surfactant is produced .
Give steroids to induce production of surfactant 
A minimum of 24- 48 hrs is required
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6
Q

When Tocolytic therapy fails , what becomes necessary

A

Anesthesia ( for delivery )

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7
Q

Terbutaline : routes, rapid route, duration of effects and MOA of that duration .

A

Routes: PO, SQ, Inhalation
Rapidly effective by SQ and Inhalation.
Effects persists 3-6 hrs partly bc its structure w/ a RESORCINOL ring preventing COMT action.
Bc of this ring , terbutaline cannot be methylated by COMT

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8
Q

When are the tocolytics Terbutaline and Ritodrine used and how is Ritodrine administered ?

A

used to manage premature labor contractions through relaxation of myometrium via their B2 effect .
Ritodrine started IV and continued PO if tocolysis is achieved

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9
Q

How is ritodrone metabolized

A

Liver
To inactive conjugated
1/2 is excreted unchanged on the urine

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10
Q

Continuous use of beta agonist prayer has been associated with:

A

hypokalemia and tachyphylaxis

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11
Q

What is the mechanism of hypokalemia in beta 2 agonists ?

A

Insulin mediated increase in uptake of extra cellular K+
or
Increased Na+/K+/ATPase activity .

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12
Q

Pulmonary edema with normal PCWP have been attributed to what medications?

A

Terbutaline and Ritodrine

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13
Q

All beta adrenergic Tocolytic drugs only have B2 receptor effects . True or False ?

A

False .

Both B1 and B2 receptor effects

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14
Q

Where are B2 receptors found ? ( PALSSS)

A 
Pancreas
Adipose Tissue 
Liver 
Smooth muscle : Uterus, blood vessels , bronchi , intestine , detrusor , spleen 
Skeletal muscle 
Salivary glands
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15
Q

B2 Smooth muscles : name organs/locations

A 
Uterus 
Blood vessels
Bronchi 
Intestine 
Detrusor 
Spleen
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16
Q

Ritrodrine and Terbutaline are relatively selective B2 and stimulation of B2 in the myometrium =

A

Relaxation of the uterine smooth muscle

Other B2 effects such as vasodilation occur as well ( can be undesired ) + some B1 effects

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17
Q

Where are Beta 1 receptors located ?

A

Predominantly: Heart and adipose tissue .

This results in increased maternal HR and CO ( can be undesired )

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18
Q

MOA Beta Adrenergic Tocolytic Drugs

A

Agonist» Beta 2 site on outer membrane of uterine myometrail cells&raquo_space;activate the enzyme adenyl Cyclase&raquo_space; adenyl cyclase catalyzes conversion of ATP to cAMP» rise in intracellular concentration of cAMP = high cAMP concentration&raquo_space;decrease in available intracellular concentration of calcium + inhibits myosin light chain kinase (MLCK)&raquo_space; inhibition of MLCK= decrease interaction between actin and myosin = myometrial relaxation

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19
Q

A delay of ____minutes often results in slowing of maternal HR after administration of Tocolytic drug . However ,______, ______and ________ often require anesthesia

A

15 minutes ;

Advanced labor , non reassuring FH status, and abnormal presentation often require anesthesia

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20
Q

Theoretically, what are the effects of epidural analgesia/anesthesia after beta adrenergic agonist when compared to spinal anesthesia ? And why ?

A

May cause less hemodynamic compromise than spinal anesthesia
Because of slowe onset of sympathetic blockade .
However this theory remains UNPROVEN

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21
Q

Aggressive hydration in patients on Tocolytic therapy . Any thought ?

A

Avoid aggressive hydration before and during induction of anesthesia in these patients
Due to :
Risk of pulmonary edema

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22
Q

GA is required in a patient who has recently received beta-adrenergic tocolysis , what agents will you avoid in order to prevent exacerbation of maternal tachycardia

A

Atropine
Glycopyrrolate
Pancuronium

  • Maternal tachycardia may make it difficult to asses volume status and depth of anesthesia
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23
Q

Why is it a bad idea to use Halothane on patients on tocolysis ?

A

Because halothane sensitizes the myocardium to catecholamine-induced-arrhythmias

It should not be used

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24
Q

Why should hyperventilation avoided ?

A

It will exacerbate the hypokalemia = hyperpolarization of the cell membrane will be potentiated

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25
Q

A study found what effects of terbutaline pretreatment in non-pregnant patients on Succs neuromuscular blockage ?

A

The terbutaline pretreatment shortened BOTH onset time and recovery time of succs- induced-NMB. Therefore :
May be pro dent to use a nerve stimulator during GA

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26
Q

What are the MOA of Magnesium :

A
  1. Extra cellular Mag = competitive antagonist of calcium either at the motor end plate or cell membrane» reducing calcium influx into the myocyte .
  2. Competes with Ca++ for low affinity calcium-binding sites on outside of the sarcoplasmic reticulum and prevents the rise in free intracellular calcium concentration.
    To sum it up :
  3. Reduce calcium influx into the myocyte
  4. Prevent rise in free intracellular calcium concentration
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27
Q

Hypermagnesemia result in

A

1) Abnormal neuromuscular function

2) Decrease the release of acetylcholine at the NMJ + decrease the sensitivity of the end plate to acetylcholine

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28
Q

True or False . Per studies , Mag Sulfate results more frequent and more severe CV side effects than beta adrenergic tocolytic agents

A

No !

Mag Sulfate = less severe and less frequent CV side effects than Tocolytic

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29
Q

Magnesium can have similar effects of beta adrenergic tocolytic agents .what side effects have been reported ?

A
  1. Chest Pain And Tightness
  2. Palpitations
  3. Nausea
  4. Transient hypotension
  5. Blurred vision
  6. Sedation
  7. Pulmonary edema
  8. May lessen normal compensatory responses to hemorrhage in the mother AND fetus
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30
Q

How is Magnesium is eliminated

A

Almost entirely by renal excretion

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31
Q

Do you give Mag in patients with abnormal renal function ?

A

Monitor carefully if they receive Mag sulfate

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32
Q

Should you D/C magnesium before administering an epidural ? Why or why not ?

A

Yes, D/C it because Mag will increased the likehood of hypotension through its generalized vasodilation properties

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33
Q

This electrolyte potentiates the action of both depolarizing and non-depolarizing muscle relaxants

A

Magnesium

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34
Q

In hypermagnesemic women, what should not be given prior to administration of Succinylcholine?

A

A defasiculating dose of NDMB

-a standard dose of muscle relaxant (ie Succ 1mg/kg) should be used b/c the extent of potentiation by mag sulfate is variable

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35
Q

During the maintenance of anesthesia, in a hypermagnesemic woman, how would you adjust muscle relaxant?

A

Lower doses

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36
Q

Parturients receiving mag sulfate often appear

A

Sedated

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37
Q

It is recommended that severely pre-eclampsia woman undergoing c/s should receive mag sulfate on what scheduling?

A
  • at least 2 hours BEFORE procedure
  • during surgery
  • 12 hours postpartum
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38
Q

Treatment for mag toxicity

A
  • immediate d/c of infusion

- IV admin of calcium gluconate 1gm over 10mins

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39
Q

Primary anesthetic considerations for women receiving magnesium sulfate are: (3)

A
  1. Interaction with NDMDs
  2. Effects on uterine tone
  3. Interaction with calcium entry -blocking agents
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40
Q

Magnesium sulfate increases the potency and duration of:

A

Mevacurium
Rocuronium
Vecuronium

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41
Q

Why do many practitioners avoid use of depolarizing drugs in parturient?

A

Concern for residual post op NMB — which can lead to respiratory complications

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42
Q

Why is NMB rarely required to facilitate surgical closure after c/s?

A

Abdominal wall distention in the term parturient

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43
Q

What patient populations are at a greater risk for awareness?

A
  • emergent c/s

- CABG

44
Q

This drug stimulates uterine muscle and is administered to induce labor, reduce/prevent uterine atony, and decrease hemorrhage in the postpartum period

A

Oxytocin

45
Q

Oxytocin preparations are all naturally occurring or synthetic?

Potency is measured in?

A

Synthetic

Potency described in units

46
Q

The synthetic preparations of oxytocin are identical to the hormone normally released from the ______ ______ but devoid of contamination by other ________ _______ & ______ found in natural proteins.

A

Posterior pituitary

Contamination by other polypeptide hormones and proteins found in natural proteins

47
Q

The sensitivity of the uterus to oxytocin increases as

A

Pregnancy progresses

48
Q

Oxytocin for the induction of labor:

A

Dilute solution of 10mU/mL

Continuous gtt beginning at 1-2mU/min. Increased 1-2mU q 15-30mins until optimal response of uterine contraction q 2-3 mins

49
Q

Average dose of oxytocin to induce labor is?

A

8-10mU/min

Gtt up to 40mU/min may be necessary to tx uterine atony after delivery.

50
Q

High and bolus doses of oxytocin are more likely to decrease ?

Via what MOA?

A

Decrease SBP and DBP

-via direct relaxant effect on vascular smooth muscles

51
Q

With high dose oxytocin, what also accompanies the transient decrease in SBP?

A

Reflex tachycardia and

Increased CO

52
Q

Hypotension after oxytocin administration is likely due to patients with: (2)

A
  1. Blunted compensatory reflex responses (may be produced by anesthesia)

Or

  1. Hypovolemia **
    HD effects of second dose of oxytocin are diminished compared to initial dose
53
Q

Hemabate: carboprost tromethamine

IM administration stimulates

A

Gravid uterus myometrial contractions similar to labor at end of full term pregnancy.

Evacuates products of conception from the uterus in most cases.

54
Q

Hemabate also stimulates the smooth muscle of?

Produces?

A

The GIT.

Produces vomiting and diarrhea or both.

55
Q

Contraindications for Hemabate administration?

A
  1. Hypersensitivity (anaphylaxis / angioedema)
  2. Acute PID
  3. Active cardiac, pulmonary, renal or hepatic disease
56
Q

Hemabate adverse reactions at completion of therapy:

A

Transient and reversible

57
Q

Most adverse reactions to hemabate are related to its

A

Contractile effect on smooth muscle

58
Q

in studies, patients who had Hemabate, approx:

2/3 experienced this reaction:
1/3 experienced:
1/8th had:
1/14th experienced:

A

2/3 experienced this reaction: VOMITING & DIARRHEA
1/3 experienced: NAUSEA
1/8th had: TEMP INCREASE GREATER THAN 2DEGREES F
1/14th experienced:FLUSHING

59
Q

Although rare, what are additional adverse reactions to hemabate?

A
  1. Vaso-vagal syndrome
  2. Faintness; light headed ness
  3. Pulmonary edema
  4. Endometritis from IUCD
  5. Uterine rupture
60
Q

Hemabate dose:

A

250mcg/ml

Deep IM

61
Q

Total dose of hemabate should not exceed:

A

2 mg’s (8 doses!)

250mcg x 8 = 2000mcg (/1000 = 2mg)

62
Q

Hemabate must be refrigerated at

A

2 - 8 degrees Celsius

36-46*F

63
Q

Methergine is a semi-synthetic ergot alkaloid used for the prevention and control of postpartum hemorrhage.

It’s available in what supply?
How may it be admin?

A
  1. 2mg/ml for IM or IV

0. 2mg tablets for PO

64
Q

Methergine acts directly on

A

Smooth muscle of the uterus

65
Q

Methergine effect on contractions?

A

Increases the tone, rate, and amplitude of rhythmic contractions

66
Q

Methergine induces a rapid and sustained titanic uterotonic effect which shortens which stage of labor and reduces ___?

A

The third stage of labor

And reduces blood loss

67
Q

Methergine onset:
IV:
IM:
PO:

A

IV : immediate
IM: 2-5 mins
PO: 5-10mins

68
Q

Pharmacokinetics of IV methergine show rapid distribution from plasma to peripheral tissues within

A

2-3 mins or less

69
Q

Methergine bioavailability after oral admin:

A

About 60%

No accumulation after repeat doses

70
Q

Methergine IM bioavailability

A

Increased to 78%

71
Q

Ergot alkaloids are mostly eliminated how?

The decreased bioavailability of PO admin is a result of?

A

Hepatic metabolism and excretion

First pass metabolism in the liver

72
Q

Methergine indication and usage following delivery of the placent, routine mgmt of uterine atony, hemorrhage and subinvolution fo the uterus,

And for control of uterine hemorrhage in the second stage of labor follow the delivery of:

A

The ANTERIOR shoulder

73
Q

Contraindications for methergine

A

HTN
Toxemia
Pregnancy
Hypersensitivity

74
Q

Methergine should not be administered IV routine b/c of

A

Sudden HTN and CVA

75
Q

If methergine is administered IV as an essential lifesaving measure, how should it be administered?

What else should be done?

A

Slowly over a minimum of 60seconds

With careful BP monitoring

76
Q

Methergine administration should be exercised with caution in the presence of

A

Hepatic or renal impairment

77
Q

Is intra-arterial or periarterial injection of methergine okay?

A

No. It should be avoided

78
Q

Patient with CAD or RF for CAD may be more susceptible to developing this with methylergonovine-induced vasospasm

A

Myocardial ischemia/infarction

79
Q

Inadvertent administration of what medication to newborn infants has occurred?

What s/s are seen as a result?

A

Methergine

S/S: respiratory depression, convulsions, cyanosis, oliguria

TX is symptomatic

Resp and CV support required in severe cases

80
Q

Caution should be exercised with methergine and concurrent use of

A

Beta blockers

81
Q

Concomitant admin of methergine and beta blockers may result in what?

A

Exchange the vasoconstrictive action of ergot alkaloids

82
Q

Most common adverse reaction to Methergine

A

HTN

Some w/seizure and/or HA.

*hypotension has been reported

83
Q

Dosing and indication for Methergine

A

IM 0.2mg/ml - after delivery of the anterior shoulder, after delivery of the placenta, or during the puerperium

May be repeated as required at intervals of 2-4hr

84
Q

IV dosing of methergine

A

0.2mg/ml slowly over a period of no less than 60s

85
Q

PO dose of methergine

A

0.2mg tablet 3-4 x day in puerperium for max of 1 wk

86
Q

IV contrast medium reactions can be divided into:

A

Renal or general and the subdivided into acute and delayed

87
Q

Contrast media induced renal impairment can be reducded with the use of

A

Low osmolarity contrast media and extracellular gold expansion

88
Q

What can IV contrast medium do if extravasates from vein?

A

Local tissue sloughing and necrosis

89
Q

ICM is typically a water soluble , iodine containing solution of two available types:

A
  1. Media that can dissociate into ions in solution

2. Media that will remain in a neutral state in solution

90
Q

ICM is also formulated as high osmolarity contrast media (HOCM) which contains few dissolved particles and iodine atoms

and low osmolarity contrast media (LOCM) contains greater number of dissolved particle with iodine.

  1. HOCM causes fluid to shift from:
  2. LOCM induces
A
  1. HOCM - fluid shift from cell to the vein

2. LOCM induces less fluid shift from the cell ; it’s closely iso-osmolar

91
Q

Reactions with ICM. occur with LOCM or HOCM? Most? Least?

A

Possible with either ICM.

Fewer with LOCM.

92
Q

Some ICM reactions can occur how long after administration?

A

A half hour to a week after admin

93
Q

ICM reaction theory is:

A

ICM molecules serve as an antigen and affix itself to either mast cells or basophils.

Release histamine mediators
Inhibit coagulation
Dilate vessels 
Release complement
Or stimulate IgE reaction
94
Q

ICM can stimulate what type of modulated immune reaction?

A

IgE

95
Q

What is a new ICM undergoing testing?

Advantages over ICM: higher radiation absorption, yielding better images w/lower XR dose, lower allergic responses, longer imaging times

A

Gold nanoparticles

96
Q

Preanesthetic assessment for a pt undergoing CT should include questions re:

A

Asthma
Allergies
Previous reactions to contrast media

97
Q

What medication must be withheld b/c of risk of lactic acidosis observed in pts w/diabetic nephropathy?

A

Metformin

98
Q

Patients with multiple medical problems (esp cardiac dx), preexisting azotemia, advanced age, being tx with nephrotoxic agents (aminoglycoside antimicrobials, gentamicin, tobramycin, streptomycin, amikcyin, kanamycin, and neomycin), NSAIDs

Are at risk for reactions to

A

IV contrast media

99
Q

IV contrast media in pregnancy

A

Is contraindicated

100
Q

Prevention of CM reactions can be taken by doing these interventions:

A
  1. Use smallest amount of contrast needed.
  2. Hyrdate to safeguard against renal failure (1hr before and 24hr after)
  3. Pretreat if at risk for anaphylactic
  4. Those with moderate or severe previous ICM reactions tx with Histamine blocker (diphenhydramine) and H2 blocker (cimetidine/ranitidine) IV or PO
101
Q

Pretreatment for ICM anaphylactic reactions:

A

Corticosteroids such as methylprednisolone or prednisone PO or IV

102
Q

The most frequent cause of anaphylactic reactions

A

ICM

103
Q

ICM anaphylactoid reactions can be initiated with what amount of contrast medium?

A

As little as 1ml of contrast

104
Q

Fluorescein and its metabolites are eliminated how?

A

Via renal elimination

105
Q

Important educational component for patients who receive Fluroescein contrast agent?

A

The urine remains slightly fluorescent for 24-36hrs.

106
Q

General caution is exercised in patient with a hx of allergy or bronchial asthma with the use of Fluorescite 10% injection to include:

A

An emergency tray should be available in the event of possible reaction

107
Q

Indications and usage for Fluorescite injection 10%?

A

Diagnostic angiography/angioscopy of retina and iris vasculature

Fall'20 Pharmacology III (14 decks)

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