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med surg pharm 1 > exam 1 > Flashcards

exam 1 Flashcards

1
Q 
Respiratory depression
GI: nausea and vomiting, constipation
CNS: dizziness, psychoses, anxiety, hallucinations, sedation
GU: ureteral spasm, urinary retention
Sweating and dependence less likely
A

narcotic agonists antagonist side effects

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2
Q

Strongly binds to opioid receptors, mu, kappa, sigma, but does not activate them

greatest affinity for mu

Blocks the effect of opioids in the system
utilized for overdose treatment

A

narcotic antagonist action

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3
Q

Ergot Derivative

sublingual
combined with caffeine in Cafergot for increased absorption from GI tract

A

ergotamine

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4
Q

Rapidly absorbed from many sites
Metabolized by the liver and excreted through the urine

(nasal spray, oral, subq)

A

triptans pharm

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5
Q 
Hemorrhage
Shock
Burns
Acute liver failure
Neonatal hemolytic disease

Use may be limited due to cost

A

colloids use

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6
Q

butorphanol (stadol)

A

narcotic agonist antagonist

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7
Q

Mainstay of treatment before development of triptans

Block/Bind alpha-adrenergic and serotonin-receptors in the brain, which causes vasoconstriction of the cranial vessels (decreased cranial artery pulsation, decrease in hyperperfusion of the basilar artery bed)

Can prevent or abort a migraine

A

ergot derivatives actions

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8
Q

0.9 nacl

A

isotonic crystalloid solution

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9
Q

3 and 5 nacl

A

hypertonic solution

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10
Q

Plasma and coagulation factors

Frozen immediately after donation and thawed before use

  • can be stored for up to a year
  • once thawed, it’s good for 24 hours

Used for bleeding caused by coagulation factor deficiency and plasmapheresis
-not used for simple volume expansion

Needs to be typed but not crossmatched

Infuse as fast as tolerated, must be within 4 hours

A

fresh frozen plasma

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11
Q

A sensory and emotional experience associated with actual or potential tissue damage

A

pain

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12
Q

small, myelinated (insulation-outside coating- for the nerves), respond quickly to pain

A

a delta fibers

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13
Q

small, unmyelinated, slow conducting (contribute to chronic pain)

1) Pain impulses are conducted through these fibers to the dorsal horn of the spinal cord
2) They are then transmitted to the brain

A

c fibers

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14
Q

large-diameter sensory nerves that enter the dorsal horn of the spinal cord

  • Do not transmit pain impulses, instead transmit touch and temperature
  • Conduct impulses more rapidly than small fibers
  • Can block smaller fibers from transmitting their signals
A

a fibers

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15
Q

The transmission of impulses can be modulated or adjusted all along the spinal cord

Interneurons act as “gates” by blocking ascending transmissions of pain

The “gate” can be closed by:

  • stimulation of the A fibers*
  • descending impulses from the cerebral cortex, limbic system and reticular activating system
  • Learned experiences, cultural expectations, individual tolerance, and placebo effect can activate descending inhibitory nerves from the upper CNS
  • Many strategies need to be considered along with medication
A

gate control theroy

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16
Q

Receptor sites that respond to naturally occurring endorphins and enkephalins (enkephalins substance that regulates substance P–makes pain signals more intense and promotes inflammation)

Found in CNS, on nerves in periphery, on cells in GI tract

Help to control blood pressure, pupil size, GI secretions, chemoreceptor trigger zone (CTZ) –(has to do with nausea, respirations), pain

A

opioid recptors

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17
Q

Endorphins are released during stress to block the sensation of pain

In the limbic system (memories and emotions), receptors incorporate an emotional response to pain

Pain is subjective and can be assessed through many methods

A pain management plan should include nonpharmacological treatments

A

pain response

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18
Q 
pain-blocking
respiratory depression
euphoria
decreased GI activity
pupil constriction
physical dependence
A

mu pain receptors

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19
Q

some analgesia
pupil constriction
sedation
dysphoria

A

kappa pain recptors

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20
Q

react with enkephalins

A

beta pain receptor

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21
Q

pupil dilation
hallucinations
dysphoria
psychoses

A

sigma pain receptor

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22
Q

React with opioid receptors throughout the body to cause analgesia, sedation, and euphoria

A

narcotic agonist action

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23
Q

IV administration is most reliable, IM and subq have varying rates of absorption

Metabolized by the liver and excreted through bile and urine

Cross the placenta and enter breast milk

A

narcotic agonist pharm

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24
Q 
Respiratory depression, cardiac arrest
Orthostatic hypotension
GI: nausea and vomiting, constipation
CNS: dizziness, psychoses, anxiety, pupil constriction, sedation (addiction)
GU: urinary retention, ureteral spasm
Sweating and dependence
A

narcotic agonist s/e

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25
Q 
Head injury, increased ICP
Alcoholism 
Respiratory dysfunction
After GI or GU surgery
Diarrhea caused by toxic poisons
Liver or renal dysfunction
Most are pregnancy category C, oxycodone is drug of choice because category B
A

narcotic agonist contraindications

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26
Q

Monitor clients for respiratory compromise with multiple CNS depressants

Rare instances of serotonin syndrome have occurred when combined with SSRIs, SNRIs, MAOIs, TCAs, and most triptans (agitation, confusion, sweating, fever, muscle rigidity, diarrhea, headache)

A

narcotic agonist interactions

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27
Q

Perform pain assessments on a regular basis
Provide medications before pain is severe
Monitor bowel movements and treat constipation proactively
Utilize non pharmacological methods
Monitor respiratory status and LOC before administering
Reassure risk of addiction is minimal when used correctly
Monitor units of measurement

A

narcotic agonist n/c

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28
Q

Narcotic Agonist

works primarily on mu receptors
rapid onset, peak in 20-90 minutes
can be used for acute or chronic pain
slow IV push, may dilute to ease titration (1mg per minute)..

A

morphine

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29
Q

narcotic agonist

moderate pain

A

hydrocodone

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30
Q

narcotic agonists

moderate to severe pain

A

oxycodone

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31
Q

narcotic agonist

moderate to severe pain

A

hydromorphone

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32
Q

narcotic agonist

for most severe pain

A

fentanyl

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33
Q

Act at specific opioid receptor sites to produce analgesia, sedation, euphoria, hallucinations

Block opioid receptors that may be stimulated by other narcotics

Three functions:
relief of moderate to severe pain
adjunct to general anesthesia
relief of pain during labor and delivery

A

narcotic agonist antagonist action

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34
Q

Readily absorbed after IM administration

Reach peak levels rapidly when given IV

Metabolized by the liver, excreted in urine and bile

A

narcotic agonist antagonist pharm

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35
Q

Use caution with physical dependence on narcotics (Withdrawal)

Respiratory dysfunction

Renal or hepatic dysfunction

Care with MI or CAD due to cardiac stimulation

A

narcotic agonist antagonist contraindications

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36
Q

Monitor for respiratory depression with multiple CNS depressants
Pentazocine combined with tripelennamine (old form of antihistamine) produces hallucinations and euphoria similar to heroin (Ts and Blues)

A

narcotic agonist antagonist interactions

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37
Q

Narcotic Agonist-Antagonist

relief of moderate to severe pain
anesthesia adjunct
has an oral form
rapid onset when given IV

A

pentazocine (talwin)

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38
Q

buprenophrine (buprenex)

A

Narcotic Agonist-Antagonist

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39
Q 
Usually due to blocking of opioid receptors
nausea and vomiting
sweating
tachycardia
hypertension
tremors
anxiety
A naloxone challenge will help avoid acute reactions
A

narcotic antagonist s/e

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40
Q 
Can be administered:
subcutaneously
IM
IV
orally
nasal spray
Metabolized by the liver and excreted in the urine
A

narcotic antagonists pharm

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41
Q

Pregnancy and lactation: category C, limited human data, will cause fetal withdrawal

Narcotic addiction: withdrawal syndrome

Cardiovascular disease: could exacerbate symptoms due reversal of depressive effects

A

narcotic antagonists contraindications

42
Q

May need larger dose to reverse narcotic agonists-antagonists

A

narcotic antagonist interactions

43
Q

Open airway, ventilate with ambu bag, administer vasopressors as needed

Provide comfort measures to assist with withdrawal

Those receiving naltrexone should be narcotic-free for 7-10 days to avoid acute withdrawal

Monitor for response, may need additional dosing

Usually supplied as 0.4mg/ml, give 0.4-2mg IV q 2-3 minutes, max dose 10mg

consider other causes of resp. depression if doses do not work

A

narcotic antagonist n/c

44
Q

Several syndromes which cause severe, throbbing headaches on one side of the head

May or may not have an aura

Signs and symptoms:
pulsating pain
nausea and vomiting
sensitivity to light and sound

Cause:

  • Thought to be due to arterial dilation, Cause of dilation not well understood
  • bradykinins
  • serotonin
  • other hormones or chemicals

Those with an aura are associated with hypoperfusion of the brain during the aura with reflex arterial dilation

A

migraine headaches

45
Q

Rapidly absorbed through many routes

Ergotamine (sublingual
combined with caffeine in Cafergot for increased absorption from GI tract)

Dihydroergotamine (nasal spray, IM, IV
drug of choice if oral is not tolerable, Onset of action 15 - 30 minutes)

A

ergot derivatives pharm

46
Q

Related to vascular constriction

CNS: numbness, tingling, muscle pain
Stimulates the CTZ - nausea, vomiting, GI upset, diarrhea

CV: pulselessness, chest pain, arrhythmias, MI

Drug dependency with prolonged use, withdrawal syndrome

may need hospitalization for safe withdrawal

A

erot derivatives s/e

47
Q

peripheral vascular disease

CAD
Impaired liver function

Pregnancy and lactation
uterotonic activity
inhibit prolactin

Pruritus could become worse

Monitor for malnutrition

CTZ stimulation

A

ergot derivatives contrain

48
Q

Care with beta-blockers due to increased risk of peripheral ischemia and gangrene

A

ergot derivatives interactions

49
Q

Ergot Derivative

nasal spray, IM, IV
drug of choice if oral is not tolerable
Onset of action 15 - 30 minutes

A

dihydroergotamine

50
Q

Bind to selective serotonin receptors, which causes vasoconstriction of cranial vessels and reduced inflammation

Used for the treatment of acute migraines, not prevention

Clients can have poor response to one triptan and respond well to another

Benefit is fewer side effects

A

triptans action

51
Q

Related to vascular constriction
CNS: numbness, tingling, burning, dizziness
GI: dysphagia, abdominal pain
CV: blood pressure alterations, chest pressure and tightness
Almotriptan has fewer side effects than others

A

triptans s/e

52
Q

As a class triptans are contraindicated during pregnancy and breastfeeding
human data is scarce
sumatriptan is generally considered safe
do the benefits outweigh the risks?

Renal and hepatic dysfunction

CAD

A

triptans contrain

53
Q

Combining triptans and ergot drugs results in risk of prolonged vasoactive reactions

Do not use within two weeks of an MAOI due to increased vasoconstrictive effects
MAO enzyme also breaks down some triptans
Almotriptan, Rizatriptan, Sumatriptan, Zolmitriptan

Care must be taken when combining with SSRIs and SNRIs due to rare risk of serotonin syndrome

A

triptans interactions

54
Q

Administer at first sign of migraine, don’t wait until severe
Provide comfort, including non-pharmocological therapies
Monitor for vasoconstrictive effects
Safe use for children has not been established
Monitor older adults closely due to chronic disease

A

triptans n/c

55
Q

Triptan

nasal spray, oral, subcutaneous
subcutaneous pen has rapid onset
oral onset 1 -1.5 hours
wait 2 hours between doses

A

sumatriptan (imitrex)

56
Q

zolmitriptan (zomid)

A

triptan

57
Q

measure of the number of dissolved particles in 1 L of water

sodium is greatest contributor
glucose and urea

normal osmolality is 275-295 nOsm/kg (300)

A

osmolality

58
Q

ability of a solution to cause a change inwater movement across a membrane due to osmotic forces

relative concentration of IV fluids
isotonic, hypertonic, hypotonic

A

tonicity

59
Q

Travel between compartments though a semipermeable membrane

Intracellular fluid - two thirds of total body water

Extracellular fluid - one third of total body water
plasma

interstitial space

There is a continuous exchange, turnover, and mixing of fluids between compartments

A

body fluids

60
Q

most important mechanism for regulation is thirst

  • hypothalamus senses the ECF is hypertonic
  • saliva decreases, leads to dry mouth, person drinks

hypothalamus directs pituitary to release ADH
-acts on kidneys to increase water reabsorption

intake average- 2500ml of fluid per day
output- kidneys, lungs, skin, feces, sweat

RAAS (rennin, aldosterone)

  • aldosterone is secreted by the adrenal glands
  • aldosterone causes kidneys to retain sodium and water
A

fluid regulation

61
Q

imbalance disorder

  • dehydration and shock
  • treated with oral and/or IV fluids
A

fluid deficit

62
Q

imbalance disorder

-treated with diuretics

A

fluid excess

63
Q

to diagnose and correct the underlying cause

-administer supporting fluids and medications to stabilize the client

A

imbalance disorders goal

64
Q

IV solutions that contain electrolytes and other agents in concentrations that closely mimic the body’s extracellular fluid

Capable of quickly diffusing across membranes, leaving the plasma, and entering interstitial fluid and ICF

Sodium is most common electrolyte, dextrose is another common additive

Isotonic
Hypotonic
Hypertonic

A

crystalloids

65
Q

Same osmolality as plasma

Expand the circulating intravenous volume, without causing major fluid shifts between compartments

Used to treat fluid loss due to vomiting, diarrhea, or surgical procedures
will help to raise the BP

Also used to treat mild hyponatremia

Care must be taken because they can cause fluid overload
increased BP, crackles, edema, dyspnea

0.9% NaCl, LR, 5% dextrose in water (D5W)*

A

isotonic solutions

66
Q

isotonic crystalloid solution

Isotonic fluid that contains sodium, chloride, potassium, and calcium

Also contains lactate which is metabolized into sodium bicarbonate by the liver

can help with metabolic acidosis

Used for fluid resuscitation following:

  • hemorrhage
  • surgery
  • burns
A

lactated ringers

67
Q

isotonic crystalloid solution*

quickly metabolized

left as hypotonic solution

A

D5W

68
Q

Raises the osmolality of the plasma and expands plasma volume by drawing water away from cells and tissues

Used to relieve cellular edema, especially cerebral edema

Overtreatment with hypertonic solutions can lead to excessive expansion of intravascular compartment

3% NaCl, 5% NaCl, 5% dextrose in normal saline (D5NS)

Infusions of 3% NaCl or greater should have the serum sodium, chloride, and bicarbonate checked after the first 100ml

A

hypertonic solutions

69
Q

hypertonic solution*

dextrose metabolized, leaving normal saline

left as isotonic (clinical effect)

A

D5NS

70
Q

Dextrose added to any solution will increase the osmolality

added as a source of calories

1L of 5% dextrose supplies 170 calories

It is quickly metabolized leaving you with the underlying fluid

D5W is isotonic but quickly becomes hypotonic after infusion

D5NS is hypertonic but clinical effects are isotonic

Water is formed during dextrose metabolism, enhancing rehydration

D5W is often used to reconstitute medications

A

dextrose

71
Q

Lower the serum osmolality, causes water to move out of the plasma and into the tissues and cells

Used for those with hypernatremia or cellular dehydration

Overtreatment with hypotonic solutions can lead to depletion of the intravascular compartment with resulting hypotension and peripheral edema

Dehydration with normal BP = hypotonic solution

Dehydration with low BP = isotonic solution

0.45% NaCl

A

hypotonic solution

72
Q

0.45 nacl

A

hypotonic solution

73
Q

Intravenous solutions containing large molecules that remain in the blood

proteins, starches, other large molecules

too large to cross the capillary membrane

Draw water from the cells and tissues into the plasma through osmotic pressure

often called plasma volume expanders

1) Blood product colloids:
albumin*, plasma protein fraction, serum globulins

2) Synthetic colloids:
dextran*, hetastarch

A

colloids

74
Q

Protein extracted from whole blood or plasma
*classified as both a colloid and blood product

Maintains osmotic pressure and binds substances for transport such as medications, hormones, enzymes

helps to maintain CO

also administered for hypoproteinemia

Allergic reactions are possible due to donor antibodies (extremely rare; fever, chills, dyspnea, rash, urticaria)

Some may refuse due to religious preferences

Monitor vitals and watch for signs of fluid overload

A

albumin

75
Q

Can double the plasma volume in a matter of minutes

effects last approximately 12 hours

Effects:

  • increased BP, CO, SV, and urine output
  • HR and blood viscosity decrease

Also reduces platelet adhesiveness, and improves blood flow through capillaries

Monitor vitals continuously during administration to prevent hypertension

Use cautiously in those with renal failure

A

dextran

76
Q

RBCs with little plasma, some platelets, and WBCs

  • platelets and WBCs not functional
  • may cause allergic reaction

Used to increase serum hemoglobin level

  • 1 unit increases hgb by 1g/dL and hct by 3%
  • transfusion usually occurs with a hgb <7g/dL

Stored in refrigeration for up to 42 days

Type and crossmatch required

Only infuse with 0.9% NaCl

Infuse as fast as tolerated, must be within 4 hours

A

prbc

77
Q

Concentrate prepared from FFP
-Factor VIII, von Willebrand factor, fibrinogen, fibronectin, Factor XIII

Frozen immediately after donation and thawed before use
-once thawed, it’s good for 6 hours

Used in the treatment of DIC, uremic bleeding, abruptio placentae, cardiothoracic surgery

Preferably ABO of recipient

Infuse as fast as tolerated, must be within 4 hours

A

cryoprecipitate

78
Q

Platelets, plasma, few RBCs and WBCs

Used to prevent bleeding

  • 1 unit increases the platelet count by 10,000/mm3
  • often pooled as 6 units
  • transfusion usually occurs with plt <10,000/mm3

Stored at room temperature for 5 days
agitated while stored to prevent clumping

Preferably ABO of recipient due to reduced cell survival when not typed, no crossmatch

Most likely to have bacterial contamination

A

platelets

79
Q

Crystalloids:

  • 0.9% NaCl - best for brain injuries
  • LR - can help with acidosis
  • hemodilution concern

O negative PRBCs:

  • 1 to 2 units
  • move to type specific when type and crossmatch done

Colloids:

  • no major advantage over crystalloids
  • can affect coagulation
  • expensive

FFP & Platelets:

  • minimize coagulopathy
  • 1 FFP for every 2 units blood
A

best fluid for hemorrhage

80
Q

Major electrolyte in extracellular fluid

Important link between water retention, blood volume, and blood pressure

NaCl is administered for hyponatremia, <130 mEq/L

  • 0.9% or 3%
  • oral available

Monitor for hypernatremia
-lethargy, confusion, tremor, hypotension

Monitor for pulmonary edema, especially with 3% NaCl

Diuretics will reduce peripheral and pulmonary edema

A

sodium

81
Q

Major electrolyte in the intracellular fluid

Plays a critical role in muscular contraction and conduction of nerve impulses

KCl is administered to treat/prevent hypokalemia

  • oral - tastes bad
  • IV - slow infusion, never push

Monitor for hyperkalemia
-dysrhythmias, heart block, twitching, fatigue, diarrhea

Overdose
-Dextrose with insulin, polystyrene sulfonate, Lasix, calcium chloride, sodium bicarbonate

A

potassium

82
Q

Posture, balance, and movement are regulated by the spinal motor neurons

These neurons are influenced by higher-level brain activity:
cerebellum - conscious muscle movement
basal ganglia - unconscious muscle movement

Injuries result in local damage to either muscle or tendons

pain and muscle spasm

Damage to CNS neurons can cause sustained muscle contractions or spasticity

Skeletal muscle relaxants can treat temporary or permanent damage

A

regulation of nerves and movement

83
Q

the result of injury to the musculoseketal system (can be fixed)

overstretching a muscle, wrenching a joint, tearing a tendon or ligament

A flood of sensory impulses come into the spinal cord, are passed through interneurons to spinal motor nerves, causing contraction

Contraction cuts off blood flow to muscle fibers, increasing lactic acid which causes pain

A

spasm

84
Q

is the result of damage to neurons within the CNS (permanent)

Results from an increase in excitatory influences or a decrease in inhibitory influences within the CNS

exact presentation is dependent on location of damage

A

spasticity

85
Q 
Heat or cold therapy
Hydrotherapy
Therapeutic ultrasound
Physical thearpy
Manipulation
Massage
Topical herbal remedies - capsaicin, caster oil, menthol
A

non pharm treatment of muscle spasticity

86
Q

NSAIDS & Tylenol

skeletal muscle relaxants should be an alternative treatment option
Research shows skeletal muscle relaxants are not more effective than NSAIDs in patients with acute back pain

A

first line treatment for muscle spasticity

87
Q

Exact mechanism of action is unclear but it is thought they involve action in the upper or spinal interneurons

sedation?

all are CNS depressants

Can be used alone or with other medications such as analgesics

A

centrally acting skeletal muscle relaxants mechanism of action

88
Q

Centrally Acting Skeletal Muscle Relaxant

Structurally similar to GABA (neurotransmitter)– primary neuro inhibit transmitter– calming down

Used for spinal cord injuries or disease (long term treatment, permanent injuries)

MS, cerebral palsy, ALS, trauma (spinal cord injury)

PO or intrathecal pump
pump allows for decreased dosing
PO: start at 5mg 3x per day and slowly increase (due to side effects), max of 80mg/day
IT: several test doses first, dosing highly individualized, 100-800mcg/day

A

baclofen (lioreseal)

89
Q

Centrally Acting Skeletal Muscle Relaxant

Acute management (hurt back carrying something)

max of 3 weeks (2-3 weeks, no longer). no added benefit of having long term. Flexeril is a short term management

Structurally similar to TCAs (no antidepressant effects except for sedation)

should not be used with heart conditions

Has anticholinergic properties
constipation, urinary retention, drowsiness, dry mouth

Can cause physical dependence with long-term use

Usually 5-10mg 3x per day, also available in an ER form

A

cyclobenzaprine (flexeril)

90
Q

Centrally Acting Skeletal Muscle Relaxant
Benzodiazapine

advantageous when anxiety precipitates spasm
2-10mg 3x per day, max 30mg/day

A

diazepam (valium)

91
Q

Centrally Acting Skeletal Muscle Relaxant
Alpha2-adrenergic agonist (inhibit motor neurons at the spinal cord level)

short acting* (Similar to baclofen but is short acting, baclofen is longer acting)

can be used for chronic conditions (MS, spinal cord injuries, etc.)

2-4mg 3x per day, max 36mg/day

A

tizanidine (zanaflex)

92
Q 
Contraindicated when spasticity contributes to locomotion, upright posture, or increased function 
Seizure disorder (*baclofen)
Cardiac dysfunction (*baclofen)
Muscle weakness 
Hepatic and renal dysfunction
especially metaxalone &amp; tizanidine
Safety during pregnancy and lactation is not known
do the benefits outweigh the risk
A

centrally acting skeletal muscle relaxant cautions

93
Q

CNS depression may increase when taken with other CNS depressants including alcohol

Cyclobenzaprine should not be used within 14 days of MAOIs (hypertensive crisis, seizures, death)

A

centrally acting skeletal muscle relaxants interactions

94
Q

Taper dosage to avoid withdrawal
(baclofen; prevent psychoses and hallucinations)

Most are on the Beers list (monitor older adults closely)

Chlorzoxazone may discolor urine, orange to purple-red

Monitor for CNS effects

A

centrally acting skeletal muscle relaxants n/c

95
Q

Enter the muscle to directly prevent muscle contraction

They do not interfere with neuromuscular communication, cause lessened CNS effects

Botulinum toxin type A (Botox Cosmetic)
Botulinum toxin type B (Myobloc)
Dantrolene (Dantrium)
Incobotulinumtoxin A (Xeomin)
A

direct acting skeletal muscle relaxants

96
Q

Direct-Acting Skeletal Muscle Relaxant

Interferes with the release of calcium from muscle tubules

prevents skeletal muscle fibers from contracting

Management of chronic muscle spasticity

  • spinal cord injury, cerebral palsy, MS
  • treatment for malignant hyperthermia

Hepatotoxicty has been reported
-women, elderly, and those on high doses at greatest risk

Oral - 25mg per day, max 100mg 4x per day
Parenteral - 1-3mg/kg (M.H.), rapid IV push, max 10mg/kg

A

dantrolene (dantrium)

97
Q
  • drowsiness, weakness, headache, diarrhea* or constipation, abdominal cramping, hepatitis
  • lower doses and gradual increase can help to avoid adverse effects
A

dantrolene (dantrium) adverse effects

98
Q

Direct-Acting Skeletal Muscle Relaxant

Bind to receptor sites of motor nerve terminals and block the release of acetylcholine
-leads to local muscle paralysis

Type A (Botox Cosmetic) - frown lines, axillary hyperhidrosis, cervical dystonia, strabismus, blepharospasm (chronic blinking), overactive bladder, chronic migraines

Type B (Myobloc) - cervical dystonia

Dose is 100 units, not to exceed 300 units/3 months

Generally not absorbed systemically
Usually lasts a few months

ADVERSE EFFECTS:

  • redness and edema at injection site, headache
  • can migrate from injection site and cause breathing and swallowing difficulties, most notably in children
A

botulinum toxin

99
Q

Contraindicated when spasticity contributes to locomotion, upright position, or increased function

Hepatic disease, concurrent use of estrogrens

Pregnancy and lactation
pregnancy category C
limited human data

Respiratory depression

Cardiac disease

A

direct acting skeletal muscle relaxants cautions

100
Q

Monitor for signs of hepatitis, discontinue medication

Monitor IV infusions of Dantrolene closely, can cause extravasation

Establish therapeutic goals at the beginning of therapy

Periodic drug “holidays” may be needed with dantrolene to ensure effectiveness

Discontinue dantrolene if diarrhea becomes severe, may need lower dose

A

direct acting skeletal muscle relaxants n/c

med surg pharm 1 (3 decks)

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