module 2

Question 1

Nociceptive pain

Answer 1

Caused by stimulation of intact nerve fibers ave to actual or potential rissue damage. Nocicepters are present in skin, joints, connective tissue, muscle and viscera. Can be stimulated by trauma or by chemical mediators released at the tissue site.

Question 2

Neuropathic pain

Answer 2

Pain caused by damage or disease of neurological system fibers. Pain may last long after the initial injury; central neurons can become hyperexcirable making minor stimuli cause severe pain.

Question 3

Osteoarthritis

Answer 3

breakdown of articular catrilage, bone and synovium that Causes nociceptive pain. can be primary or secondary. Primary = no history of injury. secondary= previous injury or inflammatory condition.

Question 4

Inflammation

Answer 4

The body is immunologic response to allergy, infection or injury that increases the migration of leukocytes and blood flow to assist in repairing tissue. Can be acute or chronic

Question 5

phases of inflammaton

Answer 5

Vascular: Blood vessels near injury dilate and blood flow to the area increases
Cellular: consists of margination, transmigration, and chemotaxis
Opsonization: marking thr bacteria to prevent infection and cause phagocytosis of bacteria

Question 6

Rheumatoid arthritis

Answer 6

Inflammation of the synovium causing swelling and joint damage. The endothelium activates chemostatic factors which attracts leukocytes to joint spaces which causes an exaggerated auto immune response in genetically susceptible individuals.

Question 7

Histamine

Answer 7

High concentration in mast cells, basophils, and platlets. It causes vasodilation, jncreases cappilary pemeability and stimulates nociceptors. Move eosinophils to injured tissue

Question 8

Bradykinin

Answer 8

Activated by tissue injury. When white blood cells ingest cells of damaged tissue, the release enzymes that activate kinins which prolong vasodilation and vascular permeability caused by histamine. Also stimulate nociceptors. Increase mucous secretion.

Question 9

Complement

Answer 9

Plasma proteins that destroy cell membranes of pathogens. Also cause vasodilation, vascular permeability and promote chemotaxis the movement of WBC to an area of injury

Question 10

Cytokines

Answer 10

Interferons and interlukins. Act locally and systemically to promote chemotaxis of white blood cells, lroduce jnflammatory response, and fever

Question 11

Prostaglandins and pain

Answer 11

Sensitize pain receptors which increase pain associated with chemical mediators

Question 12

Prostaglandins and fever

Answer 12

Mediates cytokines such as interlukins and tumor necrosis factors that are pyrogens

Question 13

Inflammation and prostaglandins

Answer 13

Induces inflammation and increases effects of other chemical mediators

Question 14

Signs and Symptoms of inflammation. Also systemic signs

Answer 14

Warmth, redness swening, pain, decreased function. Leukocytes > 11,000. Increased ESR. Fever, headache, loss of appetite, malaise, weakness

Question 15

Cox-1

Answer 15

Physiologic prostaglandins associated with GI protection, renal protection, relaxed smooth muscle tone, regulates platlet aggregation

Question 16

Cox-2

Answer 16

Pathologic prostaglandins associated with inflammation, leukocytosis

Question 17

pharmacokinetics

Answer 17

what the body does to the drug. the movement of the drug through the body

Question 18

pharmacodynamics

Answer 18

what the drug does to the body. how does it get into cells. what impact does it have

Question 19

what are the 4 phases of pharmacokinetics?

Answer 19

1. absorption: drug gets absorbed into the bloodstream
2. distribution: drug gets circulated to all tissues/ organs of the body
3. metabolism: drug is biotransformed to make it more soluble for easier elimination
4. excretion: drug is eliminated

Question 20

absorption

Answer 20

1. oral drugs are swallowed and enter the stomach. the drug must enter solution to cross cell membranes. the drug is broken down via stomach churning and stomach acid. can be absorbed via the vast vasculature in the duodenum

Question 21

what affects absorption?

Answer 21

1. amount of acid in the stomach
2. food and beverages
3. motility and blood flow of the GI tract
4. presence of other drugs
5. lipophilic drugs

Question 22

Types of meds that should not be crushed

Answer 22

SR: sustained release
LA: long acting
XL or XR: extended release
CR: controlled release

Question 23

subcutaneous absorption

Answer 23

rapid absorption: highly water soluble medication and good blood flow
slow absorption: poor blood flow due to cold, anxiety, vasoconstriction, poor cardiac output and poor circulation

Question 24

IM absorption

Answer 24

rapid: highly water soluble medication and good blood flow
slow: improper injection into fat or fascia or inadequate muscle mass. drugs dissolved in oil (can be present in the system for months)

Question 25

unique routes of entry

Answer 25

inhalation is the fastest route to the brain

transdermal is released into the bloodstream over many hours

Question 26

protein binding

Answer 26

plasma proteins (albumins) act as carries for drug molecules. bound drug stays in the bloodstream and is pharmacologically inactive but are drug is active

Question 27

circulation to the liver

Answer 27

portal circulation delivers drug to the liver for the “first pass” the liver detoxifies the blood and protects the body from poisons and toxins. after the first pass, 60% of the drug is still bioavailable.

Question 28

bioavailability

Answer 28

some of the dose becomes inactive after the first pass. this drug is made water soluble for excretion. the portion of the drug that is left after the first past is called the bioavailable drug. different drugs have different bioavailabilites. if a drug has a high first pass effect it has a low bioavailability. IV drugs are 100 % bioavailable.

Question 29

metabolism

Answer 29

also called biotransformation. the liver is the organ of metabolism. there are 6 enzyme systems in the liver that metabolize 90% of all drugs. there is genetic variability in these enzymes which is responsible for variable responses in drugs

Question 30

liver (CYP450) enzyme inducers

Answer 30

substances such as St. John wort and alcohol increase the amount of these liver enzymes meaning drugs are metabolized quicker. If someone is stable on warfarin and suddenly began taking st. johns wort, their condition could deteriorate because the warfarin is no longer at a therapeutic level

Question 31

CYP450 enzyme inhibitors

Answer 31

these drugs reduce the activity of liver enzymes. Substances such as grapefruit, protease inhibitors and certain antibiotics reduce the function of the liver enzymes making metabolism of a drug a longer process. if a patient is taking warfarin and is stable, eating grapefruit could elevate the level of warfarin in the blood and become dangerous.

Question 32

minimum effective concentration

Answer 32

the minimum plasma concentration of a drug needed to bind to receptors to produce a desired pharmacologic response. this is the lower end of the therapeutic range. the upper end is the maximum therapeutic concentration. once above the upper extreme, the patient will experience adverse events

Question 33

regular dosing vs loading dose

Answer 33

regular dosing: the longer the half life, the less frequent the dose. to reach a steady state, it takes 4-5 half lives. a loading dose is used when an immediate drug response is desire. it is a large initial dose that achieves the minimum effective concentration. there are smaller subsequent doses. Digoxin is sometimes prescribed this way

Question 34

peak and through levels

Answer 34

peak drug level: highest plasma concentration of the drug at a specific time. indicates the rate of absorption.
trough drug level: lowest plasma concentration of a drug. measures the rate at which the drug is eliminated

Question 35

adverse effects

Answer 35

undesired responses to medication administration. all drugs can produce them and they can occur within therapeutic range. more severe with high doses, IVs, high alert drugs, and in infants or elderly

Question 36

side effects

Answer 36

physiologic effects not related to desired drug effects. may resolve on their own.

Question 37

adverse reactions

Answer 37

undesired events that result from taking medication correctly. can be predictable or unpredictable. must be reported

Question 38

excretion

Answer 38

kidneys are the main organ of excretion. The GFR is the fluid filtered from the renal capillaries per unit of time. it is an estimate of creatinine clearance because it accounts for variations among individuals. normal is 90 or higher. < 60 means the kidneys are not working well and <15 means the patient needs intervention like dialysis. check for GFR, BUN, and creatinine before administration

Question 39

serum creatinine

Answer 39

creatinine is a waste product of muscle wear and tear that is normally filtered out by the kidneys but if kidneys are not doing their job, the creatinine levels will rise. >1.2 for women an > 1.4 for men is concerning

Question 40

BUN

Answer 40

urea nitrogen comes form the breakdown of proteins. nitrogen binds to waste and is filtered by the kidneys. BUN >20 is concerning. *some medications, intestinal bleeding, and blood flow problems can also affect the BUN

Question 41

how do drugs transport through cell membranes

Answer 41

1. lipid soluble drugs dissolve in the lipid layer of the cell membrane and diffuse into or out of the cell
2. gated channels regulate movement of ions
3. carrier proteins attach to drug molecules and move them across cell membranes.

Question 42

receptor theory of drug action

Answer 42

cell membranes have receptors for physiologic substances such as hormones and neurotransmitters. these substances inhibit or stimulate cellular function. drug molecules also interact with receptors to stimulate or inhibit cellular function. when drugs bind to receptors they can stimulate, inhibit, or alter cell process. they can also change permeability of membranes for ions.

Question 43

agonists and antagonists

Answer 43

a full agonist produces a maximal response. an antagonist blocks a response. a partial agonist produces a weaker response even when all other receptors are bound. because it competes with a full agonist, it is considered a part antagonist too.

Question 44

nonselective drug effect

Answer 44

nonselective drugs have and effect on all types of receptors for example adrenergic medications can affect alpha 1, beta 1 and beta 2 receptors

Question 45

drug interactions

Answer 45

interactions can increase drug effects: synergism and they can decrease drug effects like with antidote.