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PHTH 561: Pharmacology > Block 1 Exam > Flashcards

Block 1 Exam Flashcards

1
Q

What is the difference between the motor neurons in the somatic NS vs the ANS?

A

-Somatic innervates skeletal muscles; voluntary
-ANS: innervates smooth muscle, cardiac muscle, and glands; involuntary

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2
Q

What neurotransmitter is always released by the preganglionic neurons in the ANS?

A

ACh

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3
Q

What neurotransmitter is released from postganglionic neurons in the sympathetic and parasympathetic NS? What is the exception to this?

A

-Sympathetic: norepineprhine
-Parasympathetic: ACh
-Sweat glands have sympathetic input but only use ACh as a neurotransmitter

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4
Q

What is another name for the sympathetic NS?

A

-“Fight or flight”
-Thoracolumbar system

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5
Q

What is another name for the parasympathetic NS?

A

-“Rest and digest”
-Craniosacral system

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6
Q

What is the role of the parasympathetic division?

A

-SLUD
-Salivation
-Lachrymation
-Urination
-Defecation
-BP, HR, and RR are low
-GI tract activity is high
-Pupils are constricted and lenses are accommodated for close vision

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7
Q

What is the role of the sympathetic division?

A

-Mobilizes the body during activity
-Promotes adjustments during exercise or when threatened
-Blood flow is shunted to skeletal muscles and heart
-Bronchioles dilated
-Liver releases glucose

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8
Q

What are the functional aspects of the parasympathetic NS?

A

-Constricts pupils
-Stimulates salivation
-Inhibits heart
-Constricts bronchi
-Stimulates GI tract
-Stimulates gallbladder
-Contracts bladder
-Relaxes rectum

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9
Q

What are the functional aspects of the sympathetic NS?

A

-Dilates pupils
-Inhibits salivation
-Relaxes bronchi
-Accelerates heart
-Inhibits digestive activity
-Stimulates glucose release by liver
-Secretion of epinephrine and norepinephrine from kidney
-Relaxes bladder
-Contracts rectum

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10
Q

What receptors are there in the sympathetic NS?

A

-⍺-1
-⍺-2
-β-1
-β-2

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11
Q

What receptors are there in the parasympathetic NS?

A

Muscarinic

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12
Q

What types of receptors do ACh bind to?

A

-Nictonic receptors
-Muscarinic receptors

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13
Q

Where are nicotinic receptors found?

A

-Motor end plates of skeletal muscles
-All ganglionic neurons (sympathetic and parasympathetic)
-Hormone-producing cells of the adrenal medulla
-Effect of ACh at nicotnic receptors is always stimulatory

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14
Q

Where are the muscarinic receptors found?

A

-Found on all effector cells stimulated by postganglionic cholinergic fibers
-The effect of ACh at muscarinic receptors can either be excitatory or inhibitory

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15
Q

What are the two types of adrenergic receptors?

A

-Alpha
-Beta

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16
Q

What is sympathetic tone?

A

-Sympathetic NS controls BP even at rest
-Keeps blood vessels in a continual state of partial constriction
-Sympathetic fibers fire more rapidly to constrict blood vessels and cause BP to rise

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17
Q

What is parasympathetic tone?

A

-Parasympathetic NS dominates the heart and smooth muscle of GI tract and urinary tract organs
-Slows the HR
-Dictates normal activity levels of the digestive and urinary tracts

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18
Q

What are unique roles of the sympathetic NS?

A

-The adrenal medulla, sweat glands, and blood vessels only receive sympathetic fibers
-Controls thermoregulatory responses to heat
-Release of renin from the kidneys
-Metabolic effects

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19
Q

Where are β-1 receptors located that are stimulated by the sympathetic NS? What are its effects?

A

-Heart (increase HR)
-Salivary glands (increases)
-Adipose tissue (lipolysis)
-Kidney (renin secretion)

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20
Q

Where are ⍺-1 receptors located that are stimulated by the sympathetic NS? What are its effects?

A

-Skin (constricts)
-Smooth muscle sphincters (contracts)
-Pupils (dilation-mydriasis)

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21
Q

Where are β-2 receptors located that are stimulated by the sympathetic NS? What are its effects?

A

-Bronchioles (dilates)
-Blood vessels to skeletal muscle (dilates)
-Smooth muscle walls (relaxes)
-Bladder wall muscle (relaxes)
-Liver (gluconeogenesis, glycogenolysis)

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22
Q

Where are ⍺-2 receptors located that are stimulated by the sympathetic NS? What are its effects?

A

Smooth muscle walls (relaxes)

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23
Q

What are cholinergic agonists? What is another name for them?

A

-Mimic the effects of acetylcholine
-Also referred to as “parasympathomimetics”

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24
Q

What are the two types of cholinergic agonists?

A

-Direct: mimic the activity of ACh at the cholinergic receptors
-Indirect: inhibit the actions of acetylcholinesterase

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25
Q

What are some examples of direct acting cholinergic agonists?

A

-Bethenechol
-Pilocarpine
-Methacholine
-Carbachol

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26
Q

What is the mechanism of action of bethanechol? What is its purpose?

A

-Targets muscarinic receptors in the GI and urinary tract
-Purpose is to increase tonicity in the destrusor muscle and stimulate gastric motility

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27
Q

What are adverse effects of bethanechol?

A

-Abdominal discomfort
-Urinary urgency
-Flushing of skin
-Bronchial constriction
-Asthma attacks

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28
Q

What is the mechanism of action of pilocarpine? What is its purpose?

A

-Targets muscarinic receptors in the lacrimal glands
-Its purpose is to decrease fluid in the eye which decreases pressure
-Used to treat glaucoma

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29
Q

What are the adverse reactions of pilocarpine?

A

-Blurred vision
-Decreased night vision
-Eye irritation
-Headache
-Increase sweating and salivation

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30
Q

What is methacholine used for?

A

To diagnose asthma

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31
Q

What is carbachol used for?

A

To treat glaucoma

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32
Q

What are indirect acting cholinergic agonists/cholinesterase inhibitors used for alzheimer’s?

A

-Donepezil
-Rivastigmine
-Galantamine

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33
Q

What are indirect acting cholinergic agonists/cholinesterase inhibitors used for myasthenia gravis?

A

-Neostigmine
-Pyridostigmine
-Edrophonium
-Ambenonium

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34
Q

What are indirect acting cholinergic agonists/cholinesterase inhibitors used for glaucoma?

A

-Physostigmine
-Echothiopate

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35
Q

What is myasthenia gravis?

A

Weakness of the skeletal muscle and fatigue

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36
Q

What is glaucoma?

A

Increase in intraocular pressure which can lead to blindness

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37
Q

What are common adverse effects of cholinergic stimulants?

A

-GI distress
-Increased salivation
-Increased lachrymation
-Bronchoconstriction
-Bradycardia
-Difficulty in visual accommodation

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38
Q

What are common anti-cholinergic drugs?

A

-Atropine
-Scopolamine
-Ipratropium bromide
-Tiotropium bromide
-Oxybutynin
-Tolterodine
-Benztropine
-Tropicamide
-Dicyclomine
-Hyoscyamine

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39
Q

What are common ⍺-1 selective agonists? What is their use?

A

-Phenylephrine
-Pseudoephedrine
-Oxymetazoline: reduces redness of the eye
-Xylometazoline
-Decrease nasal congestion

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40
Q

What are adverse effects of ⍺-1 agonist?

A

-Increased BP
-Headache
-Slow HR due to reflex bradycardia

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41
Q

What are common ⍺-2 selective agonists? What is their use? What is the mechanism of action?

A

-Clonidine
-Methyldopa
-Antihypertensive agent
-Binds to ⍺-2 receptors on the presynaptic neuron and blocks neurotransmitter release

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42
Q

What are adverese effects of ⍺-2 agonists?

A

-Dizziness
-Drowsiness
-Dry mouth

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43
Q

What are common β-1 selective agonists? What is their use?

A

-Dobutamine: positive inotrope
-Dopamine: congestive HF

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44
Q

What are adverse effects of β-1 selective agonists?

A

-Chest pain
-Arrhythmias
-SOB or difficulty breathing

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45
Q

What are common β-2 selective agonists? What is their use?

A

-Albuterol: bronchodilator
-Salmeterol: bronchodilator
-Terbutaline: delay preterm labor (slows uterus contractions)

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46
Q

What are adverse effetcs of β-2 selective agonists?

A

-Nervousness
-Restlessness
-Trembling

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47
Q

What are some common non-selective adrenergic drugs? What are their uses?

A

-Amphetamines: treat ADHD in children, or narcolepsy
-Epinephrine: anaphylactic shock
-Norepinephrine: to treat hypotension during shock

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48
Q

What are the adverse effects of non-selective adrenergic drugs?

A

-CNS excitation
-Anxiety
-Arrhythmias
-Hypertension

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49
Q

What are common ⍺-1 selective antagonists? What is their use?

A

-Prazosin: antihypertensive
-Doxazosin: antihypertensive
-Alfuzosin: treats urinary retention
-Tamulosin: treats urinary retention

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50
Q

What is phenooxybenzamine? When is it used?

A

-⍺-1 selective antagonist
-Used to control BP prior to and during the removal of a pheochromocytoma (cancer of adrenal gland)

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51
Q

What are the adverse effects of ⍺-1 selective antagonists?

A

-Reflex tachycardia
-Orthostatic hypotension
-Dizziness

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52
Q

What are common β-1 selective antagonists? What are their uses?

A

-Atenolol: antihypertensice
-Bisoprolol: treats HF
-Metroprolol: treats HF
-Esmolol: treats arrhythmias

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53
Q

What are some common non-selective β blockers? What are the adverse effects of them?

A

-Propranolol: antihypertensive
-Timolol: treats glaucoma
-Could cause bradycardia and bronchoconstriction

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54
Q

What are the adverse effects of β-adrenergic antagonists?

A

-Bronchoconstriction
-Increase in airway resistance
-Bradycardia
-Dizziness
-Depression
-Lethargy

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55
Q

What are physical therapy considerations for anyone taking medications that influence the ANS?

A

-BP and HR may be low
-Respiratory conditions
-Dizziness and fall risk
-Endurance and fatigue: may have exercise intolerance
-Heat tolerance: anticholinergics can decrease sweating
-Cholinesterase inhibitors can cause bradycardia
-Diuretics are often prescribed with ANS agents and can cause dehydration and electrolyte imbalances

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56
Q

What are the health threats from high BP?

A

-Stroke
-Vision loss
-HF
-MI
-Kidney disease
-Sexual dysfunction

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57
Q

What are the two types of hypertension?

A

-Essential
-Secondary

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58
Q

What is essential hypertension?

A

Cause is not known

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59
Q

What is secondary hypertension?

A

-Cause is known
Can be caused by the following:
-Renal artery constriction
-Phenochromocytoma (tumor of adrenal glands)
-Primary aldosteronism

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60
Q

What is the calculation for blood pressure?

A

BP= CO x total peripheral resistance (TPR)

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61
Q

What is elevated BP?

A

SBP 120-129 and DBP less than 80

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62
Q

What is stage 1 hypertension?

A

SBP 130-139 or DBP 80-89

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63
Q

What is stage 2 hypertension?

A

SBP 140 or higher or DBP 90 or higher

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64
Q

What is a hypertensive crisis?

A

SBP higher than 180 and/or DBP higher than 120

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65
Q

What is the stepped approach to treatment of hypertension?

A
  1. Lifestyle changes
  2. Medication management
  3. Multiple medications
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66
Q

What is non-pharmacological treatments for hypertension?

A

-Dietary salt restriction
-Potassium supplementation
-Weight loss
-Dietary Approaches to Stop Hypertension diet (DASH)
-Aerobic exercise

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67
Q

What are the anti-hypertensive drug categories?

A

-A: Angiotensin converting enzyme inhibitors
-B: Blockers of the angiotensin receptor
-C: calcium channel blockers
-D: diuretics
-Beta blockers
-Alpha blockers
-Alpha 2 agonists
-Renin inhibitors
-Vasodilators

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68
Q

What are diuretics? What are the different types?

A

-Acts on the kidneys to increase excretion of sodium and water
-Thiazide diuretics
-Loop diuretics
-Potassium sparing diuretics

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69
Q

What is the mechanism of action of thiazide diuretics? What are common thiazide diuretics?

A

-Ibhibits sodium reabsroption in the distal convoluted tubule
-Chlorothiazide
-Hydrochlorothiazide

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70
Q

What is the mechanism of action of loop diuretics? What are common loop diuretics?

A

-Inhibits reabsorption of sodium & chloride in the Loop of Henle
-Furosemide
-Torsemide

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71
Q

What is the mechanism of action of K+ sparing diuretics? What are common K+ sparing diuretics?

A

-Prevents secretion of K+
-Not as good of a diuretic but it prevents hypokalemia
-Spironolactone
-Triamterene

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72
Q

What are side effects and adverse reactions of diuretics?

A

-Fluid loss: can lead to orthostatic hypotension
-Electrolyte imbalance: can lead to cardiac arrhythmias
-Hypokalemia

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73
Q

How does the renin-angiotensin system work?

A

-Decreased BP, blood volume, or decreased sodium content
-Kidneys release renin
-Renin converts angiotensinogen (in the liver) to Angiotensin I
-Angiotensin I travels to the lungs
-Angiotensin converting enzyme (ACE) in the lungs, converts angiotensin I to angiotensin II

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74
Q

What are the effects of angiotensin II?

A

-Causes vasoconstriction, thereby increasing BP
-Stimulates the release of aldosterone from the adrenal cortex
-Stimulates the release of antidiuretic hormone which increases water retention and blood volume
-Induces thirst leading to increased fluid intake

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75
Q

What can occur with chronic activation of the renin-angiotensin system?

A

Can lead to persistent increases in blood pressure, contributing to the development of hypertension

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76
Q

What is the function of aldosterone?

A

It leads to sodium and water retention in the kidneys, which increases blood volume and pressure

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77
Q

What is the mechanism of action of ACE inhibitors?

A

-Inhibits angiotensin converting enzyme (ACE) therefore preventing angiotensin II from being made
-Inhibits aldosterone secretion as there is no angiotensin II
-Prevents remodeling of the blood vessels and heart

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78
Q

What are common ACE inhibitors?

A

-Benazepril
-Captopril
-Cilazapril
-Enalapril
-Fosinopril
-Lisinopril
-Quinipril
-Ramipril

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79
Q

What are side effects or adverse effects of ACE inhibitors?

A

-Dry cough
-Hyperkalemia
-Acute kidney damage
-Angioedema (skin & mucous membranes)
-Fetotoxi and should not be used by pregnant women!!!

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80
Q

What is the mechanism of action of angiotensin receptor blockers (ARBs)?

A

-Blocks the angiotensin II receptors to prevent vasoconstriction, release of aldosterone from the adrenal glands
-Same therapeutic effect as ACE inhibitors

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81
Q

What are the side effects and adverse effects of ARBs?

A

-Acute kidney damage
-Hyperkalemia
-Fetotoxic and should not be used by pregnant women

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82
Q

What are common ARBs?

A

-Candesartan
-Irbesartan
-Losartan
-Telmisartan
-Valsartan
-Olmesartan

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83
Q

What is the mechanism of action of calcium channel blockers (CCBs)?

A

Blocks calcium entry into the cells of the vascular smooth muscle and the heart

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84
Q

How does smooth muscle activation work in the vascular and heart smooth muscle?

A

-Influx of extracellular calcium releases stored calcium from the sarcoplasmic reticulum
-Intracellular calcium binds to calmodulin, which then activate myosin light chain kinase (MLCK)
-Activation of MLCK enables myosin to interact with actin to induce contraction

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85
Q

What are side effects of CCBs?

A

-Dizziness
-Flushing
-Headache
-Fatigue
-Peripheral edema

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86
Q

What are common CCBs?

A

-Verapamil
-Dilitiazem
-Amlodipine
-Felodipine
-Nifedipine

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87
Q

How do β-1 blockers effect blood pressure?

A

-Bind to β-1 receptors
-Blocks the effects of epinephrine and norepinephrine
-Decreases HR and contractility which results in reduced CO and BP

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88
Q

How do ⍺-1 blockers effect blood pressure?

A

Binds to ⍺-1 receptors on vascular smooth muscle to cause decrease in vascular resistance which decreases BP

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89
Q

How do ⍺-2 agonists effect blood pressure?

A

Stimulates ⍺-2 adrenergic receptors in the brain to reduce sympathetic outflow

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90
Q

What are common vasodilators? What are their uses?

A

-Hydralazine and minoxidil directly relax arteriolar smooth muscle resulting in vasodilation
-Minoxidil is a more potent vasodilator than hydralazine
-Used to treat moderate-severe hypertension

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91
Q

What is the mechanism of action of vasodilators?

A

-Activation of K+ channels
-Increased K+ efflux induces hyper-polarization of the smooth muscle membrane
-Calcium influx is inhibits and the arteriolar smooth muscle relaxes

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92
Q

What are side effects and adverese effects of vasodilators?

A

-Reflex tachycardia
-May prompt angina pectoris, MI, or cardiac failure
-Increase plasma renin concentration resulting in sodium and water retention
-Orthostatic hypotension

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93
Q

What is the mechanism of action of renin inhibitors? What is their use?

A

-Aliskiren
-Similar to ACE inhibitors and ARBs
-Ibhibits renin
-Monitors serum K+ and kidney function
-Must not be used during pregnancy

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94
Q

What are physical therapy considerations for anyone taking anti-hypertensives?

A

-BP monitoring
-Orthostatic hypotension
-Fatigue and dizziness
-Exercise intensity
-Dehydration
-Electrolyte imbalances
-Patient education

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95
Q

What are the different classes of antiarrhythmic drug classes?

A

-Class I: sodium-channel blocker
-Class II: beta-blocker
-Class III: potassium-channel blocker
-Class IV: calcium-channel blocker

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96
Q

What is class IA anti-arrhythmic drugs? What is their mechanism of action?

A

-Block fast Na+ channels
-Cause moderate phase 0 depression
-Prolong repolarization
-Increased duration of action potential

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97
Q

What are common class IA anti-arrhythmic drugs?

A

-Quinidine
-Procainamide
-Disopyramide

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98
Q

What are class IB anti-arrhythmic drugs? What is their mechanism of action?

A

-Weak phase 0 depression
-Shortened repolarization
-Decreased action potential duration

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99
Q

What are common class IB anti-arrhythmic drugs?

A

-Lidocaine
-Mexiletine

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100
Q

What are class I anti-arrhythmic drugs used to treat?

A

Ventricular arrhythmias

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101
Q

What are class IC anti-arrhythmic drugs? What is their mechanism of action?

A

-Strong phase 0 depression
-Little effect on repolarization

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102
Q

What are common class IC anti-arrhythmic drugs?

A

-Flecainide
-Propafenone

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103
Q

What are class II anti-arrhythmic drugs? What are their mechanism of actions?

A

-β-adrenergic blockers
-Blockade of myocardial β-adrenergic receptors
-Direct membrane stabilizing effects related to Na+ channel blockage

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104
Q

What are common class II anti-arrhythmic drugs?

A

-Propranolol
-Other β-adrenergic blockers

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105
Q

What are class II anti-arrhythmic drugs used to treat?

A

-Atrial tachycardias
-Ventricular arrhythmias

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106
Q

What are class III anti-arrhythmic drugs? What is their mechanism of action?

A

-K+ channel blockers
-Cause delay in repolarization

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107
Q

What are common class III anti-arrhythmic drugs?

A

-Amiodarone
-Dronedarone
-Ibultilide
-Dofetilide

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108
Q

What are class IV anti-arrhythmic drugs? What is their mechanism of action?

A

-Ca2+ channel blockers
-Slows rate of AV conduction in patients with a-fib

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109
Q

What are common class IV anti-arrhythmic drugs?

A

-Verapamil
-Diltiazem
-Slows SA node in tachycardia

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110
Q

What are other drugs that are used in arrhythmias?

A

-Adenosine: inhibits AV conduction
-Digoxin: reduces conduction through AV node
-Atropine: blocks vagal effects on the SA node to treat sinus bradycardia

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111
Q

What are physical therapy considerations for patients taking anti-arrhythmic drugs?

A

-Monitor vital signs
-Recognize side effects
-Pace and progression
-Consider exercise type
-Educate patients
-Be prepared
-Coordination with healthcare providers

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112
Q

What are skeletal muscle relaxants used to treat?

A

Used to treat conditions associated with hyper excitable skeletal muscle- specifically spasticity and muscle spasms

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113
Q

What is spasticity vs spasm?

A

-Spasticity: velocity dependent increase in muscle tone caused by the increased excitability of the muscle stretch reflex
-Spasms: involuntary muscle contractions

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114
Q

What are common symptoms of severe spasticity?

A

-Muscle stiffness
-Muscle spasms
-Rapid muscle contractions
-Fixed joints: contractures
-Exaggerated muscle jerks
-Pain or tightness around joints

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115
Q

What is the primary goal of skeletal muscle relaxants?

A

-Selective decrease in skeletal muscle excitability
-Decrease pain without causing a profound decrease in muscle function

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116
Q

What are common anti-spasticity drugs?

A

-Baclofen
-Dantrolene
-Tizanidine
-Botulinum toxin
-Gabapentin
-Diazepam (Benzodiazepines)

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117
Q

What are common spasmolytics?

A

-Carisoprodol (Soma)
-Cyclobenzaprine (Flexeril)
-Methocarbamol (Robaxin)
-Orphenadrine (Norflex)

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118
Q

What is the mechanism of Carisoprodol? What is a brand name of this drug?

A

-Its exact mechanism is unknown, but is believed to alter interneuronal activity in the spinal cord and descending reticular formation
-Polysynaptic inhibitor
-Decrease alpha motor neuron excitability
-Soma

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119
Q

What is the mechanism of Cyclobenzaprine? What is a brand name of this drug?

A

-Works centrally, likely by decreasing activity in the brainstem to relieve muscle spasms
-Flexeril

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120
Q

What is the mechanism of Methocarbamol? What is a brand name of this drug?

A

-Central muscle relaxant properties
-Robaxin

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121
Q

What is the mechanism of Orphenadrine? What is a brand name of this drug?

A

-Anticholinergic properties are believed to be responsible for this drugs mechanism
-Norflex

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122
Q

What are the key differences in the mechanisms for anti-spasticity drugs vs spasmolytics?

A

-Anti-spasticity drugs often have more specific targets
-Spasmolytics are less clear and can be diverse

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123
Q

What are the uses of polysynaptic inhibitors?

A

-Adjuncts to rest and PT for relief of muscle spasms associated with acute painful MSK injuries
-The same compounds sometimes incorporated into the same tablet with analgesic (Norgesic)

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124
Q

What are adverse effects of polysynaptic inhibitors?

A

-Drowsiness, dizziness
-Nausea, lightheadedness, vertigo, ataxia, headache
-Tolerance and physical dependence

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125
Q

What are the most common polysynaptic inhibitors?

A

-Carisoprodol (Soma)
-Cyclobenzaprine (Flexeril)
-Methocarbamol (Robaxin)
-Orphenadrine citrate (Norflex)

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126
Q

What is the mechanism of Diazepam (Valium)?

A

-Increases the inhibitory effects at CNS synapses that use GABA
-Binds to GABA A receptors: positive allosteric modulation
-Increases GABA-mediated inhibition of alpha motor neuron ——> less excitability

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127
Q

What are therapeutic uses of Diazepam?

A

-Treats muscle spasms associated with MSK injuries, especially low back strains
-Controls muscle spasms associated with tetanus toxin (inhibits spasms of larynx)

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128
Q

What are adverse effects of Diazepam?

A

-Sedation and a general reduction in psychomotor ability
-Long-term use also limited by tolerance and dependence
-Sudden withdrawal after prolonged use can cause seizures, anxiety, agitation, tachycardia, and even death
-Overdose can result in coma or death

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129
Q

What is an antidote for diazepam?

A

Flumazenil is antidote for Diazepam and other benzodiazepines

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130
Q

What drugs work on GABA A receptors?

A

Benzodiazepines (Valium/diazepam)

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131
Q

What drugs work on GABA B receptors?

A

Baclofen

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132
Q

What drugs work on alpha 2 receptors in the spinal cord?

A

Tizanidine

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133
Q

What drugs work directly on the skeletal muscle?

A

Dantrolene

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134
Q

What is the chemical name of Baclofen (Lioresal)? What is the mechanism?

A

-Chemical name: beta-(p-choloro-phenyl)-GABA
-Derivative of the central inhibitory GABA
-Binds to GABA B receptors in spinal cord
-Inhibits transmission within the spinal cord at specific synapses causing an inhibitory effect on alpha motor neurons within spinal cord

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135
Q

What are common uses of Baclofen?

A

-Administered orally to treat spasticity with spinal cord lesions (paraplegia, quadriplegia, SC demyelination)
-Drug of choice with MS because of fewer side effects
-Does not cause as much generalized muscle weakness as direct-acting relaxants such as Dantrolene

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136
Q

What are the adverse effects of Baclofen?

A

-Transient drowsiness which usually disappears within a few days
-Sometimes confusion and hallucinations in patients with CVA or in elderly
-Nausea, muscle weakness
-Headache

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137
Q

What are intrathecal injections? What are they used for? What is the benefit?

A

-Spinal injections
-Used in severe spasticity (Baclofen)
-Catheter and “pump” deliver drug to subarachnoid space
-May decrease spasticity with less drug, fewer systemic side effects

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138
Q

What is an itrathecal baclofen pump?

A

-Smaller catheter usually implanted surgically
-Open end of the catheter is attached to some type of programmable pump
-Pump is implanted subcutaneously in the abdominal wall
-Adjusted to deliver drug at slow, continuous rate
-Rate of infusion titrated over time to achieve best clinical reduction in spasticity

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139
Q

What are adverse effects of intrathecal baclofen?

A

-Disruption in delivery system
-Pump malfunction
-Increased drug delivery can cause overdose
-Abrupt stoppage of drug secondary to pump dysfunction can cause withdrawal syndrome (fever, confusion, delirium, seizures)
-Tolerance with long-term use

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140
Q

What is the mechanism of adrenergic alpha-2 receptor agonists? What is the primary agent?

A

-Primary agent: Tizanidine (Zanaflex)
-Stimulate alpha-2 receptors located on spinal interneurons
-Cause inhibition of interneurons which decreases excitatory input onto alpha motor neuron
-Tizanidine decreases excitability by both pre and post synaptic inhibition
-Efficacy similar to Baclofen but with less generalized muscle weakness

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141
Q

What are the uses of alpha-2 agonists?

A

-Control spasticity from spinal lesions and central lesions
-As effective in decreasing spasticity as oral baclofen or diazepam
-Milder side effects and less generalized muscle weakness
-Tizanidine is better than Clonidine because it has less cardiovascular side effects and hypotension

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142
Q

What are the adverse effects of alpha-2 agonists?

A

Sedation, dizziness, dry mouth

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143
Q

What is the mechanism of Gabapentin (Neurontin)?

A

-Calcium channel blocker
-Developed originally as anti-seizure drug
-Enhances GABA effect in spinal cord (exact mechanism unclear)

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144
Q

What are the uses of Gabapentin (Neurontin)?

A

-Decrease spasticity associated with SCI and MS
-Best use may be in combination with other anti-spasticity agents (Gabapentin + Baclofen)
-May help in reducing certain types of chronic pain

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145
Q

What are adverse effects of Gabapentin?

A

-Sedation and fatigue
-Dizziness
-Ataxia

146
Q

What is the mechanism of Dantrolene (Dantrium)?

A

-Only direct acting muscle relaxant
-Inhibits release of calcium from skeletal muscle sarcoplasmic reticulum

147
Q

What are the uses of Dantrolene?

A

-Effective in treating severe spasticity
-Not prescribed to treat muscle spasms caused by MSK injury

148
Q

What are adverse effects of Dantrolene?

A

-Generalized muscle weakness most common
-Use of Dantrolene therefore can be counterproductive because increased motor function with decreased spasticity is offset by muscle weakness
-Severe hepatotoxicity and fatal hepatitis

149
Q

What is the mechanism of Botulinum Toxin?

A

-Injected locally for severe spasms such as torticollis, laryngospasms
-Increased use in spasticity
-Inhibits release of acetylcholine at neuro-muscular junction

150
Q

Where is Botulinum injected into? How long does it last? How does it help with spasticity?

A

-Injected into skeletal muscle
-Relaxation/paralysis occur within 3-7 days and lasts 2-3 months
-Remove spastic dominance in certain patients
-Volitional motor function can be facilitated
-Improved gait and other functional activities in patients with cerebral palsy or TBI
-Helps to stretch muscle and prevent joint contractures
-Enables patients to wear orthotic devices

151
Q

What are the problems and limitations with Botulinum Toxin?

A

-Local irritation at injection site
-Only a limited number of muscles can be injected during a given treatment
-Must limit total dose (300-400 units of Type A, 2500-5000 units Type B)
-Exceeding recommended dosage can cause immune response which will create antibodies against toxin making subsequent treatments less effective

152
Q

How do effects of Botulinum Toxin wear off?

A

-New presynaptic terminal sprouts from axon that originally effected by toxin
-New motor end plate with new source of acetylcholine
-Another injection needed to block sprout

153
Q

What is the duration of action of carisoprodol (Soma)?

A

4-6 hours

154
Q

What is the duration of action of chlorzoxazone?

A

3-4 hours

155
Q

What is the duration of action of cyclobenzaprine (Flexeril)?

A

12-24 hours

156
Q

What is the duration of action of Diazepam (Valium)?

A

Up to 24 hours

157
Q

What is the duration of action of Metaxalone?

A

4-6 hours

158
Q

What is the duration of action of Methocarbamol (Robaxin)?

A

Unknown

159
Q

What is the duration of action of Orphenadrine citrate (Antiflex, Norflex)?

A

12 hours

160
Q

What are alternatives to skeletal muscle relaxants?

A

-Physical therapy
-Ibuprofen/NSAIDS
-Tramadol
-Opioids

161
Q

What are special concerns for rehab patients who use skeletal muscle relaxants?

A

-Meds are used to compliment PT interventions
-Long term use is not recommended: addiction
-PT can reduce the need for meds
-Possible drastic change in muscle tone over short period of time
-Pt’s sometimes rely on muscle spasms or spasticity for functioning

162
Q

What effects of anti-spastic and spasmolytic drugs can interfere with rehabilitation?

A

-Motor control problems
-Functional decline for daily activities
-Decreased alertness
-Weakness
-Tolerance and physical dependence

163
Q

What are possible PT solutions to effects of anti-spastic and spasmolytic drugs?

A

-Schedule PT for time of day when sedative effects are less marked
-Discuss with pt’s PCP
-In pt’s with spasticity due to neurological injury, use intensive PT to return pt to normal physiologic motor control
-Use intensive therapy for acute MSK injuries
-Improve muscle strength, posture, and flexibility which can decrease need for medications

164
Q

What is allodynia?

A

Pain due to a stimulus that does not normally provoke pain

165
Q

What is hyperalgesia?

A

Increased pain from a stimulus that normally provokes pain

166
Q

What is hypoalgesia?

A

Diminished pain in response to a normally painful stimulus

167
Q

What is neuralgia?

A

Pain in the distribution of a nerve or nerves

168
Q

What is neuritis?

A

Inflammation of a nerve or nerves

169
Q

What is nociception?

A

The neural process of encoding noxious stimuli

170
Q

What is a nociceptor?

A

A high threshold sensory receptor of the peripheral somatosensory nervous system that is capable of transducing and encoding noxious stimuli

171
Q

What is nociceptive pain?

A

Pain that arises from actual or threatened damage to non-neural tissue and is due to the activation of nociceptors

172
Q

What is neuropathic pain?

A

Pain caused by a lesion or damage or disease of the neurons or somatosensory nervous system

173
Q

What is the WHO analgesic ladder?

A

-Step 1: Mild pain
-Step 2: Moderate pain
-Step 3: Severe pain
-Step 4: Acute, chronic, and palliative

174
Q

What medications or treatment is used for step 1 on the WHO analgesic ladder?

A

-PT
-OT
-Non-opioid analgesics
-NSAIDs
-Adjuvant pain medications

175
Q

What medications or treatment is used for step 2 on the WHO analgesic ladder?

A

-PT/OT
-Weak opioids
-Psychology, behavioral therapy, etc.

176
Q

What medications or treatment is used for step 3 on the WHO analgesic ladder?

A

-Strong opioids
-PT/OT
-Psychology, behavioral therapy, etc.

177
Q

What medications or treatment is used for step 4 on the WHO analgesic ladder?

A

-PT
-OT

178
Q

What treatments can be used at every step on the WHO analgesic ladder?

A

-NSAIDs
-PT/OT
-Acupuncture
-Massage
-TENS

179
Q

What is adjuvant pain medications?

A

Medications that are not typically used for pain but may be helpful for its management

180
Q

What are some examples of adjuvant pain medications?

A

-Anti-depressants
-Anti-seizure medications
-Muscle relaxants
-Sedatives
-Anti-anxiety medications
-Botulinum toxin

181
Q

What are medications that help to alter the perception of pain in the brain?

A

-Opioids
-TCAs
-SSRI
-SNRIs
-⍺-2 agonists

182
Q

What are medications that help to modulate the ascending/descending pain pathway?

A

-TCAs
-SSRIs
-SNRIs

183
Q

What are medications that limit the transmission of pain in the peripheral nerves?

A

-LAs (ask Dr. Pattipatti what this is)
-Opioids
-⍺-2 agonists

184
Q

What are medications that limit the transduction of peripheral nociceptors?

A

-LAs
-Capsaicin
-Anticonvulsants
-NSAIDs
-ASA (what is this?)
-Acetaminophen
-Nitrate

185
Q

What are examples of TCAs and SSRIs?

A

-Amitriptyline
-Noritryptiline
-Duloxetine

186
Q

What are examples of topical agents?

A

-Capsaicin
-Lidocaine patch

187
Q

What are examples of opioids?

A

-Tramadol
-Tapentadol
-Hydrocodone
-Oxycodone
-Methadone

188
Q

What are examples of NMDA inhibitors?

A

-Ketamine
-Amantidine
-Memantine

189
Q

What are examples of anticonvulsant agents?

A

-Pregabalin
-Gabapentin
-Carbamazepine

190
Q

Where does opioids come from? What is the history of its use?

A

-Exudate from the opium poppy
-Has been used for 2,000-6,000 years
-Known to relieve pain, diarrhea, and produce euphoria
-Serturner isolated and puriphied morphine in 1803
-Semisynthetic compounds (Heroin- 1874)
-Fully synthetic opioids (Meperidine- 1939)
-Medicinal and recreational uses firmly established

191
Q

Where are endogenous opioids derived from?

A

Peptides

192
Q

Where are endorphins derived from? What types of endorphins are there? What receptors do they work on?

A

-Derived from proopiomelanocortin (POMC)
-2 types of β-endorphins: β-endorphin-1 and β-endorphin-2
-Primarily µ agonist and also has 𝛿 action

193
Q

Where are enkephalins derived from? What types are there? What receptors do they work on?

A

-Derived from proenkephalin
-Met-ENK
-Leu-ENK
-Met-ENK: µ and 𝛿 agonist
-Leu-ENK: 𝛿 agonist

194
Q

Where are dynorphins derived from? What types are there? What receptors do they work on?

A

-Derived from prodynorphine
-DYN-A
-DYN-B
-Potent 𝜿 agonist and also have µ and 𝛿 action

195
Q

What are the 3 opioid receptors? What therapeutic effects does agonists of these receptors create?

A

-Mu (µ)
-Kappa (𝜿)
-Delta (𝛿)
-Creates spinal and supraspinal analgesia

196
Q

What are other effects of µ agonists?

A

-Sedation
-Respiratory depression this is why opioid overdose can cause death
-Constipation
-Inhibits neurotransmitter release (ACh, dopamine)
-Increases hormonal release (prolactin, growth hormone)

197
Q

What are other effects of 𝜿 agonists?

A

-Sedation
-Constipation
-Psychotic effects

198
Q

What are other effects of 𝛿 agonists?

A

-Increases hormonal release (growth hormone)
-Inhibits neurotransmitter release (dopamine)

199
Q

What are opioid receptor agonists?

A

Activate one or more opioid receptors

200
Q

What are opioid receptor antagonists?

A

Occupy receptors and prevent agonist binding (e.g. Naloxone)

201
Q

What are opioid mixed receptor agonist-antagonists?

A

Agonist activity at one type of receptor and antagonist activity at another type of receptor (e.g. Buprenorphine)

202
Q

What is the difference between and opioid and an opiate?

A

-Opioid: any naturally occurring, semi-synthetic, or fully synthetic compound that binds to opioid receptors and share the properties of one or more of the naturally occurring endogenous opioids
-Opiate: any naturally occurring opioid derived from opium

203
Q

What are examples of strong opioid receptor agonists? What receptor do they primarily interact with?

A

-Strong agonists are used to treat severe pain
-Interact primarily with µ receptors
-Fetanyl (Duragesic, Sublimaze)
-Morphine (MS Contin)
-Hydromorphone (Dilaudid)
-Oxymorphone (Numorphan)
-Meperidine (Demerol)
-Methadone (Dolophine)
-Oxycodone (Oxycontin)

204
Q

What are examples of mild to moderate opioid receptor agonists?

A

-These are used for mild to moderate pain
-Codein
-Hydrocodone (Hycodan)

205
Q

What are examples of mixed opioid receptor agonist-antagonist?

A

-Some of these bind to 𝜿 receptors while block or partially block µ receptors making them µ receptor antagonists or partial agonists
-Buprenorphine (Buprenex)
-Nalbuphine (Nubain)

206
Q

What are examples of opioid receptor antagonists?

A

-Particular affinity for µ
-Naloxone (Narcan)
-Naltrexone (ReVia, Vivitrol)

207
Q

What are other uses of Naltrexone?

A

-Can be used in conjunction with behavioral therapy to maintain an opioid-free state for recovering opioid addicts
-Can be used in treating alcohol dependence

208
Q

What is the mechanism of action of opioids?

A

-Bind to opioid receptors
-Two well established direct G-protein coupled actions
-They close voltage gated Ca2+ channels on presynaptic nerve terminals which reduces neurotransmitter release (glutamate and substance P)
-They open K+ channels on postsynaptic neurons and hyperpolarize them and inhibit postsynaptic neurons

209
Q

What are the sites of putative action of opioid analgesics?

A

-Primary afferent nociceptor terminals
-Dorsal horn
-Ventral posterolateral nucleus (VPL) of the thalamus
-Possibly in the amygdala as well

210
Q

What are the key pharmacological actions of morphine and other opioid agents?

A

-Analgesia
-Respiratory depression
-Spasm of smooth muscle of the gastrointestinal (GI) and genitourinary (GU) tracts, including the biliary tract (bile ducts)
-Pinpoint pupils (miosis)

211
Q

What is a way to determine if someone if overdosing from opioids or another drug?

A

If someone’s pupils are constricted/has pinpoint pupils, they are overdosing from opioids

212
Q

What are the CNS effects of opioids?

A

-Analgesia
-Euphoria
-Sedation
-Respiratory depression
-Cough suppression
-Miosis
-Truncal rigidity
-Nausea and vomiting
-Body temperature
-Sleep disturbances

213
Q

What are the effects of opioids on the cardiovascular system?

A

-Typically no significant effects
If there are effects:
-Bradycardia
-Hypotension
-Increased cerebral blood flow
-Increased intracranial pressure (opioids contraindicated in brain injury patients)

214
Q

What are the effects of opioids on the gastrointestinal system?

A

Constipation

215
Q

What are the effects of opioids on the biliary tract?

A

Biliary colic (blockage of bile ducts- contraction of biliary smooth muscles)

216
Q

What are the effects of opioids on the renal system?

A

-Decreased renal function
-Anti-diuretic effect
-Urinary retention

217
Q

What are the effects of opioids on the endocrine system?

A

-Decreased testosterone with chronic use
-Decreased libido, energy, and mood
-Dysmenorrhea or amenorrhea in women

218
Q

What are the effects of opioids on the skin?

A

-Pruritis (itchy feeling of the skin)
-Produce flushing and warming of the skin accompanied sometimes by sweating, urticaria (itchy red bumps), and itching
-Peripheral histamine release

219
Q

What is the duration of action of fentanyl?

A

1 hour

220
Q

What is the duration of action of methadone?

A

8 hours

221
Q

What is the duration of action of morphine?

A

4 hours

222
Q

What is the duration of action of oxycodone?

A

4 hours

223
Q

What is the duration of action of codeine?

A

4 hours

224
Q

What is the duration of action of hydrocodone?

A

4 hours

225
Q

What is the duration of action of tramadol?

A

4 hours

226
Q

What is the duration of action of buprenorphine?

A

5 hours

227
Q

What is the duration of action of naloxone?

A

2 hours

228
Q

What is the duration of action of naltrexone?

A

24 hours

229
Q

What are the clinical used for opioids?

A

-Analgesia
-Acute pulmonary edema
-Cough
-Diarrhea
-Anesthesia

230
Q

What are the signs & symptoms of opioid overdose?

A

-Euphoria
-Unconsciousness
-Respiratory depression
-Miosis
-Pulmonary edema
-Seizures
-Hypothermia
-Death

231
Q

What is the opiate toxicity triad?

A

-CNS depression (coma)
-Respiratory depression (cyanosis)
-Pupillary miosis

232
Q

What are adverse effects with chronic opioid use?

A

-Hypogonadism
-Immunosuppression
-Increased feeding
-Increased growth hormone secretion
-Withdrawal effects
-Tolerance, dependence
-Abuse, addiction
-Hyperalgesia
-Impairment while driving

233
Q

What does a person develop tolerance for on opioids?

A

-Analgesic effect
-Sedating effect
-Respiratory depressant effects
-Antidiuretic, emetic, and hypotensive effects

234
Q

What tolerance does not develop on opioids?

A

-Mitotic effect
-Convulsant effect
-Constipating effect

235
Q

What is physical dependence of opioid use?

A

An invariable accompaniment of tolerance to repeated administration pf an opioid of the µ type

236
Q

What are symptoms of withdrawal to opioids?

A

-Rhinorrhea
-Lacrimation
-Yawning
-Chills
-Gooseflesh
-Hyperventilation
-Hyperthermia
-Mydriasis
-Muscular aches
-Vomiting
-Diarrhea
-Anxiety
-Hostility

237
Q

What is psychological dependence of opioids or other drugs?

A

Addiction

238
Q

What are benefits of patient controlled anesthesia?

A

-May allow better pain control with fewer side effects
-Requires patient awareness and cognitive ability
-Increases patient satisfaction

239
Q

What are special concerns for rehab with opioids?

A

-Schedule therapy when drugs reach peak
-Consider respiratory depression
-Constipation: pts may be uncomfortable
-Withdrawal symptoms or addiction

240
Q

What are non-opioid analgesics?

A

-Non-steroidal anti-inflammatory drugs (NSAIDs)
-Acetaminophen (Tylenol)

241
Q

What are the primary therapeutic effects of NSAIDs?

A

-Analgesic
-Anti-inflammatory
-Antipyretic (reduces body temp.)
-Anticoagulant
-Anticancer (colorectal cancer)

242
Q

What are prostaglandins (PGs)?

A

-Small lipid compounds produced in almost all cells
-Cells begin to synthesize PGs in response to damage

243
Q

What are the function of PGs?

A

-In the hypothalamus: thermoregulation
-Responsible for coagulation
-PGs can exaggerate pain
-Promote inflammation
-Abnormal coagulation

244
Q

How are PGs synthesized?

A

Prostaglandings are made by an enzymatic reaction where cyclooxygenase (COX-1, COX-2) converts arachidonic acid into prostaglandins

245
Q

What is the mechanism of action of NSAIDs?

A

NSAIDs inhibit cyclooxygenase (COX-1, COX-2) from converting arachidonic acid to prostaglandins

246
Q

What are non-selective NSAIDs? What are examples of them?

A

-Inhibit COX-1 and COX-2
-Diclofenac
-Ibuprofen
-Naproxen

247
Q

What are COX-2 selective NSAIDs? What are examples of them?

A

-Specifically inhibit COX-2
-Celecoxib (Celebrex)
-Rofecoxib

248
Q

Why if Rofecoxib banned?

A

Due to cardiovascular side effects

249
Q

What are the functions of the prostaglandins that COX-1 produces?

A

-PGs that mediate homeostatic functions
-Constitutively expressed
-Homeostatic protection of gastric mucosa
-Platelet activation
-Renal functions
-Macrophage differentiation

250
Q

What are the functions of the prostaglandins that COX-2 produces?

A

-PGs that mediate inflammation, pain, and fever
-Induced mainly in sites of acute inflammation by cytokines
-Pathologic inflammation
-Pain
-Fever
-Dysregulated proliferation

251
Q

What are common NSAIDs?

A

-Aspirin
-Ibuprofen
-Naproxen
-Indomethacin
-Meloxicam
-Diclofenac
-Celecoxib

252
Q

What are common side effects of NSAIDs?

A

-Nausea and vomiting
-Diarrhea
-Constipation
-Decreased appetite
-Rash
-Dizziness
-Headache
-Drowsiness

253
Q

What are side effects associated with chronic use of NSAIDs?

A

-Kidney failure
-Liver failure
-Ulcers

254
Q

What are uncommon side effects of NSAIDs?

A

-Prolonged bleeding after injury or surgery
-Fluid retention/edema

255
Q

What is the benefit of selective COX-2 NSAIDs vs non-selective NSAIDs?

A

-May decrease pain & inflammation with less toxicity (less gastritis)
-Better for long term use

256
Q

What are the benefits of acetaminophen?

A

-Analgesic and antipyretic effects
-No gastric irritation
-No anticoagulant effects
-No anti-inflammatory effects

257
Q

What are side effects of acetaminophen if taken in high doses?

A

Liver toxicity

258
Q

What are indications for acetaminophen?

A

-Frequently 1st drug used to control pain in early stages of OA and other MSK conditions that do not have an inflammatory
-Children and teenagers

259
Q

What is a contraindication for acetaminophen?

A

-Reyes syndrome
-This syndrome is a rare but serious condition that causes confusion, swelling in the brain, and liver damage

260
Q

What is the mechanism of action of acetaminophen?

A

-Not fully understood
-Inhibits cyclooxygenase (COX)
-Unclear why it does not exert anticoagulant & anti-inflammatory effects: thought to preferentially inhibit CNS PG production vs peripheral

261
Q

Why can high doses of acetaminophen cause liver toxicity?

A

-Acetaminophen metabolizes into a toxic intermediate
-It is quickly detoxified and eliminated via the urine
-High doses can result in accumulation of the toxic intermediate with subsequent toxicity to liver proteins

262
Q

What are common acetaminophen + opioid combinations?

A

-Lortab, Lorcet: hydrocodone + acetaminophen
-Darvocet: propoxyphene + acetaminophen
-Percocet: oxycodone + acetaminophen

263
Q

What are physical therapy considerations for patients on NSAIDs or acetaminophen?

A

-Pain masking
-GI effects
-Cardiovascular risks
-Renal effects
-Hepatotoxicity
-Therapy timing
-Patient education
-Monitoring side effects

264
Q

What are steroidal anti-inflammatory drugs (SAIDs)?

A

-Glucocorticoids
-Derived from cholesterol

265
Q

What three 1° adrenal steroids does the adrenal cortex produce?

A

-Glucocorticoids (cortisol, corticosterone)
-Mineralocorticoids (aldosterone)
-Sex hormones

266
Q

What are the physiological functions of glucocorticoids?

A

-Control glucose metabolism
-Controls the body’s ability to deal with stress
-Decrease inflammation
-Suppress the immune system

267
Q

What is the precursor to steroids?

A

Cholesterol

268
Q

What is the mechanism of action of glucocorticoids?

A

-Act on inflammatory cells
-Drug binds to glucocorticoid receptors in cytoplasm
-Drug-receptor complex travels to nucleus of the cell and alters gene expression
-Decreases expression of inflammatory proteins
-Increases expression of anti-inflammatory proteins

269
Q

What is the clinical use of glucocorticoids?

A

-Endocrine conditions: normalize adrenal cortical hypofunction
-Nonendocrine conditions: RA, tenosynovitis, myositis, collagen disease

270
Q

How are glucocorticoids for nonendocrine conditions such as RA or tenosynovitis administered?

A

Injections into specific tissues to help localize effects

271
Q

What are some common glucocorticoids?

A

-Cortisone
-Dexamethasone
-Prednisone
-Hydrocortisone

272
Q

What glucocorticoid is typically used for anaphylaxis?

A

Dexamethasone

273
Q

What are methods of administering glucocorticoids?

A

-Oral: systemic
-Injections: local
-Dose packs: provide large dose but tapers off over 4-5 day period

274
Q

What are adverse effects of glucocorticoids?

A

-Adrenocortical suppression
-Peptic ulcers
-Drug induced Cushing Syndrome
-Adrenal crisis/shock
-Breakdown of supporting tissues
-Decreases body’s ability to absorb calcium and can lead to osteoporosis

275
Q

What are side effects of glucocorticoids?

A

-Headache
-Irregular heartbeat
-Sweating
-Dizziness
-Irritability

276
Q

How does breakdown of supporting tissues occur from glucocorticoid use?

A

-Bone, ligaments, tendons, and skin are subject to a wasting effect from prolonged use
-Inhibits the genes responsible for production of collagen and other tissue components by increasing the expression of substances that promote breakdown of bone, muscle, etc.
-Interferes with muscle protein synthesis
-Can cause skeletal muscle atrophy

277
Q

What are the signs & symptoms of drug induced Cushing Syndrome?

A

-Roundness and puffiness in the face
-Fat deposition and obesity in the trunk
-Muscle wasting in extremities
-Hypertension
-Osteoporosis
-Increased body hair
-Glucose intolerance

278
Q

What are signs & symptoms of adrenal crisis/shock?

A

-Vasodilation of the organs
-Vascular collapse
-Severe hypotension
-Pain in legs, low back, abdomen
-Low BP, syncope
-Vomiting and diarrhea
-Hyperkalemia
-Hyponatremia

279
Q

How can glucocorticoids lead to osteoporosis?

A

-Shifts the balance of bone metabolism leading to increased breakdown
-Stimulates osteoclast-induced bone resorption
-Inhibits osteoblast-induced bone formation

280
Q

What are other side effects of glucocorticoids?

A

-Salt/water retention
-Increased infection
-Gastric ulcers due to decreased good PGs in stomach
-Glucose intolerance
-Glaucoma-effect vitreous humor drainage
-Adrenal suppression

281
Q

What are PT considerations for glucocorticoid use?

A

-Increased risk of fractures, falls, and infection
-Strengthening exercises to maintain muscle mass
-Encourage weight bearing activities such as walking
-Inspection for skin breakdown
-Monitor blood pressure

282
Q

What is arthritis?

A

-A general term that refers to a group of more than 100 disorders affecting the joints
-Inflammation, pain, and stiffness in the joint

283
Q

What are different types of arthritis?

A

-Osteoarthritis
-Rheumatoid arthritis
-Psoriatic arthritis
-Gout
-Ankylosing spondylitis

284
Q

What is rheumatoid arthritis?

A

-Autoimmune disorder
-The body’s immune system attacks the joints

285
Q

What are signs and symptoms of rheumatoid arthritis?

A

-Often affects joints symmetrically
-Commonly affects wrists, fingers, knees, feet, and ankles
-Usually starts at middle age
-Joints may be swollen, warm, and puffy
-Morning stiffness > 30 minutes
-Systemic inflammation
-Pain worse after periods of inactivity
-May be accompanied by fever, fatigue, and weight loss

286
Q

What drugs can be used to treat RA?

A

-Disease modifying antirheumatic drugs (DMARDS)
-NSAIDs
-Corticosteroids
-Biologic agents

287
Q

What is osteoarthritis?

A

-Degenerative disorder
-Wear and tear of the joint cartilage

288
Q

What are the signs and symptoms of osteoarthritis?

A

-Usually affects weight bearing joints (hips, knees, spine)
-Usually starts at middle age or older adults
-Morning stiffness < 30 minutes
-Reduced ROM
-Inflammation localized to affected joint
-No systemic symptoms

289
Q

What drugs can be used to treat osteoarthritis?

A

-Acetaminophen
-NSAIDs
-PT
-Weight management
-Joint injections
-Surgery

290
Q

What is typically the first-line treatment for pain relief in osteoarthritis?

A

Acetaminophen

291
Q

What is the most significant concern with high doses of acetaminophen?

A

Liver toxicity

292
Q

What are common side effects from acetaminophen?

A

-Nausea or vomiting
-Loss of appetite
-Allergic reactions like skin rash, itching, or hives

293
Q

What is the maximum recommended daily dose of acetaminophen?

A

4,000mg for adults but lower limits are often recommended

294
Q

What are the most common NSAIDs used for osteoarthritis?

A

-Ibuprofen
-Naproxen sodium
-Celecoxib
-Diclofenac
-Meloxicam

295
Q

What is the mechanism of action of hyaluronic acid injections for osteoarthritis?

A

-Hyaluronic acid is a polysaccharide similar to the natural joint fluid that lubricates the joint
-When injected into the joint, it acts as a lubricant and shock absorber
-Helps to reduce pain and friction in the joint

296
Q

What are the side effects of hyaluronic acid injections?

A

-Pain at the injection site
-Joint stiffness
-Headache

297
Q

What is the mechanism of action of chondroitin sulfate for osteoarthritis?

A

-Chondroitin sulfate is one of the building blocks of cartilage
-It is believed to help prevent the breakdown of cartilage and stimulate its repair mechanism
-Also thought to have anti-inflammatory properties and improve the consistency of synovial fluid

298
Q

What are side effects of chondroitin sulfate?

A

-Stomach pain
-Nausea
-Diarrhea
-Constipation
-Headache
-Swelling of the eyelids or legs

299
Q

What are physical therapy considerations when working with patients with osteoarthritis that are taking medication?

A

-Medication schedule
-Monitor for overuse
-Educate on medication limits
-Check for side effects
-Patient feedback

300
Q

What is the prevalence of rheumatoid arthritis?

A

1% of the population and is more common in women

301
Q

What is the pathogenesis of RA?

A

-Antigen presenting cells process and present antigens to T cells, which may stimulate B cells to produce antibodies and osteoclasts to destroy and remove bone
-Macrophages stimulated by immune response can stimulate T cells and osteoclasts to promote inflammation
-Activated T cells and macrophages release factors that promote tissue destruction, increase blood flow, and result in cellular invasion of synovial tissue and fluid

302
Q

What are the main pro-inflammatory cytokines that are involved in the pathogenesis of RA?

A

-Interleukin-1 (IL-1)
-Tumor necrosis factor-⍺ (TNF-⍺)

303
Q

What is the difference between traditional Disease Modifying Anti-Rheumatic Drugs (DMARDs) and targeted DMARDs?

A

-Traditional DMARDs restrict your immune system broadly
-Targeted DMARDs block precise pathways inside immune cells

304
Q

How are biologic drugs produced? How do they work?

A

-Produced by living cells
-Work on individual immune proteins called cytokines

305
Q

What is the general strategy of biologic drugs for RA?

A

-Inhibit autoimmune response underlying RA
-Inhibition of cytokines
-Inhibit cellular activation

306
Q

What is the mechanism of action of Methotrexate for RA?

A

Inhibits dihydrofolate reductase enzyme, which reduces nucleotide synthesis

307
Q

What are the adverse effects of Methotrexate?

A

-Hepatic fibrosis
-Rash
-Thrombocytopenia
-Leukopenia

308
Q

What is the mechanism of action of hydroxychloroquine for RA? What are the adverse effects?

A

-Not well understood
-Thought to be an immunomodulator
-Retinal damage
-Rash

309
Q

What is the mechanism of action of Leflunomide for RA? What are the adverse effects?

A

-Inhibits pyrimidine synthesis
-Hepatitis

310
Q

What is the mechanism of action of Sulfasalazine for RA? What are the adverse effects?

A

-Not well understood
-Rash
-Photosensitivity

311
Q

What are common TNF-⍺ blockers used for RA?

A

-Etanercept
-Infliximab
-Adalimumab
-Certolizumab
-Golimumab

312
Q

What are adverse effects of TNF-⍺ blockers?

A

-Local injection site reactions
-Infection
-Immune reactions
-Malignancy

313
Q

What are common non-TNF-⍺ biologics that are used to treat RA?

A

-Rituximab
-Abatacept
-Tocilizumab
-Baricitinib
-Anakinra

314
Q

What are physical therapy considerations for patients on medications for RA?

A

-DMARDs can cause fatigue or reduced tolerance to exercise
-Injection site
-Steroids can increase risk of fx
-Pain masking: monitor for signs of overuse
-Understanding interactions of medications and PT

315
Q

What is osteoporosis?

A

A bone disease characterized by a decrease in bone density and an increases risk of fractures

316
Q

What is the prevalence of osteoporosis?

A

-10 million diagnosed with osteoporosis
-34 million with low bone density
-1.5 million fractures annually

317
Q

What are risk factors for osteoporosis?

A

-Postmenopausal women
-Old age
-Medications
-Endocrine disorders
-Inflammatory arthropathy
-Hematopoietic disorders
-Nutrition disorders

318
Q

What is used to diagnose osteoporosis and measure bone density?

A

Dual X-ray absorptiometry (DEXA)

319
Q

What are the different bone cell types?

A

-Osteogenic cell: bone stem cell
-Osteoblast: bone forming cell
-Osteoclast: bone resorption
-Osteocyte: maintains bone tissue

320
Q

How does parathyroid hormone effect bone density?

A

-In low and intermittent doses, it increases bone formation
-In excess doses, it increases bone resorption

321
Q

What stimulates the release of parathyroid hormone? What does this cause?

A

-Low Ca2+ levels in the blood trigger the release of PTH which increases bone resorption to release calcium from bone tissue
-PTH release increases renal reabsorption of Ca2+

322
Q

How does vitamin D effect bone formation?

A

It stimulates intestinal absorption of Ca2+ and phosphate

323
Q

How does calcitonin effect bone tissue?

A

Lowers blood levels of Ca2+ and phosphate by inhibiting osteoclast activity

324
Q

What is involved in normal bone homeostatis?

A

-PTH binds to receptors on osteoblasts
-Osteoblasts secrete RANKL and OPG (decoy receptor for RANKL)
-Osteoclasts are activated by RANKL
-There is a balance between osteoblast activity and osteoclast activity

325
Q

What is involved in osteoporsis bone formation and resorption physiology?

A

-Osteocytes upregulates RANKL and down regulates OPG synthesis
-RANKL binds to osteoclasts and increases osteoclast proliferation
-Activated osteoclasts cause significant resorption

326
Q

What are some common drugs that are used to treat osteoporosis?

A

-Bisphosphonates
-Selective estrogen receptor modulators (SERMs)
-Calcitonin
-RANKL inhibitors
-Parathyroid hormone (low doses)
-Calcium and vitamin D supplements

327
Q

What is the mechanism of action of bisphosphonates?

A

-Binds to osteoclasts and promotes apoptosis
-Binds to hydroxyapatite and prevents osteoclast activity

328
Q

What are common bisphosphonates used to treat osteoporosis?

A

-Alendronate
-Risedronate
-Ibandronate
-Zoledronic acid

329
Q

What are side effects of bisphosphonates?

A

-GI disturbances: acid reflux
-Osteonecrosis of the jaw
-Atypical femur fractures

330
Q

What are special instructions for patients taking bisphosphonates? Why?

A

-Swallow whole with water 30 minutes before breakfast
-Sit or stand upright for 30 minutes after taking the tablet
-To avoid gastric reflux

331
Q

What is the mechanism of action of selective estrogen receptor modulators (SERMs)?

A

Mimic estrogen in bone, reducing bone resorption without stimulating breast or uterine tissue

332
Q

What are common side effects of SERMs?

A

-Hot flashes
-Leg cramps
-Increased risk of venous thromboembolism

333
Q

What is a common SERM used to treat osteoporosis?

A

Raloxifene

334
Q

What is the mechanism of action of calcitonin?

A

Inhibits osteoclast activity

335
Q

What are common side effects of calcitonin?

A

-Nasal irritation (with nasal spray)
-Hot flashes

336
Q

What is a common calcitonin used to treat osteoporosis?

A

-Miacalcin
-Salmon calcitonin

337
Q

What is the mechanism of action of parathyroid hormone analogs?

A

Stimulates osteoblast activity

338
Q

What are common side effects of parathyroid hormone analogs?

A

-Leg cramps
-Dizziness
-Nausea

339
Q

What are common parathyroid hormone analogs used to treat osteoporosis?

A

-Teriparatide
-Abaloparatide

340
Q

What is the mechanism of action of monoclonal antibodies for osteoporosis?

A

Binds and inhibits RANKL, reducing osteoclast activity

341
Q

What are some common side effects of monoclonal antibodies used to treat osteoporosis?

A

-Skin reaction at the injection site
-Osteonecrosis of the jaw
-Hypocalcemia

342
Q

What is a common monoclonal antibody that is used to treat osteoporosis?

A

Denosumab (Prolia, Xgeva)

343
Q

How does low levels of vitamin D effect PTH?

A

Low levels of vitamin D can stimulate the parathyroid gland to produce more PTH (secondary hyperparathyroidism)

344
Q

What is the role of calcium in bone?

A

It forms hydroxyapatite crystals, which gives bone its hardness

345
Q

What are PT considerations for patients taking bisphosphonates?

A

-Be aware of GI issues
-Have pt take medication at least 1 hour prior to session
-Rare risk of atypical femur fracture or osteonecrosis of the jaw

346
Q

What are PT considerations for patients taking SERMs?

A

-Hot flashes or leg cramps
-Watch for signs of venous thromboembolism

347
Q

What are PT considerations for patients taking calcitonin?

A

Monitor for nasal irritation side effects

348
Q

What are PT considerations for patients taking parathyroid hormone analogs?

A

Monitor for leg cramps and dizziness

349
Q

What are PT considerations for patients taking monoclonal antibodies?

A

-Monitor for joint pain: back and/or arm or leg pain
-Pts may have low calcium levels

350
Q

What are schedule I drugs?

A

-Drugs or substances that have no currently accepted medical use and a high potential for abuse
-Ex: heroin, LSD, marijuana, MDMA

351
Q

What are schedule II drugs?

A

-Drugs or substances with a high potential for abuse but has accepted medical use
-Ex: fetanyl, cocaine, oxycodone, morphine, etc.

352
Q

What are schedule III drugs?

A

-Drugs with moderate or lower abuse potential compared to schedule II
-Ex: anabolic steroids, testosterone, codeine, ketamine, etc.

353
Q

What are schedule IV drugs?

A

-Drugs with lower abuse potential compared to schedule III
-Ex: diazepam, lorazepam, tramadol, etc.

354
Q

What are schedule V drugs?

A

-Drugs with the lowest abuse potential
-Ex: low dose opioids in cough medicine, pregabalin, lamotil, etc.

355
Q

What is pharmacokinetics?

A

What the body does to the drug

356
Q

What is pharmacodynamics?

A

What the drug does to the body

357
Q

What are the principles of pharmacokinetics?

A

-Absorption (stomach/intestines)
-Distribution
-Metabolism (liver)
-Excretion (kidney)

358
Q

What is the median effective dose (ED50)?

A

Dose at which 50% of the population responds to the drug in a specific manner (positively)

359
Q

What is the median toxic dose (T50)?

A

Dose at which 50% of the population experiences adverse effects

360
Q

What is the median lethal dose (L50)?

A

Dose that causes death in 50% of the population

361
Q

What is the therapeutic index (TI)?

A

-Indicator of the drugs safety
-Median toxic dose (TD50) divided by median effective dose (ED50)
-TI= TD50/ED50
-The greater the TI, the safer the drug

PHTH 561: Pharmacology (5 decks)

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