Pharm Lecture #6: Pca & Oa

Front 1

What is PCA & how is it typically administered

Back 1

Patient-Controlled Analgesia: Pt can deliver small doses of pain meds relatively frequently for optimal pain control

Via IV or into Spinal Canal

Front 2

Give the Pros and Cons of PCA

Back 2

Pro: Pain control is achievable with less drug often times resulting in less side effects

Con: Potential user error (not clicking button); operator error (nurse types dosage in wrong); mechanical problems with pump

Front 3

Give the main benefit of PCA use

Back 3

Tighter control of concentration of drug in pt's bloodstream--results in less fluctuations with PCA vs oral or bolus administration b/c of more smaller dosages ---results in decreased sedation side effects

Front 4

What is the loading dose

Back 4

Initial large dose that brings concentration up to analgesic range

Front 5

Demand dose

Back 5

Amount administered when the patient clicks the button

Front 6

Lockout Interval?

Back 6

Minimum amount of time alotted b/t doses--won't deliver dose if button pushed earlier than lockout interval

Front 7

What is the background infusion rate?

Back 7

Occasionally their is a small amt of drug being given continuously without button push--(during sleep)

Not used as much b/c its more difficult to avoid side effects b/c pt cant stop pushing button if dose becomes to large & side effects ensue

Front 8

What are total demands? Successful demands?

Back 8

Total demands are the # of times pt has tried to receive medicine

Successful demands are the # of times the pt pushes the button & receives demand dose of drug

Front 9

What drugs are used with PCA

Back 9

1. Opiod--pain relief
2. Opiod/Non-opiod combination--Tylenol or NSAID
3. Opiod/Anesthetic
4. Anesthetic

Front 10

What are options for PCA delivery

Back 10

1. IV
2. Epidural
3. Transdermal--patch

--Cancer/chronic pain pts may have PCA for long term use

Front 11

Define RA

Back 11

Chronic, systemic disease primarily characterized by synovitis & articular tissue destruction

Front 12

S&S of RA

Back 12

Pain, Swelling, inflammation, stiffness

Front 13

Give typical joints affected with RA

Back 13

Smaller joints--hands, wrists, & feet

Front 14

Describe RA's typical disease course

Back 14

Progressive disease--pts will be in periods of remission

Their are juvenile and adult forms but they are treated similar

Front 15

Describe the etiology and treatment goals with RA

Back 15

Etiology-- somewhat unknown--an autoimmune response occurs, with the end result of synovitis and articular destruction

Txt Goals: 1. Dec inflammation
2. Stop disease progression

Front 16

What are options for decreasing inflammation associated with RA

Back 16

1. NSAIDs--very common txt
-Have analgesic and anti-inflammatory effects with less side effects than glucocorticoids

-Acetaminophen--not used bc no anti-inflammatory effects

Front 17

What are DMARDs

Back 17

Disease-modifying antirheumatic drugs
-Heterogeneous group that seem to slow or stop the RA disease process
-Most modify the immune response --for many unknown MOA

-Slow acting: often take 6 weeks to 6 months to see an effect
- Somewhat controversial: some have serious side effects--trying to combine different DMARDs together to reduce side effects

Essentially they attack the autoimmunity

Front 18

Give Examples of Types of DMARDs

Back 18

1. Anticancer drugs (Methotrexate or Rheumatrex) --oftin 1st choice & key drug in combination therapy txt

2. Immune Suppressants (Azathioprine or Imuran)--for severe & active RA---not used if pt is in remission--potentially has flu-like symptoms and increases fatigue

3. Anti-Inflammatory (Gold Compounds) : used if others are ineffective

4. Anti-Inflammatory via TNF-a inhibition (Infliximab or Remicade) --Newer

There is a broad variety of drugs used and they are mostly used in combination

Front 19

Why is TNF-a inhibition potentially helpful in treatment of RA

Back 19

TNF-a is involved in the inflammatory response in RA

It binds with tissue to cause inflammation but Infliximab binds to TNF-a & modifies its shape so that it cannot bind to the joint tissue--the drug may also mimic TNF-a shape & compete for tissue receptors

Front 20

What could be potential problems with RA pts exercising

Back 20

Increased fatigue and immune response

Front 21

What is another worry for RA pts

Back 21

Liver and kidney toxicity d/t increased drug intake

Front 22

What are 2 options for non-pharmaceutical treatment of OA

Back 22

PT & joint replacement

Front 23

What types of drugs are used to treat RA

Back 23

1. NSAIDs
2. Acetominophen (depending if jts are highly inflamed)
3. Disease -modifying OA drugs--Viscosupplementation and supplementation of precursors to joint tissue constituents

Front 24

Describe Viscosupplementation in the Txt of OA

Back 24

-Administered with injection of hyaluron into the joint--may restore lubricating properties of the joint

-Relatively transient response but can last up to 6 mo

-Can delay need for sx & usually tolerated well

Adverse effect: local pain and inflammation can occur

Front 25

Describe precursor to joint constituents supplementation

Back 25

Glucosamine: one of the substrates for cartilage production

Chondroitin Sulfate: key component of synovial fluid along with glucosamine

PROs: may decrease pain/inflammation
CONs: may cause GI problems

These are usually well tolerated so it doesn't hurt to try--usually takes a # of weeks to start working

Front 26

Describe the immune basis for RA

Back 26

Some type of autoimmune response occurs in genetically susceptible pts after some sort of precipitating factor such as a virus or infection

The precipitating factor seems to initiate the formation of antibodies that are later recognized at antigens--results in destruction of art cartilage and bone

Front 27

Give criteria for classification of RA

Back 27

1. Morning stiffness
2. Arthritis of 3 or more joint areas
3. Arthritis of hand joints
4. Symmertric Arthritis
5. Serum Rhematoid factor

Front 28

What are the 2 goals of RA drug txt

Back 28

1. Decrease joint inflammation
2. Arrest the progression of this disease

Front 29

What are 3 categories of drugs used for RA

Back 29

1. NSAIDs
2. Glucocorticoids
3. Disease Modifying Antirheumatic drugs (DMARDs)

Front 30

Define DMARDs and give their indication

Back 30

DMARDs are medications that retard or halt the progression of RA

Early and aggressive use of DMARDs can slow the progression of RA before there is extensive damage to affected joints

Front 31

How do DMARDs work?

Back 31

Attempt to induce remission by inhibiting certain aspects of the immune resonse thought to be underlying RA

Inhibit the fxn of monocytes and T & B lymphocytes that are responsible for perpetuating joint inflammation and destruction