Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
68 Cards in this Set
- Front
- Back
|
Describe Opiods main Mechanism of Action
|
Opiods bind to opiod G-protein coupled receptors
-Inhibit afferent pain transmission in ascending pain pathways (spinothalamic tract) |
|
|
What is the main opiod analgesic drug
|
Morphine
Has natural, semisynthetic (drug has a precursor that is naturally occurring & then is further refined synthetically, & synthetic forms |
|
|
What is morphine used for
|
1. Moderate/Severe Pain control (most common)
2. Cough suppression 3. Component of anesthesia 4. Decrease GI motility 5. Adjunct for pulmonary edema --Can be abused |
|
|
How do opiods affect the pain pathways pre & post-synaptically
|
Presynaptic: G-proteins inhibit Ca+ entry and cAMP release, causing less NT release
Postsynaptic: G proteins open k+ channels (K+ outflow) & hyperpolarize the membrane--making it harder to excite the neuron |
|
|
Describe Opiods main Mechanism of Action
|
Opiods bind to opiod G-protein coupled receptors
-Inhibit afferent pain transmission in ascending pain pathways (spinothalamic tract) |
|
|
What is the main opiod analgesic drug
|
Morphine
Has natural, semisynthetic (drug has a precursor that is naturally occurring & then is further refined synthetically, & synthetic forms |
|
|
What is morphine used for
|
1. Moderate/Severe Pain control (most common)
2. Cough suppression 3. Component of anesthesia 4. Decrease GI motility 5. Adjunct for pulmonary edema --Can be abused |
|
|
How do opiods affect the pain pathways pre & post-synaptically
|
Presynaptic: G-proteins inhibit Ca+ entry and cAMP release, causing less NT release
Postsynaptic: G proteins open k+ channels (K+ outflow) & hyperpolarize the membrane--making it harder to excite the neuron |
|
|
What is an endogenous opiod
|
Body's natural way of using opiods
Enkephalins, endorphins, and dynorphing are examples of endogenous opiods |
|
|
When are endogenous opiods released
|
Released during stress or for pain control
|
|
|
What are the 3 major types of opiod receptors
|
1. Mu
2. Kappa 3. Delta |
|
|
Describe Mu receptors
|
Have the strongest analgesic effect but cause the most different side effects & most severe ones at that
Include Decreased RR, constipation, and increased dependance |
|
|
Describe Kappa receptors
|
Fxn in analgesia but not as serious side effects as Mu
Include sedation, hallucination--not as severe |
|
|
Describe Delta receptors
|
Have analgesic effect but have very minor side effects--increased hormonal release
|
|
|
What type of receptors do opiods bind to
|
Opiod G-Protein coupled receptors in CNS (and possibly PNS)
|
|
|
Give the 2 was opiods decrease pain
|
1. Inhibit afferent pain transmission in ascending pain pathways
2. Active descending pain control pathways via disinhibition |
|
|
What is disinhibitition
|
Inhibition of the initial inhibition during resting state--so net result is facilitation
|
|
|
Describe the disinhibition that opiods cause
|
Nerves in the PAG region are normally inhibiting descending pain control--when this inhibition is inhibited (disinhibition) pain control occurs via opiods
|
|
|
Do exogenous opiods work in the same way as endogenous
|
They bind to the same receptors--they make work together with endogenous opiods on peripheral nerve terminals causing decreased excitability of primary nerve endings that transmit pain signals to the CNS
|
|
|
Give some adverse effects of opiods
|
1. Sedation
2. Euphoria (possible) 3. Respiratory depression--dec RR (especially if pt has another co-morbidity) 4. May cause additional CV problems--like OH 5. GI distress/constipation |
|
|
Give main administration routes for opiods
|
1. Oral--less effective for severe pain
2. Parenteral--IV (Use PCA pump for safety) -Epidural, intrathecal, patches (transdermal) |
|
|
Where are opiods mainly metabolised
|
Inactivated in the liver
|
|
|
What are two important things for effective txt of pain
|
Route & dosing schedule
|
|
|
Give possible problems with opiod use
|
1. Addiction--compulsive drug use
2. Tolerance--need an increase in drug does to have the same functional effect d/t changes in receptor sensitivity or enzyme induction 3. Physical dependence--occurs when onset of withdrawal occur with discontinued use of drug |
|
|
Opiod Withdrawal symptoms
|
1. Flu-like symptoms
2. Insomnia 3. Irritability 4. Tachycardia 5. Uncontrollable yawning 6. Muscle aches--treatable by PT Elimination of physical symptoms does not mean the pt no longer desires the drug |
|
|
Describe the different opiod types
|
1. Strong Agonists (Mu Agonist)
-Morhpine--severe pain 2. Mild-to-moderate Agonists -Codeine (generic)--moderate pain 3. Mixed agonist-antagonists (stimulate kappa or delta receptors but block or only partially stimulate Mu) 4. Antagonists--binding to opiod receptor nut not causing a fxn effect |
|
|
Give mechanism of codeine
|
Stimulates all opiod receptors but at lower affinity & efficacy
|
|
|
When are Mixed agonist-antagonists used
|
When pt is recovering from dependance since Mu is not stimulated
Not used for normal pain control |
|
|
How is opiod addiction treated
|
Usually use methadone
-Strong opiod agonist -Milder withdrawal symptoms than other opiods so more easily tapered off Can also use Buprenophine (Buprenex) -Mixed Agonist- Antagonist that partially activates Mu receptors and strongly antagonist for kappa--thus no hallucinations bc no kappa effects |
|
|
Give the 2 pathways affected by non-opiod analgesics
|
Lox--involves leukotriene enzymes
Cox--involves Thromboxanes and Prostaglandins |
|
|
What are 3 uses for NSAIDs
|
1. Relieve Moderate pain
2. Decrease fever 3. Anticoagulants Glucosteroids are also often used for anti-inflammatory purposes |
|
|
What are NSAIDs mechanism of action
|
Anti-inflammatory and analgesic effects are d/t inhibition of eicosanoid synthesis
More specifically the effects of NSAIDs are d/t inhibition of Prostaglandins and Thromboxanes synthesis (via inhibition of COX enzyme systems) |
|
|
Give 4 different types of NSAIDs
|
1. Aspirin
2. Ibuprofen 3. Alieve 4. Motrin |
|
|
Describe the differences between the COX-1 & COX-2 pathways
|
COX-1 : Normally produced in normally fxn cells
COX-2: Emergency pathway--produced in cells that are injured--stimulated with inflammation |
|
|
Are NSAIDs selective
|
Aspirin & most NSAIDs are non-selective--thus they affect both types of COX pathways causing some side effects in both situations
|
|
|
How does one determine which inflammatory enzymes NSAIDs will inhibit
|
NSAIDs only inhibit COX pathway so they dont effect leukotrienes
Depends where the pathway is blocked whether PGs or TXs will be inhibited |
|
|
What is one of the functions of the COX-1 pathway
|
Functions in protection of GI tract lining
|
|
|
What are Eicosanoids? What are the 3 main types?
|
Have a wide variety of effects on many different body systems
1. PGs 2. TXs 3. Leukotriens |
|
|
Describe the 3 main eicosanoids
|
1. Prostaglandins--endogenous lipidlike compounds that help regulate a wide array of cell fxns; pro inflammatory
2. Thromboxanes: vasoconstriction & platelet aggregation 3.Leukotrienes: pro-inflammatory esp. in airway |
|
|
Describe some of the problems that PGs and TXs can cause when not working correctly
|
Can cause inflammation, pain, fever, thrombus formation, & mentrsual problems when not working correctly
|
|
|
Describe the main uses for Aspririn
|
Aspirin (acetylsalicylic acid; ASA)
Uses: 1. Txt mild-moderate pain & inflammation, especially musculoskeletal & joint--also dysmenorrheal pain 2. Treat fever in adults (not children) 3. Treat vascular disorders--low doses 4. prevent colorectal cancer |
|
|
Give adverse effects of aspirin
|
1. GI problems--(main problem with NSAIDs)
2. Renal and liver problems if pre-existing disease or decreased body water 3. Overdose 4. Reye Syndrome: (rare) high fever, vomitting, liver dysfunction, leads to unresponsiveness & possibly death--usually after chicken pox 5. Aspirin Intolerance (supersensitivity)--allergy 6. Slowed Bone healing--may not be advisable after fx or bone sx |
|
|
What are the S&S of aspirin OD
|
HA, decreased hearing, confusion, GI distress, possibly metabolic acidosis & dehydration
|
|
|
Compare & contrast NSAIDs and Tylenol (Acetominophen)
|
-Same analgesic and antipyretic effects (decreased fever)
-No apparent anti-inflammatory or anticoagulant effects in oral doses of tylenol -No GI irritation or Reye Syndrome(in children) -Tylenol can cause high doses of liver toxicity |
|
|
What are used 1st with OA and other MS conditions
|
Tylenol
|
|
|
When to use tylenol or NSAID
|
If pt has GI problem or their is decreased inflammation use tylenol
If pt has liver issues or inc inflammation use NSAIDs |
|
|
GIve the mechanism of tylenol
|
Inhibits COX--probably inhibits PGs--may preferentially inhibit CNS PG's (COX-3 ?)
Not fully understood |
|
|
List all the aspirin-like NSAIDs and the differences bt them and aspirin
|
1. Advil
2. Motrin 3. Naproxen )Naprosyn) 4. Naproxen Sodium (Aleve) Main differences are in side effects/safety and cost No risk of reye syndrome Used similar to aspirin |
|
|
Give the Pharmakokinetics of NSAIDS
|
-Most is bound (80-90 %) to plasma proteins (albumin)--thus it stays in the bloodstream
The components of the drug that are unbound in the plasma are hydrolyzed to active metabolite (biotransformation occurs in bloodstream)--further broken down in the liver & excreted Aspirin-like NSAIDs have similar pharmakokinetics |
|
|
What is the main COX-2 selective inhibitor? What is the benefit?
|
Celecoxib (Celebrex): inhibits COX-2 only so less GI problems
|
|
|
Give the adverse effects of COX-2 inhibitor
|
1. Risk of MI & ischemic CVA
2. Shifts to favor increased platelet activity and increased risk of clotting in coronary and carotid arteries in some pts -Vioxx & Bextra were two COX-2 inhibitors used and found to increased risk of MI and CVA so now banned |
|
|
Give the pharmakokinetics of acetaminophen?
|
-Absorbed rapidly--compared to aspirin
-Much less is bound to plasma proteins -Biotransformation occurs mostly in the liver -Toxic metabolite (NAPQI) must be conjugated for detoxification & excretion |
|
|
Give 2 examples of Mixed opiod/non-opiods
|
1. Vicodin (Tylenol & hydrocodeine)--goal is pain control effect without serious side effects
2. Tylenol + Codeine |
|
|
Give the 4 main properties of NSAIDS
|
1. Ant-Inflammatory
2. Ability to relieve mild-moderate pain (analgesia) 3. Ability to decrease elevated body temperature associated with fever (antipyresis) 4. Ability to decrease blood clotting by inhibiting platelet aggregation (Anticoagulation) |
|
|
What is the difference b/t acetominophen and aspirin
|
Acetaminophen lack anti-inflammatory and ant-coagulant properties
|
|
|
What is aspirins main MOA
|
Inhibition of prostaglandin production
|
|
|
Give 3 main Eicosanoids
|
1. PGs
2. TXs 3. Leukotrienes |
|
|
Give the two enzyme systems that break down arachadonic acid
|
1. COX (cycloxygenase enzyme)
-Synthesizes TX's & PGs 2. LOX (Lipoxygenase enzyme) -Synthesizes Leukotrienes |
|
|
Where do leukotrienes mediate effects
|
Respiratory tissues
|
|
|
Discuss the role and effects of PGs
|
PGs are increased in cells that are subject to trauma or disturbances in homeostasis
PGs may be important in the protective response to cellular injury PGs mediate some of the painful effects of inflammation & also help produce the elevated body temperature during a fever |
|
|
Give one negative effect of TXs
|
Cause platelet aggregations that result in blood clot formation
|
|
|
Describe the differences between the Cox-1 and COX-2 enzymes
|
COX-1 is a normal cell component that synthesizes prostaglandins to help regulate and maintain cell activity
COX-2 represents an emergency enzyme that often synthesizes prostaglandins in response to cell injury |
|
|
Describe how aspirin acts on the COX pathways
|
Aspirin are non-selective--inhibiting both COX pathways
Thus aspirin causes primary beneficial effects by inhibiting the COX-2 enzyme and decreasing pain and inflammation However, these drugs also inhibit the COX-1 enzyme, they also decrease the production of the beneficial and protective PGs--loss of protective PGs in the stomach and kidneys result in gastric damage |
|
|
Give symptoms or Reye Syndrome
|
Occurs in children and teenagers usually following a bout of chicken pox or influenza
|
|
|
What is the mechanism of COX-2 inhibitors?
|
These drugs inhibit COX-2 enzymes selectively and don't affect COX-1 beneficial PGs
As a result the mediate the pain and inflammation affects without the side effect of GI irritation |
|
|
What is the mechanism of COX-2 selective drugs causing MI or Stroke
|
By inhibiting the COX-2 enzyme these drugs also inadvertently inhibit prostacyclin--a prostaglandin that promotes vasodilation and prevents platelet-induced occlusion in the coronary and carotid arteries
These drugs also don't inhibit TXs from the COX-1 enzyme--which facilitates platelet aggregation and clot formation These results in increased risk of clotting |
|
|
Describe the pharmokinetics of aspirin
|
Absorbed readily from the stomach and small intestine--80-90% remains in the bloodstream bound to plasma proteins
The unbound drug exerts the therapeutic effects throughout the body Hydolyzed to an active metabolite in the bloodstream |
|
|
Describe th pharmokinetics of acetaminophen
|
Absorbed rapidly in the upper GI tract
Plasma protein binding is 20-50% Metabolism occurs in the liver via conjugation with an endogenous substrate |
