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Pharmacology > Summer Exam 1 > Flashcards

Summer Exam 1 Flashcards

1
Q

Epithelial Prostatic Tissue

A

Produces prostatic secretions

Growth stimulated by androgens

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2
Q

Stromal Prostatic Tissue

A

Smooth muscle with alpha-1-adrenergic receptors

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3
Q

How is dihydrotestosterone (DHT) created?

A

Testosterone and androstenedione are converted by 5a-reductase

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4
Q

What does DHT do in the prostate?

A

Induces growth and enlargement of the prostate gland

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5
Q

What are the two types of 5a-reductase?

A

Type 1: sebaceous glands in scalp, skin and liver causing acne and facial hair
Type 2: localized to prostate, genital tissue and hair follicles

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6
Q

What is the normal ratio of stromal to epithelial tissue in the prostate? In BPH?

A

stromal:epithelial 2:1

In BPH its 5:1

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7
Q

What drug class reduces size of enlarged prostate and by how much?

A

5a-reductase inhibitors by 25% (reduces production of DHT)

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8
Q

What drug class provides symptomatic relief in BPH patients?

A

Alpha-1-adrenergic antagonists (allow urinary flow by relaxing the contracted smooth muscle in prostate and bladder)

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9
Q

What do Static Factors cause in the Prostate

A

Cause anatomic enlargement of the gland blocking bladder neck obstructing urinary flow

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10
Q

What do Dynamic Factors do in the Prostate

A

Excessive a-adrenergic tone of stromal component causing contraction of the smooth muscle of the prostate gland around the urethra

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11
Q

Questions to ask for BPH screening

A

Any issues with starting/stopping urine stream, need to urinate >once a night, unable to reach toilet in time

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12
Q

Management of mild asymptomatic BPH

A

No treatment, just watch every 12 months to check for worsening

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13
Q

Management of mod-severe symptoms in BPH

A

Drug therapy (5a-reductase inhibitors and alpha1-adrenergic antagonists)

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14
Q

Three types of BPH drug therapy

A
  • Drugs that interfere with testosterones effect on gland enlargement (5alphas)
  • drugs that relax smooth muscle (alpha 1s)
  • drugs that relax bladder detrusor muscle (alpha 1s)
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15
Q

What are surgical options for BPH?

A

TURP (transurethral resection), allows for biopsy

Green light therapy, does not allow for biopsy

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16
Q

Risk factors of ED

A

Hypertension (bc of diuretics), hyperlipidemia, diabetes, smoking, alcohol abuse, metabolic syndrome, psychological

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17
Q

What types of medications cause ED?

A

Anticholinergics (effects point mechanism), dopamine antagonists (inhibit testicular testosterone production), estrogens/antiandrogens (suppress libido), CNS depressants (suppress perception of psychogenic stimuli), diuretics/B adrenergic antagonists/sympatholytics (reduce arteriolar flow)

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18
Q

Types of ED Treatments

A

Oral PDE5’s (often first line)
Vacuum erection devices (least invasive, good in cardio patients)
Intracavernosal injections/ intraurethral inserts, prosthesis

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19
Q

When is testosterone replacement indicated?

A

With hypogonadism (low T) confirmed with decreased libido and low serum concentration of testosterone

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20
Q

Low Testosterone Symptoms

A

decreased libido, ED, gynecomastia small testes, reduced body/facial hair growth, decreased muscle mass, increased body fat
Can develop anemia and osteoporosis

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21
Q

When should you not give testosterone?

A

Normal T levels, asymptomatic hypogonadism, isolated ED without hypogonadism

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22
Q

What is considered “low” testosterone?

A

<300ng/dL

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23
Q

What does testosterone treatment do?

A

Directly stimulates androgen receptors in CNS for normal sex drive, stimulates nitric oxide synthase enhancing PDE5 effects in cavernosal tissue

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24
Q

Oral Testosterone Therapy

A

Methyltestosteroe, fluoxymesterone
Check levels in 2-3 hours
Not commonly recommended because high association with hepatic toxicity

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25
Q

Buccal Testosterone Cons

A

Must be timed to be removed every morning/evening causing compliance issues

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26
Q

Parenteral Testosterone Treatment Issues

A

Contraindicated with severe hepatic or renal impairments

Can cause mood swings due to supra physiologic serum concentrations of testosterone

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27
Q

Parenteral Testosterone Treatment Types

A

Testosterone cypionate IM (depo)

Testosterone enthanate IM (delatestryl)

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28
Q

Transdermal Testosterone

A

Androderm
Administer at bedtime to form normal circadian pattern, inject in arm, back, tummy, thigh
Avoid water on the site for 3 hours

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29
Q

Transdermal Testosterone Gels/Sprays

A

Cover application to avoid transfer to others, apply on shoulder, upper arms and tummy (thighs for sprays)
Avoid water on application site for 2 hours

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30
Q

Subcutaneous Testosterone

A

Testopel

Onset is delayed for 3-4 months and must be administered by health care provider

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31
Q

Which testosterone regimen achieves normal serum concentrations?

A

Oral alkylated androgens, but they cause hepatotoxicity

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32
Q

Benefits of transdermal testosterone

A

They get normal serum concentrations, normal circadian pattern, normal androgen metabolites, works in 3-12 hours; low AEs (dermatitis and transfer to others)

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33
Q

Intramuscular testosterone Pros/Cons

A

Cypionate or enanthate

Achieve normal serum levels but not circadian pattern, cause mood swings, gynecomastia, polycythemia, hyperlipidemia

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34
Q

Buccal Testosterone System Pros/Cons

A

Achieves normal serum concentrations but not normal circadian pattern, causes gum irritation and bitter taste

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35
Q

Intracavernosal Medications

A

Alprostadil (preferred), papaverine, phentolamine

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36
Q

What nerves innervate the detrusor and what type of impulses?

A

S2-S4, parasympathetic

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37
Q

What is the primary neurotransmitter in the lower urinary tract and what does it do?

A

acetylcholine; volitional and involuntary contractions of the detrusor

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38
Q

What do M3 receptors do?

A

Emptying contractions and involuntary contractions of bladder

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39
Q

Drug of choice for bladder overactivity/urge incontinence?

A

Anticholinergics or antispasmodics (prevent contractions)-darifenacin, fesoterodine, oxybutinin, solifenacin, tolterodine
Trospium second line

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40
Q

First line treatment for urinary incontinence

A

behavioral therapy (bladder training, bladder control strategies, pelvic floor strengthening, fluid management)

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41
Q

Drug of choice for Stress incontinence/ urethral under activity?

A

a-adrenergic receptor agonists (norfenefrine and norephedrine) and topical estrogens

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42
Q

What do we monitor with anticholinergic meds?

A

Mental status and fall risk

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43
Q

How do we reduce anticholinergic med AEs?

A

Use extended release forms of drugs

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44
Q

Contraindications to Anticholinergics

A

Urinary/gastric retention, angioedema, glaucoma, renal/hepatic conditions

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45
Q

Mirabegron MOA

A

Improves urine storage by stimulating B3 adrenoreceptors reducing frequency of bladder contractions

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46
Q

What is mirabegron used for?

A

Overactive bladder incontinence, good for elderly because no anticholinergic AEs

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47
Q

Mirabegron AEs

A

Hypertension, urinary retention (caution in cardiovascular disease)

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48
Q

Mirabegron Drug Interactions

A

Inhibits CYP2D6, lowering dose of tricyclics, SSRIs, beta blockers, antipsychotics

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49
Q

Botox Use and MOA

A

Paralyzes detrusor muscle, helps with overactive bladder

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50
Q

Botox AEs

A

dysuria, hematuria, UTI, urinary retention

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51
Q

Norfenefrine and Norephedrine MOA and use

A

Vasoconstrictors

Used for stress incontinence

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52
Q

Norfenefrine and Norephedrine AEs

A

Hypertension, HA, dry mouth, nausea, insomnia, restlessness

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53
Q

Other Stress Incontinence drugs (not a-adrenergics)

A

Duloxetine, vaginal estrogen, imipramine (used for bedwetting)

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54
Q

Duloxetine MOA

A

Dual inhibitor of serotonin and norepinephrine reuptake-controls urethra and urethral sphincter increasing muscle tone

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55
Q

Duloxetine AEs

A

Nausea, headache, constipation, dry mouth, insomnia

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56
Q

Overflow (atonic bladder) Drugs and AEs

A

Cholinomimetics- bethanecol and BPH drugs

AEs: salivation, lacrimation, urination, defecation, GI upset, emesis, cardiac/resp issues

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57
Q

Osteoporosis Prevention

A

Regular exercise, nutritious diet, tobacco avoidance, minimal alcohol, fall prevention

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58
Q

Osteoporosis Causes

A

Deficiencies in hormones (estrogen), calcium and vitamin D

Drugs (steroids, thyroid drugs, antiepileptics

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59
Q

Osteoporosis Predictive tools

A

FRAX tool and garvan calculator-predict 5/10 year fracture risks

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60
Q

Diagnosis of Osteoporosis

A

low trauma fracture or central hip/spine dual-energy X-ray absorptiometry with T-score

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61
Q

T score between -1 and -2.5

A

Osteopenia

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62
Q

T score below -2.5

A

osteoporosis (-3.5 is severe)

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63
Q

Z-score

A

Used to diagnose osteoporosis in kids, premenopausal women and men <50 (should be -2.0)

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64
Q

Antiresorptive Therapies in Osteoporosis

A

Calcium, Vit D, disposphonates, calcitonin, estrogen, testosterone, teriparatide, denosumab

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65
Q

Drug of Choice in Osteoporosis

A

Bisphosphonates with calcium and vitamin D

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66
Q

Calcium in Osteoporosis and AEs

A

Carbonate or citrate (carbonate causes GI/gas probs)

AEs: hypophosphatemia, hypercalciumia

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67
Q

3 forms of vitamin D

A

Natural-D3/cholecalciferol
Plant derived-D2/ergocalciferol
Active- 1, 25, (OH) vit D (calcitrol)

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68
Q

Which form of Vitamin D is used for deficiency?

A

Ergocalciferol/D2

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69
Q

Cholecalciferol AEs

A

Hypercalcemia (headache, weakness, cardiac rhythm disturbance) and hypercalcuria

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70
Q

How is Calcitrol (active) formed?

A

Vit D metabolized into 25(OH)D in the liver, then metabolized to 1, 25 (OH) D in the kidney

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71
Q

Indications for Active Vitamin D

A

Renal osteodystrophy, hypoparathyroidism, refractory rickets

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72
Q

Types of bisphosphonates

A

Alendronate, risendronate, zoledronic acid (IV), denosumab

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73
Q

Bisphosphonates MOA

A

Endogenous bone resorption inhibitor-decreased osteoclast maturation, number, recruitment, bone adhesion and life span

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74
Q

Special instructions with Bisphosphonates

A

Take on empty stomach with lots of water and don’t lay down for 30-60 minutes after and don’t take with other meds

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75
Q

Contraindications of Bisphosphonates

A

CrCl is <35mL/min
Serious GI conditions
Pregnancy

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76
Q

Monitoring of Bisphosphonates

A

1-2 years after initiation then every 2 years for efficacy

Bone turnover markers

77
Q

Bisphosphonate AEs

A

Oral: nausea and dyspepsia
IV: flu-like illness
Can have GI bleed, perforation, ulcers, fractures, MSK pain

78
Q

Black Box warning in Bisphosphonates

A

Osteonecrosis of the jaw or subtrochanteric femoral fracture

79
Q

When can we stop osteoporosis drugs?

A

when T score gets above -2 with no evidence of low-trauma fracture; followed with bone turnover markers serially

80
Q

Calcitonin in Osteoporosis/MOA

A

3rd line/last resort! Provides pain relief with vertebral fracture
antagonizes effect of PTH (promoting calcium deposition into bones)

81
Q

Estrogen Agonist/Antagonist in Osteoporosis

A

Raloxifene and Bazedoxefene

decreases bone resorption increasing bone mineral density, decreasing fracture incidence

82
Q

Teriparatide (what it is and who its for)

A

Recombinant representing first 34 amino acids in PTH, used for post menopause, men, and patients on steroids with T score

83
Q

Teriparatide MOA

A

Increases bone formation, bone remodeling rate and osteoblast number/activity

84
Q

Denosumab in Osteoporosis MOA

A

Binds to RANKL inhibiting osteoclastogenesis and increasing osteoclast apoptosis, decreases vertebral/hip fracture rates

85
Q

Denosumab AEs/Treatment

A

Subcutaneous every 6 months-one of first lines (bisphosphonate)
AEs: back, extremity and MSK pain, increased cholesterol, cystitis, decreased calcium, skin probs

86
Q

Osteomalacia

A

“soft bones”, caused by vit D deficiency (<10ng/mL), treated with ergocalciferol BID for 8 weeks

87
Q

Spasmolytics for Chronic Use

A

CNS action: baclofen, diazepam, tizanidine, cyclobenzaprine

Muscle action: dantrolene and botox

88
Q

Spasmolytics for Short Term Use

A

Cyclobenzaprine

89
Q

Conditions Treated with Spasmolytics

A

Spasticity from UMN lesions

90
Q

Conditions treated with antispasmodics

A

spasms from peripheral musculoskeletal conditions

91
Q

Baclofen MOA

A

Facilitates spinal inhibition of motor neurons through release of excitatory transmitters in brain and spinal cord
Centrally acting on Pre and Post synaptic GABA receptors

92
Q

Baclofen Uses and AEs

A

Severe spasticity from cerebral palsy, MS, stroke

AEs: sedation, muscle weakness/falls

93
Q

Diazepam MOA

A

Facilitates GAA transmissions in CNS increasing interneuron inhibition of primary motor afferents in spinal cord
Centrally acting on Postsynaptic GABA receptors for central sedation

94
Q

Diazepam Uses/AEs

A

Chronic spasm from cerebral palsy, stroke, spinal cord injury AND acute spasm due to muscle injury
AEs: sedation, additive with other CNS depressants, antegrade amnesia, abuse potential

95
Q

Which antispasmodics can be used for acute spasm due to muscle injury?

A

Diazepam, cyclobenzaprine

96
Q

Tizanidine MOA

A

a2 agonist in spinal cord

Centrally acting on pre and post-synaptic inhibitors of reflex motor output

97
Q

Tizanidine Use/AEs/Elimination

A

Spasm due to MS, stroke, amyotrophic lateral sclerosis
Eliminated in renal/hepatic
AEs: weakness, sedation, hypotension

98
Q

Cyclobenzaprine MOA

A

Inhibits spinal stretch reflex, reduces hyperactie muscle reflexes
Centrally acting

99
Q

Cyclobenzaprine Uses/AEs

A

Acute spasm due to muscle injury/inflammation

AEs: antimuscarinic effects, sedation (take at night!), confusion, ocular effects

100
Q

Which antispasmodic should we avoid and why?

A

Soma/carisoprodol

Schedule IV drug, metabolized to meprobamate, very addictive!

101
Q

Dantrolene MOA

A

Blocks RyR1 Ca release channels in SR of skeletal muscle, weakens muscle contraction by reducing myosin-actin interaction

102
Q

Dantrolene Uses/AEs

A 
Malignant hyperthermia (given IV), spasm from cerebral palsy, spinal cord injury, MS (given orally)
AEs: muscle weakness
103
Q

Botox as antispasmodic (MOA)

A

Cleaves fusion proteins in nerve endings

104
Q

Botox as antispasmodic Uses/AEs

A

Spasm from cerebral palsy, MS, over-active bladder, migraine

AEs: muscle weakness, falls

105
Q

Which drugs should we avoid in fibromyalgia?

A

NSAIDs and opioids

106
Q

Non-pharmacological treatment of Fibromyalgia

A

Patient education, exercise (tai chi, yoga), CBT, alternative medicine (acupuncture), CNS neurostimulatory therapy

107
Q

Medications used in fibromyalgia

A

Amitriptyline, cyclobenzaprine, duloxetine, milnacipran, gabapentin, pregabalin

108
Q

Amitriptyline in Fibromyalgia (MOA and alternate)

A

Tricyclic antidepressant blockade of NET and SERT channels

Can use Desipramine

109
Q

Amitriptyline AEs

A

dry mouth, constipation, fluid retention, weight gain, grogginess, difficulty concentrating
Possible cardio toxicity limit in elderly

110
Q

Cyclobenzaprine MOA in Fibromyalgia

A

Centrally acting skeletal muscle relaxant related to tricyclics (has mild antidepressant effect), used for mild-mod symptoms, helps with good nights sleep

111
Q

Cyclobenzaprine AEs (fibromyalgia)

A

drowsiness, dry mouth, mental change, consitpation, weakenss, blurred vision

112
Q

Duloxetine in Fibromyalgia use

A

SNRI, preferred in patients with depression needing therapy, taken with breakfast
Helps with mental fatigue but not gen fatigue

113
Q

Duloxetine AEs

A

Nausea, headache, dry mouth (in first 3 months)

114
Q

Milnacipran MOA, Use, AEs

A

SNRI
Used for severe fatigue and pain
AEs: nausea, headache, constipation

115
Q

Venlafaxine in Fibromyalgia

A

Not generally used bc of short half life

116
Q

Gabapentin in Fibromyalgia (MOA)

A

Cellular calcium channels exert their analgesic effects by blocking release of neurotransmitters

117
Q

Gabapentin Use

A

Reduce pain and improve sleep and quality of life in fibromyalgia

118
Q

Gabapentin AEs

A

Dizziness, sedation, lightheadedness, weight gain

119
Q

Pregabalin in Fibromyalgia (MOA)

A

Binds to alpha-2 delta subunit of Ca channels in CNS inhibiting excitatory neurotransmitter release reducing connectivity between pain regions

120
Q

Pregabalin Uses/AEs

A

More severe sleep disturbance in addition to pain

AEs: peripheral edema, dizziness, ataxia, dry mouth, tremor, blurred vision

121
Q

Medication Overuse Headache

A

Use meds for <10 days/month to avoid

One of the most common causes of chronic daily headache

122
Q

Pathogenesis of Migraines

A

Complex dysfunctions in neuronal and broad sensory processing
Activation of trigeminal nerves triggers release of vasoactive neuropeptides and vasodilates>neurogenic inflammation

123
Q

OTC Migraine meds

A

Analgesics- acetaminophen, exedrin (acetaminophen+caffein+aspirin)
NSAIDs- aspirin, ibuprofen, naproxen, diclofenac

124
Q

Triptans MOA/Uses

A

Selective 5-HT1B and 5-HT1D receptor agonists- enhanced vasoconstriction, inhibition of vasoactive peptide, inhibition of transmission through second order neurons to thalamus
Migraines and cluster headaches

125
Q

Ergots MOA

A

Nonselective 5-HT1 receptor agonists- constrictive blood vessels and inhibit neurogenicinflammation through central inhibition of trigeminal pathway

126
Q

First line treatment in mild-severe migraines

A

Triptans (after OTC fails)

127
Q

Triptans Dosing

A

Most have max dose of 2 daily, rizatriptan nd frovatriptan can have 3/day
Rizatriptan dose halved if patient on propranolol

128
Q

Ergotamine Tartrate main AE

A

nausea, vomitting, give with anti-emetics!

129
Q

Adjunct Migraine Therapies

A

Metoclopramide and Prochlorperazone- these are good for acute relief

130
Q

Triptan AEs

A

Tightness, pressure, heaviness, pain in chest neck or throat

possible coronary vasospasm

131
Q

Serotonin Syndrome Cause/Treatment

A

Caused by SSRIs, antidepressants, sumatriptan, others

Treated with benzos and removal of causative drug

132
Q

Neuroleptic Malignant Syndrome Causes/Treatment

A

Caused by D2 blocking antipsychotics

Treated with diphenhydramine, cooling, benzos for sedation

133
Q

Neuroleptic Malignant Syndrome Presentation

A

hyperthermia, acute severe Parkinson’s reduced bowel sounds, onset 1-3 days

134
Q

Malignant Hyperthermia Causes/Treatments

A

Causes by anesthetics, succinylcholine

Treated with Dantrolene and cooling

135
Q

Malignant Hyperthermia Presentation

A

Hyperthermia, muscle rigidity, hypertension, tachycardia, onset within minutes

136
Q

When should we start preventive migraine therapy?

A

If they have frequent headaches >2 times/week with risk of medication overuse headache

137
Q

Medications approved for migraine prevention

A

Propranolol (first line), timolol, divalproex sodium/valproic acid, topirmate, ibuprofen/frovatriptan (esp for menstrual)
Can use naproxen

138
Q

How long does migraine prevention take to work?

A

Takes 2-3 months to start seeing effects, usually maxed effects in frequency by 6 months, but can take 12 months for severity to decrease

139
Q

CGRP Mabs for migraine prevention

A

Usually only used if all other fail, can cause formation of neutralizing antibodies

140
Q

What is the most common type of headache?

A

Tension type

141
Q

Where does tension headache pain originate from?

A

Myofascial factors and peripheral sensitization of nociceptors

142
Q

Treatment for tension headaches

A

CBT (stress management, relaxation training, biofeedback), analgesics (acetaminophen), NSAIDs (naproxen, aspirin, ibuprofen, etc)
Combo NSAIDs with Tylenol are good too

143
Q

Max times to take medications for tension headaches per month

A

Butalbital containing: 3 days
Combination analgesics: 9 days
NSAIDs: 15 days

144
Q

Preventative Tension headache meds

A

Tricyclics, SSRIs, can use topiramte and gabapentin, botox (but not highly recommended)

145
Q

Where does cluster headache pain generate?

A

Hypothalamus

146
Q

Abortive therapy of cluster headaches

A

100% oxygen*

triptan sprays/injections, IV dihydroergotamine

147
Q

Prophylaxis of cluster headaches

A

Verapamil (first line), lithium, steroids

148
Q

What kind of pain does large-diameter, sparsely myelinated A-delta fibers evoke?

A

sharp and well localized

149
Q

What kind of pain does unmyelinated small-diameter C fibers produce?

A

dull, aching, poorly localized

150
Q

Treatment options for neuropathic pain

A

Anticonvulsants (gabapentin), tricyclics, serotonin, opioids (second line), topical analgesics

151
Q

Gabapentin MOA

A

decrease neuronal excitatory neurotransmitters and nociception through calcium channels

152
Q

Gabapentin AEs

A

Dizziness, fatigue, ataxia, abnormal gait, amnesia, abnormal thinking, tremor, weight gain

153
Q

Pregabalin MOA

A

binds to alpha2-delta subunit calcium channels within CNS inhibiting excitatory neurotransmitter release
Exerts antnociceptive and anticonvulsant activity

154
Q

Pregabalin AEs

A

Peripheral edema, weight gain, tremor, dizziness, ataxia

155
Q

Chronic pain adjunctive therapies

A

Tricyclics, serotonin, norepinephrine reuptake inhibitors

First line and cheap

156
Q

Duloxetine MOA

A

Potent inhibitor of neuronal serotonin and norepinephrine reuptake (dual mechanism)

157
Q

Duloxetine AEs

A

Headache drowsiness, fatigue, nausea, dry mouth, insomnia, agitation

158
Q

Regional Analgesia AEs

A 
High plasma concentrations>CNS excitation and depression
Cardiovascular effects (hypotension, decreased cardiac output, heart block, bradycardia, cardiac arrest
159
Q

Types of local anesthetics (2)

A

Esters (only have 1 i)

Amides (have 2 i’s)

160
Q

Opioids used for epidural, intrathecal and subarachnoid routes

A

Morphines and fentanyl

161
Q

Ziconotide MOA

A

Selectively binds to N-type calcium channels on the nociceptive afferent nerves of dorsal horn blocking excitatory neurotransmitter release and reduces sensitivity to painful stimuli

162
Q

Ziconotide AEs

A

Confusion, dizziness, hallucinations, urinary retention, sedation, nausea, headache

163
Q

What is the first thing we should do for low back pain?

A

Nonpharma therapy! heat, massage, acupuncture, CBT, etc

164
Q

First line meds for low back pain

A

NSAIDs

Duloxetine and tramadol are second lines

165
Q

Heroin MOA

A

Diacetylmorphine metabolizes to morphine and gets past the blood brain barrier
Naturally occurring from poppies

166
Q

What qualifies a true allergy?

A

bronchospasm and angioedema

167
Q

Pseudoallergy

A

Itching, flushing, sweating

Common reaction to opioids, caused by histamine release

168
Q

Which opioids most commonly cause pseudo allergy?

A

Codeine, morphine, meperidine (they release the most histamine)

169
Q

Esters vs Amides

A

Esters have higher allergic potential, 1 i. metabolized by plasma
Amides are longer acting, 2i’s, metabolized in the liver

170
Q

Local Anesthetic MOA

A

Blocks sodium channels reducing influx of sodium ions and preventing depolarization of the membrane
Blocks conduction of action potential

171
Q

What are the roles of ionized and nonionized anesthetics?

A

Nonionized helps drug reach the site moving through the tissues
Ionized is active form, causes the effect

172
Q

What is the role of sodium bicarbonate in local anesthetic?

A

Accelerates the onset of action, enhances intracellular access of basic compounds

173
Q

Epinephrine’s effect on local anesthetic

A

prolongs the duration of action, lowers total systemic absorption
Its an a-agonist sympathomimetic vasoconstrictor

174
Q

Are myelinated or unmyelinated fibers easier to block?

A

Myelinated

175
Q

Which fiber type has the most sensitivity to blocks?

A

Type C, then type B, then type A-delta, we need to block to type A-beta (touch and pressure)

176
Q

When is motor paralysis desirable?

A

Surgery except childbirth

177
Q

What is the order of nerve blocking?

A

Sympathetic transmission>temperature> pain> light touch> motor block (surgical should include loss of touch in addition to ablation of pain)

178
Q

Caudal epidural block

A

needle inserted into caudal canal

179
Q

Perineural block

A

injections around peripheral nerves

180
Q

Spinal block

A

Injection into cerebrospinal fluid in subarachnoid space

181
Q

What drug is banned in obstetrics for cardio toxicity?

A

0.75% bupivicaine

Antidote is lipid emulsion

182
Q

Toxicities of amides

A

seizures, vasodilation, hypotension, arrythmias

183
Q

Toxicities of esters

A

vasoconstriction, hypertension, seizures, cardiac arrythmias

184
Q

Side effect of prilocaine

A

converts hemoglobin to methemoglobin

185
Q

Side effect of esters

A

Can cause antibody formation

186
Q

Side effect of high concentrations of anesthetics

A

may cause permanent impairment of function

187
Q

Treatment of anesthetic toxicity

A

Diazepam for convulsions, no antidote for anything else

188
Q

Side effects of anesthetics

A

Light-headed, sedation, restless, nystagmus, convulsions, vasodilation, heart block, arrythmias, hypotension

189
Q

What makes up emla cream and what is it used for?

A

Lidocaine and prilocaine

used in meds to numb skin for IV placement

Pharmacology (7 decks)

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