Opioids

130

non fatal > fatal

45
70

50

1990s

2010

2013

-Opioids used when a person's endogenous opioid or reward system is not enough to combat the experience of pain
-Exogenous opioids given in a larger amount than the body normally produces
-Exogenous opioids attach to same opioid receptors in the body and cause a large release of dopamine
-Opioids block reuptake of dopamine, therefore the dopamine receptors are continously activated

-opioids attach to receptors and release dopamine which results in inhibition of pain experience
-opioids and dopamine agonist (DA) return to homeostatic levels after danger input gone via reuptake
-patients with persistent pain are primed to develop misuse because of already existing physiological changes

overly sensitized long term depression
decreased excretion of dopamine in response to same levels of opioids

released via DA and danger messages
forms "pain" memories
increased with prolonged use

helps protect brain from addiction
decreased BDNF

Still multimodal
Still biopsychosocial
likely to include many healthcare providers
manual therapy
exercise

Neurophysiological response - decreasing pain modulation circuit
Different types of manual therapy effective through different mechanisms
-massage therapy elicits an oxytocin repsonse, utilizes serotonergic and dopaminergic pathways
Different spinal manipulations elicit different neurochemical responses indicative of different descending pain modulation mechanisms
Patients with central sensitization are less likely to benefit from joint mob for pain relief

Benefits of Exercise:
-Increased abstinence rate
-decreased anxiety
-decreased depression
-ease withdrawal symptoms
Exercise more effective in depression reduction in opioid abuse sufferers than alcohol abuse sufferers
Exercise more effective at increasing abstinence rates in opioid abuse than in alcohol abuse

Glutamatergic and dopaminergic signaling
Regulate BDNF
Change concentrations of
-norepinephrine, serotonin, GABA, endocannabinoids
Helps to return DA, Glut, and BDNF to normal levels

moderate levels of exercise most beneficial
chronic high levels of exercise have been shown to create the same neuroadaptations in the brain as drugs of abuse

Thiazide diuretic
Loop diuretic
K+ sparing drugs

blocks Na+ and K+ from being reabsorbed back into the blood
Often ends in -thiazide

act on the loop of henle
reduce NaCl reabsorption
Often ends in -mide

cause Na+ to be excreted but conserves the K+

Antacid drugs for heartburn
H2 Blockers for Heartburn
Proton pump inhibitor of peptic ulcer disease
Gastrointestinal spasms

weak base that neutralizs hydrochloric acid
decreases mucous membrane irritation

blocks receptor cells that allow the release of hydrochloric acid
often ends in -idine
Ranitidine (zantac), cimetidine (tagament)

decrease gastric acid by blocking acid production within the gastric parietal cell
Often ends in -azole
Omeprazole (prilosec)

block the effect of acetylcholine to decrease the amount of acid and stop the spasms
atropine is most common

Bone resorption inhibitor drugs
Estrogen drugs for osteoporosis
Calcium supplements
Salicylate class
Acetaminophen
NSAID's
Cox 2 Inhibitors
Corticosteroid drugs

often ends in -dronate
Ibandronate (Bonivia)

with declining estradiol levels, bone resorption rates increase

calcium with added Vitamin D
Stimulate new bone formation

Aspirin

Analgesic
No anti-inflammatory action

inhibit prostaglandin production
produce analgesic and anti-inflammatory effect
gastric irritability
often ends in -profen
ibuprofen

selectively inhibit the enzyme cyclooxygenase -2 (COX-2)
decreases production of prostaglandins
less gastric irritability
questionable risk for cardiac complications
celebrex

replicate the effect of gluco corticoid hormones secreted by the adrenal gland
powerful anti inflammatory action
often used to treat acute inflammation
-orally (methylprednisolone-medrol dose pack)
-injected into the joint or soft tissue (cortisone)
medication often ends in -one

relax the smooth muscle that surrounds the bronchioles allowing dilation and increased airflow
often ends in -terol or -phylline
Sympathomimetric bronchodilator
Xanthine derviative
Anticholinergic
Corticosteroids
Leuko triene receptor blocker drugs

stimulate beta 2 receptors in the smooth muscle
mimic the action of epinephrine

act directly on the smooth muscle around the bronchioles and stimulate the respiratory centers in the brain

blocks the action of acetylcholine or muscarinic receptors in the smooth muscle

suppress the inflammatory response of the immune system
reduce inflammation and edema associated with asthma and other chronic lung disorders
Do not dilate bronchioles
should not be used in an cute episode
Often ends in - lide, -nide, -lone, and -sone

leukotriene is produced in response to inhaled antigens and causes airway edema, bronchospasm and inflammation
block the action of leukotriene at the receptor level
used to prevent asthma
often end in -lukast: montelukast (singulair)

Hypertension:
Diuretics
Beta Blockers
Alpha Blockers
Calcium Channel Blockers
ACE Inhibitor
Angiotensin II receptor blockers

Hyperlipidemia:
Bile acid sequestrant drugs
HMG - CoA
Hypercholesterolemia and Hypertriglyceridemia

CHF:
Digitalis
Diuretics
ACE Inhibitors

Angina Pectoris:
Nitrate Drugs
Beta Blockers
Calcium Channel blockers

Myocardial Infarct:
Thrombolytic Drugs

Drugs for Bradycardia
Drugs for heart block

antiarrythmic drugs

excretion of Na+ and water lowers total blood volume which lowers blood pressure

block the action of epinephrine at all beta receptors to decrease the heart rate and dilate the blood vessels
often ends in -olol: atenolol (tenormin)

blocks alpha receptors in the peripheral blood vessels causing dilation, thus decreasing BP
often ends in -azosin

block the movement of calcium ions into the heart muscle and smooth muscle of the blood vessels
decreases heart rate, dilates the arteries and lowers blood pressure
often ends in -dipine

blocks enzyme that converts angiotensin I into angiotensin II
Angiotensin II is a vasoconstrictor, when blocked the blood vessels dilate
often ends in -pril: Fosinopril (Monopril)

prevents angiotensin II from binding to and activating receptor on the smooth muscle of the blood vessel
allows vasodilation
often ends in -sartan: Eprosartan (teveten)

lowers cholesterol in blood by binding with bile so it cannot be used to produce more cholesterol

enzyme that is involved in cholesterol production - blocks it
often ends in -statin
Atorvastatin (Lipitor)

reduce serum level of cholesterol
reduce amount oif lipoprotein carrier LDL and HDL
Fenofibrate (Tricor)

makes the heart pump more slowly and more strongly
Digoxin is most common

Increase Na+ and H2O excretion to reduce edema

causes vasodilation which reduces the force the heart must pump against

dilate the coronary arteries
decrease arterial blood pressure
nitroglycerin is most common

decrease heart rate which decreases the need for myocardial oxygen

smooth muscle dilation

dissolves clots

blocks acetylcholine to maintain a slow and normal rhythm
atropine

changes the elctrical impulses from the SA node
Ephedrine

blocks the flow the K+ ions and delays the contraction of the heart muscle

Heparin
Warfarin
Platatet aggregation inhibitor drugs

inhibits clotting factor X

blocks vitamin K and keeps the liver from producing clotting factors

prevents platelets from adhering to the site of injury

thrombolytic enzyme drugs

clot dissolves
often ends in -ase
Streptokinase (Streptase)

drugs for hypothyroidism
drugs for hyperthyroidism

supplemental existing levels of T3 and T4

inhibits the production of T3 and T4

Antianxiety and antidepressant medication

elevate mood and have antihistamine effect that relieves skin sensation, it can produce mild sedation

Antipsychotics
Depressants
Hallucinogens
Stimulates
-Complex + overlapping

block dopamine, histamine, and serotonin receptors in the brain
often ends in -azine
Chlorpromazine (thorazine)

tricyclic antidepressant drugs
selective serotonin reuptake inhibitor

inhibit the reuptake of and prolong the action of norepinephrine or serotonin
increase sensitivity of receptors
often ends in -triptyline or -ipramine
Amitriptyline

block the normal reuptake of free serotonin
often ends in -talopramt or - oxetine
Citalopram (celexa), paroxetine (paxil)

benzodiazepine
antidepressants

bind to several specific receptor sites to provide sedation
often ends in -azepam
Diazepam (valium)

tricyclic antidepressants
SSRI
Norepinephrine Reuptak inhibitor

Antidepressants and or tricyclic antidepressants (TCA's)
Anticonvulsants

amitriptyline and nortriptyline
SSRI not as effective as tricylic antidepressants
reduce transmission in the spinal cord

gabapentin, carbamazepine, clonazepam
stabilizing nerve cells