8.1 Concepts Psych Meds Portage

Pain 2 functions

Warning of imminent danger/something wrong in body

Accompany normal healing process

Time difference between acute and chronic pain

Acute: <6 weeks

Chronic: 3-6 months or >1 month after healing of acute injury

Tolerance

State in which effectiveness of drug is significantly reduced following prolonged use

Body adapts, drug is unable to achieve the same initial physiological effect

Withdrawal

Unpleasant physical and mental symptoms

Physical Dependence

Need to continue taking drug to avoid unwanted side-effects without it

Addiction

Chronic neurobiological disease in which genetic, psychosocial, and environmental factors induce changes in the individual’s behavior to compulsively use drugs despite the harm they may cause

2 categories of analgesics

Opioid and nonopioid

Opioid

Synthetic drugs that bind to the opiate receptors in the brain and relieve pain

Nonopioid

Painkillers that DO NOT work on opioid receptors

NSAIDS - what are they and what 2 functions do they have

NONopioid drug class that are analgesics with anti-inflammatory and antipyretic activity

Neuropathic pain

Resulting from a damaged nervous system or damaged nerve cells

T/F: Neuropathic pain responds well to both opioids and NSAIDS

FALSE - it is very difficult to manage

How is neuropathic pain treated?

It is extremely difficult to manage and is treated with a variety of meds from different classes

Antiseizure, antidepressants, etc

What is the most common neuropathic pain?

Fibromyalgia

Fibromyalgia main symptom

Widespread musculoskeletal pain

Fibromyalgia lesser symptoms

Fatigue and sleep/memory/mood issues

What do researchers think fibromyalgia does to the brain?

Researchers believe that fibromyalgia amplifies painful sensations by affecting the way your brain processes pain signals.

Opioid 3 chemical classes & science names

1) Morphine-like drugs — Phenanthrenes

2) Meperidine-like drugs — Phenylpiperidines

3) Methadone-like drugs — Phenylheptanes

Opioid MOA

Bind to opioid receptors in brain → Analgesic response

They stimulate opioid receptors

Do opioids bind to one receptor? why or why not?

No

Multiple different receptors (mu, kappa, delta)

T/F: Opioids differ in relative potency

TRUE

Morphine Equivalents

Using morphine as standard drug, they compared potency of each opioid.

Opioids with LESS potency than morphine

Codeine

Hydrocodone

Opioids with SAME potency as morphine

Oxycodone

Methadone

Meperidine

Opioids with GREATER potency than morphine

Oxymorphone

Hydromorphone

Fentanyl

Which med is 7x more potent than morphone?

Hydromophone

Which opioid med is available in 72-hour patch?

Fentanyl

Is oxymorphone available in IR or ER?

ER only

Why is Meperidine not recommended for long term use?

Accumulation of toxic metabolites can cause seizures

Which opioid med is primarily used for addiction tx?

Methadone — clinics available

Is hydrocodone typically available in combo with other opioids?

NO — only nonopioids like acetaminophen and ibuprofen

What is Codeine typically used in combo with?

Other nonopioids

Or drugs that are used for cough suppressant

What are some major adverse effects (besides abuse) of opioids and what is this caused by?

Histamines are released

Itching, rash, hemodynamic changes (flushing, orthostatic HypoTN)

Which opioids release the most histamine? The least?

Most: Morphine-like (Phenanthrenes)

• Morphine, hydromorphone, oxymorphone, codeine, hydrocodone, oxycodone

Least: Meperidine-like (Phenylpiperidines)

• Meperidine, fentanyl

Most serious adverse event (besides abuse) for opioids

CNS depression → Respiratory Depression

Typical cause of death from opioids

Less serious but common side effects with opioid meds

GI tract — N/V/D

Why do opioids cause GI tract issues? Why is constipation occuring?

When the GI opioid receptors are stimulated → CTZ is triggered → N/V & constipation occur

Constipation occurs because opioids slow peristalsis and increase the absorption of water from the intestines.

2 opioid antagonists to treat opioid overdose

Naloxone and Naltrexone

Naloxone is available as…

Narcan (nasal spray) and Evzio (autoinjector)

and

OTC

Opioid drug interactions

CNS depressants — respiratory depression

(Barbiturates, Benzos, Alcohol)

Name 5 FDA approved indications for NSAIDS

Acute gout	Mild to moderate pain
Acute gouty arthritis	Osteoarthritis
Ankylosing spondylitis	Primary dysmenorrhea
Bursitis	Rheumatoid arthritis
Fever	Tendinitis
Juvenile rheumatoid arthritis	Various ophthalmic uses

Inflammation

Localized protective response stimulated by injury to tissues that destroy, dilute, or wall off both the injurious agent and injured tissue

Causes enhanced blood flow to the site of injury

Signs of Inflammation

Pain, fever, redness, swelling, and loss of function.

2 pathways arachidonic acid can be metabolized

(1) the prostaglandin pathway

(2) the leukotriene pathway

Prostaglandin Pathway

Involved cyclooxygenase (COX) that converts arachidonic acid into various prostaglandins →

Increase vasodilation and vasopermeability → this is inflammation

Increases the action of other proinflammatory substances like histamine and bradykinin

Leukotriene pathway

Involves lipoxygenase

Converts the AA to various leukotrienes

this increases inflammatory response

NSAID MOA

Either inhibit Leukotriene or Prostaglandin pathway →

Block COX

(LOL COX-block)

COX-1

Maintain intact GI tract

COX-2

Conversion of prostaglandins that lead to inflammation

NSAID inhibition of COX-1

Ulcerogenic — Puts pt at risk for GI bleed

Reduces Thromboxane A2 (promotes platelet aggregation)

NSAID Adverse events

Heartburn, GI bleeds, AKI, increased risk of MI or stroke

NSAIDS Drug Interactions

Anticoagulants: Increased bleed risk

Corticosteroids: Increased ulcer risk

ACE-Inhibitors: Reduced hypotensive and diuretic effects

Diuretics: Inhibiting prostaglandin synthesis

Gabapentin MOA

Build up GABA in brain

Minimize brain activity that is signalling sensation of pain

Gabapentin adverse events

Dizziness, drowsiness, nausea, visual and speech changes, and edema.

Gabapentin Drug interactions

Increased CNS depression when combined with alcohol.

Pregabalin MOA

Binds to Alpha2-Delta receptor sites

Affects Ca channels in the CNS tissue

Pregabalin Adverse events

Dizziness, drowsiness, peripheral edema, and blurred vision.

Pregabalin drug interaction

none but caution w/ CNS depressive/sedating drugs

Milnacipran Drug Class

Selective Serotonin adn Norepinephrine Reuptake Inhibitor

SNRI

Milnacipran (Savella) Indications

Fibromyalgia

Milnacipran (Savella) MOA

Potent inhibitor of Norepinephrine and Seroonin Reuptake

Does not affect uptake of dopamine/other neurotransmitters

Milnacipran (Savella) Adverse Events

Nausea, headache, constipation, dizziness, insomnia, hot flush, excessive sweating, vomiting, palpitations, heart rate increased, dry mouth, and hypertension.

Milnacipran (Savella) Drug Interactions

Digoxin: Hemodynamic effects — HypoTN and Tachycardia

Clonidine: Inhibit anti-HTN effect

CNS drugs: CNS depression