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Glossary of Pharmacology Midterm 2

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Which parenteral technique poses the greatest risk for rapid drug toxicity to a patient?
IV route. Especially in cases of continuous IV infusion.
Drug Enzyme Interaction
Interaction with a drug and an enzyme. Drugs can increase/decrease enzyme action to produce a reponse. A common one is ACE inhibitor.
How can antagonists affect cell function?
By blocking vitamins, decreasing fluids, and working with antibiotics.

By attaching to a receptor, they prevent somrthing else from attaching and causing an effect. Also called a blocker.
Non-specific antagonists/effects
Changing the cell environment; changing cell pH, or permeability.
Additive Effect
2 like drugs are combined and the result is the sum of the drugs effects. 1 + 1 = 2.
Synergistic effects
2 or more unlike drugs are used together and the sum is greater than either drug alone. 1 + 1 = 3.
Antagonist Effects
The combined response of 2 drugs is less than 1 drug given alone. 1 + 1 = 0.
Potentiation effect
2 drugs given together, one drug increases the effect of the other drug.
Iatrogenic reaction
Unexpected response; mimics a pathological disease.
Agonist versus antagonist
Antagonists competes with agonist at the receptor site; it's reversible. Relies on the concentration
levels, whoever has more wins.

An agonist drug binds to a receptor of a cell and triggers a response by the cell. An agonist often mimics the action of a naturally occurring substance.
Antagonist
Drug combines with receptor but fails to produce an effect itself. It prevents an agonist from illiciting a response (prevents it from happening). Has affinity but not intrinsic activity.
Agonist
Has affinity (to locate receptor) and has intrinsic activity (to create changes in a cell). Creates 3 bonds with receptors to bind with receptor and changes occur within cell.

They attach to a receptor and stimulate the cell to act.
Drug receptor interaction
(lock and key) A portion of the drug will seek out and either combine or interact with a receptor. The drug with the best fit will create a higher/greater response.
Intrinsic activity
Causes cellular changes. Initiates biologic activity or efficacy.
Affinity
The ability for drugs to locate a receptor.
Receptor
Reactive cellular site on a molecule or cell; what the drug interacts with.
Drug effect
Response from the drug action.
Drug action
Interaction at the cellular level.
Trough
Lowest drug level. 1/2 hour before next dose below MEC.
Peak
Highest blood concentration. It's highest 1/2hr to 1hr after administration.
Therapeutic drug level
drug level is between MEC and MTC.
Maintenance dose
maintains the therapeutic state; a steady state.
Loading dose
1st dose to get level to MEC (large dose to reach therapeutic level).
**Drug Efficacy**
Effectiveness. Maximum response or effect achieved when the dose-response curve reaches its plateau.
**Drug potency**
Relative (min) amount of drug required to produce the desired effect, dosage.
Plasma level profile/drug response curve
The relationship between plasma concentration of the drug and the level of therapeutic effectiveness over time.
Therapeutic index
Area between MEC and MTC
MTC
Minimum toxic concentration. This is where we see the first signs of toxicity.
MEC
Minimum effective concentration
Duration
Length of time the drug concentration is sufficient to produce a therapeutic effect (above MEC).
Onset of action
The interval between time of drug administration and the first sign of effect.
Steady state
The rate of administration equals the excretion rate. Usually after 5 - 6 doses.
When are most drugs elilminated from the body?
4 -5 half-lifes
t1/2
Half-life. The time required for the total amount of the drug in the body to be diminished by half.
Clearance rate
Rate of removal of the drug from circulation.
P-450 system
Hepatic microsomal enzyme system. The major liver enzymes. Can increase/decrease the metabolism of a drug with this system.
Biotransformation
Converting the drug to a form that is easily removed by the body.
The byproduct of metabolism
Metabolite
Drug barriers
1. Blood/brain barrier
2. Placenta
What 3 factors affect drug administration?
1. The degree of blood flow
2. Binding of the drug to protein
3. Drug/protein complex
Drug distribution
The movement of the drug by the circulatory system to the site of action.
Where are most drugs absorbed?
In the small intestine.
What affects absorption of the drug?
1. Increased concentration
2. Blood flow
3. Motility/movement
First pass effect
The loss of effectiveness of the drug because the drug is going to pass through the liver and be broken down.
Drug absorption
The process of the drug transferring from the site of entry into the blood stream.
When is a drug most effective?
If they are lipophilic.
In what 3 ways do drugs cross the cell membrane?
1. Pass between spaces of the cell membrane. 2. Move with a carrier (with or without h2o); a transport system 3. Penetrates membrane directly.
Pharmacokinetics
Movement of the drug: distribution, metabolism, and excretion.
Pharmacology
The scientific study of the origin, nature, chemistry, effects, and use of drugs.
Controlled Substance Act (1970)
Established the DEA. Defined drug dependency and addiction. Strict control. Helped with education and addiction. Helped to classify drugs as controlled substances. Created a schedule of drugs.
Harrison Narcotic Act (1914)
Defines the term narcotic. First federal control on narcotics for habit-forming substances. Classified certain drugs as narcotics. Helped to regulate the importing, selling, and dist of the drug.
Federal Food Drug and Cosmetic Act (1906)
Prevents fraudulent claims about drug benefits. Makes sure that the drug is pure.
Drug safeguards
1. Post-marketing surveillance
2. Watchdog org.
3. Agencies

1980 gov't estab safeguards to protect unborn fetus; rating system estab
Compassionate use
(1988) It allowed certain drugs to be made available to a patient without complete FDA approval.
Orphan drug
A drug of limited use that's used to treat rare or unusual diseases.
What do the 4 phases of drug development look at?
Purity of the drug. Should have one active component, potency/strength, bioavailablility, efficacy, safety, and toxicity.
How long do the 4 drug phases take? How many drugs pass this phase?
5 - 10 years.

10%
4 phases of drug development when IND is approved
Phase 1: sm. pop. 25 - 75
Phase 2: 100 - 200
Phase 3: Large pop. 1000-5000
Phase 4: Post-marketing surv.
Preliminary steps to drug development
1. Discovery
2. Preclinical testing on animals. Can take up to 3 yrs. Looks at saftey and toxicity levels.
3. Company applies for an Investigational New Drug App (IND)
Who monitors drug development?
FDA
Trade Name
Brand Name
Official Name
Similar to generic name.
Generic Name
Identitifies the active ingredient. Derived from the chemical name. Assigned by the drug manu. who first dev. drug.
Chemical Name
Chemical comp of drug.
Enteric coating
A wax-like layer that is used on some tablets. It resists the acid environment of the stomach but dissolves in areas wher the local pH is neutral or slightly alkaline.
Sustained-release drugs
Formulated to release a drug slowly over time.
What does the topical route involve?
Eyes, ears, nose, vagina, rectum, and lungs
Parenteral route
Associated with all forms of injections.
Enteral route
Uses the GI tract for ingestion and absorption of drugs.
3 routes of drug administration
1. Enteral
2. Parenteral
3. Topical
Troche
lozenges
Which route is most frequently used?
Enteral route for oral drugs.
What is the advantage to an enteric-coated tablet?
Prevents drug from breaking down in the stomach. Sustained release may also occur with enteric coating.
Why might a parenteral route of a drug be prescribed instead of an enteral route?
Someone is unable to swallow and when the drug has a high first-pass effect.
Drug rating system
A - Safe
B - Risks but safe
C - There's fetal risk
D - Causes fetal harm
X - No benefit, harmful/deadly to fetus
Noncompetitive Antagonist
Inhibits the agonist response regardless of concentration. Irreversible. Combines with a different part of the receptor and inactivates the receptor. Exists for the lifetime of the cell.
Schedule of drugs
Schedule 1 - Most Poten. for abuse

Schedule 5 - Least poten. for abuse.
3 Principles of pharmacology
1. Drugs do not confer any new function on a tissue or organ, they only modify existing functions.
2. Drugs in general exert multiple actions rather than a single effect.
3. Drug action results from a physiochemical interaction between a drug and a functionally important molecule on the body.
6 Classifications of Laxatives
Hyperosmolar (saline/osmotic)
Bulk Forming
Emollient
Stimulant
Lubricant
Misc
2 Antidiarrheal Agents
Diphenoxylate HCL
Pepto Bismol
Diphenoxylate HCL
MOA: Acts on the smooth muscles of the intestine to slow intestinal motility.
S/E: drowsiness, dizziness. Increased dosages can cause dry mouth, flushing, tachycardia, urinary retention.
Pepto Bismol
MOA: Locally acting antidiarrheal salicylate (aspirin); antisecretory effect. Bismuth has a direct antimicrobial effect. Promotes secretion of bicarbonate and prostaglandins, promotes ulcer healing, suppresses H. Pylori.
NI: Can turn tongue and teeth black; don’t give to children.
3 Classifications of Antiemetics
SSR Antagonists
Antidopaminergics (Phenothiazides)
Anticholinergics
SSR Antagonists
MOA: Blocks serotonin receptors (5HT3) in CTZ and vagal nerve stimulation in the upper GI.
S/E: Headache and GI (const., gastric upset).
N/I: Admin w/ steroids increases effectiveness. Given IV.
Antidopaminergics (Phenothiazides)
MOA: Blocks dopamine receptors in the CTZ and GI Tract. Also sedative properties. Crosses b/b barrier, can have CNS effect.
S/E: Sedation, hypotension, decreased B/P, EPS, ataxia, dystonia, lip-smacking, rigidity, akathesia. Treat EPS w/ anticholinergics.
Anticholinergics
Neuro drugs. Balance Ach with dopamine (decrease Ach). Titrate down.

These drugs cross the b/b barrier.

Adverse s/e - see notes on neuro.
Drugs to Treat Peptic Ulcer Disease
Antacids
H2 Blockers
Proton Pump Inhibitors
Cytoprotective Agents (Carafate)
Antacids
MOA: React w/ gastric acid to create neutral salts. Neutralize gastric acid, raise pH (decreases the action of pepsin and damage to gut wall). Greater than 4 decreases pepsin, 2-4 increases pepsin.
NI: Watch Na and K levels.
Classifications of Antacids
Mag: MOM, can give diarrhea
Al: Maalox, Constipates people, increases Na
Ca: Tums, short-term, can give constipation, belching, gas
Na Bicarbonate: Alka Seltzer, increases Na, frees up CO2 and can cause belching and gas
H2 Blockers
MOA: Blocking of H2 (histamine) receptors in parietal cells of stomach. Decreases acid secretion 50-80%. Decreases stimulation of acid by Ach.
S/E: Well tolerated; headache, confusion
NI: Do not admin with antacids, smoking decreases effectiveness. Give at meals and bedtime. Lasts up to 8 hrs. Works w/in 1 hr.
Proton Pump Inhibitors
MOA: Converts active form in parietal cells; causes irreversible inhibition of the H+/K+. ATPase (enzyme – generated gastric acid). Therefore inhibits basal and stimulation of acid release (HCL). Blocks the last step of acid production. Can last up to 24hr. Single dose can decrease acid production by 99%.
S/E: less than 1%, headache
NI: Do not crush, best on empty stomach, impairs metab of many drugs (changes pH).
Cytoprotective Agents (Carafate)
MOA: w/ mild acid conditions, reacts with HCL acid to form a paste-like substance that adheres to gastric mucosa. Creates a barrier. Likes to bind to ulcer site. Promotes healing by creating barriers.
S/E: Constipation
NI: Not absorbed systemically, interactions with antacids (can’t create paste b/c there’s low acid). Give 30 min. apart. Best on stomach.
6 Mechanisms Of Action for Antibiotics
Inhibition of bacterial cell wall synthesis
Alteration in cell membrane function
Inhibition of protein synthesis
Inhibition of nucleic acid synthesis
Interference with intermediate cell metabolism
Unknown
Antibiotics that Affect Bacterial Cell Walls
Penicillin
Cephalosporins
Triglycerides Glycopeptide (Vancomycin)
Penicillin
Least toxic. Classified as a beta-lactam antibiotic; beta-lactam ring. Interferes with cell wall synthesis.
Binds to PBP (Penicillin binding proteins) on the bacteria.
How Penicillin Works
Activate Autolysins (holes in cells)
Inhibits transpeptidases (causes cell wall to weaken)
4 Subcategories of Penicillin
Natural Penicillin
Penicillase resistant Penicillin
Broad spectrum
Extended Spectrum
Natural Penicillin
Penicillin G is the safest. Given IM or IV, least toxic. Penicillin V is given PO. Works best against gram +.
Penicillase resistant Penicillin
Penicillin that is resistant to penicillinase, an enzyme made by gram + bacteria. Works best against gram + bacteria. AKA betalactamase.
Broad spectrum
Good against gram + and -.
Extended Spectrum
Gram + and -. Also good against pseudomones and proteins (everything).
Cephalosporins
Also beta-lactam antibiotics. MOA: Disrupt cell wall synthesis. They bind to CBPs (Cephalosporin binding proteins). 1. Activate autolysins 2. Inhibit transpeptidases.
They are broad spectrum and most beneficial against actively growing bacteria (better against gram +)
Cephalosporin Resistance & S/E
Resistance: By spontaneous mutation; causes changes; occurs w/ activation of beta-lactamases.
S/E: Similar to penicillin: hypersensitivity, rashes, itching; hematological; nephrotoxic; causes GI distress (nausea and vomiting)
Cephalosporins - NI
Careful admin. With other nephrotoxic drugs; beware of mult. Drug interactions, esp. when given IV; assess for bleeding. No alcohol consumption, can cause alcohol intolerance. Impairs alcohol metab., causes increased acetaldehyde and patient gets a hang-over effect (antabuse effect); disulfiram reaction (**within 72 hours of taking antibiotic)
How are Cephalosporins Classified?
According to Spectrum
Triglycerides Glycopeptide (Vancomycin)
MOA: Inhibits biosynthesis of bacterial cell wall.
Spectrum/uses: Best against gram +. Does not cross b/b barrier; not the drug of choice. Reserved for resistant or serious infections.
S/E: Ototoxicity, tinnitus, can cause renal damage, thrombophlebitis. Given over 1-2 hours; anaphylaxis, hypotension, nephrotoxicity; redneck syndrome. R/t release of histamines.
Triglycerides Glycopeptide (Vancomycin) NI
N/I: Monitor for renal function (BUN and creatine); monitor drug levels (trough less than 10 mcg/mL. Toxic levels over 50mcg/mL; give IV slowly, diluted, have good IV site.
Antibiotics that Affect Protein Synthesis
Aminoglycosides
Tetracycline
Macrolides (Zithromax)
Aminoglycosides
MOA: Disrupt protein synthesis by binding to 30S ribosomal subunit in bacteria which causes a misread in the RNA/DNA. Genetic code misstep.
Broad spectrum: works best against aerobic gram – bacteria. Can work with some gram +. Does not cross the b/b barrier well.
Aminoglycosides S/E & NI
S/E: 1. Ototoxicity, 2. nephrotoxicity, 3. neuromuscular rx and can lead to paralysis & resp. depression, 4. GI.
Relation b/w renal damage & increased BUN and creatine.
NI: Monitor BUN & creatine, changes in hearing; caution with nephro drugs; keep well hydrated to prevent renal damage. Cannot give IV w/ IV penicillin (the penicillin will inactivate the aminoglycoside.
Tetracycline MOA
MOA: Inhibits protein synthesis by binding to the 30S ribosomal subunit. Increased doses inhibit replication of DNA.
Spectrum: Broad, good against both + and -.
Tetracycline S/E
S/E: GI (esophageal irritation, nausea, vom). Bonds to the calcium in developing teeth and causes discoloration and hypoplasia of the enamel; affects long bone growth in children; superinfection, hepato/renal toxicity; photosensitivity.
Tetracycline NI
NI: Not given to children under 8 yrs or after 4 months of pregnancy; chelate.
Admin minerals 2 hrs apart fm Tetracycline; give on empty stomach. Check for s/s of superinfection. Take w/ 8 ounces of water.
Macrolides (Zithromax)
MOA: Inhibits protein synthesis, prevents cells from dividing.
Spectrum: More effective against gram +. Good for upper resp., ear, sinus infections.
S/E: GI
NI: Best on empty stomach. Long duration, good all day.
Misc. Antimicrobials
Fluoroquinolones (Tequin)
Anti Infective/Anti Protozoal Agent (Flagyl)
Fluoroquinolones (Tequin) MOA
Synthetic broad spectrum antibiotic against both + and – bacteria (anaerobic and aerobic).
MOA: Inhibition of DNA gyrase thereby interfering with replication, transmission, and repair of bacterial DNA.
Uses: Acute and chronic bronchitis, sinusitis, UTI, pyelonephritis, STDs.
Usual dosage: 200 – 400 mg/day (over age 18)
Fluoroquinolones (Tequin) S/E and NI
S/E: Generally well tolerated. N/V/Abd. Pain, D, dizziness, h/a, palpitations, rash, sweating. Arthropathy (joint discomfort - pain).
NI: Can give regardless of food. Don't give w/in 4 hrs of Fe, Zinc, Mg, Al.
IV dose should be admin over 1 hr.; limited info re: compatibility. Flush IV b/f and after Tequin admin. Caffeine decreases action cipro. Post-antibiotic effect for 2-6 hrs.
Anti Infective/Anti Protozoal Agent (Flagyl)
MOA: Disrupts DNA synthesis, causes cell to not replicate.
Spectrum/uses: Broad, gram + and -, protozoa, ambicides, worms, etc.
S/E: Vertigo, headaches (mj), GI, can cause neutrapenia, makes urine dark.
NI: Give with meals to decrease GI upset, avoid alcohol for 48 hrs after d/c, increases risk for bleeding; has a metallic taste.
ASA Preparations (ASA Aminosalicylates)
Used for ulcerative colitis and Crohn’s Disease.
MOA: 5-ASA (mesalamine) diminish inflammation by blocking cyclooxygenase & inhibiting prostaglandin production. Local effect in bowel.
S/E: Mild, headache
NI: 5-ASA preps similar to structure of aspirin. Some preps have sulfa products.
Pancreatic Enzymes MOA & SE
Uses: Digestant, replaces oxogenous exocrine pancreatic juices (in Cystic Fibrosis). Aids in the digestion of starches, fats, & protein in absorption in the small intestine.
MOA: Replacement therapy.
S/E: Increased doses – abd. Cramping, nausea, diarrhea
Pancreatic Enzymes NI
NI: Sensitive/allergy to pork (it’s made from pork) Eff. Treatment: decreased stools, decreased diarrhea. Take as prescribed, do not change brands, take with meals. Careful with powder as it can irritate skin. Enteric coated to decrease b/d in the stomach.
Example: Viokase, Pancrease.
Antiflatulents
MOA: Defoaming action, produces a film in the intestine & collapses gas bubbles. Disperses and facilitates the passage of gas through belching & flatus. Lasts for 3 hrs.
S/E
NI: Admin w/ meals & at bedtime to increase effectiveness.

Ex.- Simethicone (in Mylanta)
Reglan (GI Stim)
MOA: Sensitizes tissue to Ach. Increases peristalsis, increases gastric emptying, blocks dopamine in the CTZ.
S/E: R/T dosage. CNS, EPS, dystonia, lip smacking, decreased memory in children, dizziness, fatigue.
NI: Multiple drug interactions. Best given 30 min. b/f meals. If EPS occurs, give Benedryl.
Centrally acting skeletal muscle relaxants: Uses & MOA
Uses: Relief of pain assoc with muscle spasms. Decreases spasticity.
MOA: Act at diff levels of the CNS. Decreases synaptic transmission (Often works on GABA), an inhibitory neurostransmitter that slows impulses down.
Centrally acting skeletal muscle relaxants: S/E & NI
S/E: CNS, drowsiness, resp. depression.
NI: Safety concerns. Assess for CNS depressants and careful admin with other CNS depressant and drugs.
Direct Acting Skeletal Muscle Relaxants - Uses & MOA
Uses: Relief of muscle spasm/spasticity. Treatment of malignant hyperthermia.
MOA: Direct effect on skeletal muscle fibers. Interfers with release of Ca from the SR. Decreases the ability of the muscle to contract.
Direct Acting Skeletal Muscle Relaxants - S/E & NI
S/E: Low risk of CNS S/E
NI: Effects may take up to 2 weeks to be seen. Can increase liver enzymes. Contains lactose. Monitor drug interactions; safety concerns.
Most common side effects of direct acting skeletal muscle relaxants.
Weakness, malaise, fatigue, GI upset
Valium
Centrally acting skeletal muscle relaxant
Baclofen
Centrally acting skeletal muscle relaxant
Define glucocorticoid
A class of steriod hormones characterized by an ability to bind with the cortisol receptor and trigger similar effects.
What is the most important human glucocorticoid?
cortisol
What mechanism produces glucocorticoids in the body?
Negative feedback.
How do glucocorticoids work in the body (MOA)?
They control the rate of protein synthesis; they react with receptor proteins.
What 2 major effects do glucocorticoids cause?
1. Effects on metabolism and electrolytes
2. Anti-inflammatory effects (with increased doses)
What effects on metabolism and electrolytes do glucocorticoids have?
1. CHO metabolism
2. Protein metabolism
3. Fat metabolism
4. Cardiovascular
5. Fluids and lytes
6. During times of stress
7. CNS
(Gluco)

Effects on CHO metabolism
Increases blood sugar/glucose levels.
(Gluco)

3 ways gluco. increase blood sugar/glucose levels
1. Stimulates gluconeogenesis
2. Decreases peripheral glucose use.
3. Increases storage of glucose as glycogen.
(Gluco)

Effects on (Alt)protein metabolism
Promotes protein catabolism. Decreases use of amino acids for protein. Poor wound healing. Negative nitrogen balance.
(Gluco)

Effects on fat metabolism
Causes lipolysis (breakdown of fats) and fats get redistributed.
(Gluco)

Effects on cardiovascular
Potentiates the action of noepinephrine. Increases b/p by vasconstrcting. Increases the number of RBCs and neutrophils.
(Gluco)

Effects on fluids and lytes
Works like aldosterone (are similar to mineralcorticoids). Causes Na and H2O to be reabsorbed. Increases b/p.
(Gluco)

During times of stress
Increases stimulation of glucorticoids. Helps with fight or flight mechanism. Elevates blood glucose and stimulates the nervous system.
(Gluco)

CNS Effects
Affects mood, mood swings, irritability, restlessness
Anti Inflammatory effects (increased doses) of glucocorticoids
1. Interferes with biosynthesis, storage, and release of substances assoc with inflammation such as histamines, kinases, prostaglandins
2. Stabilizes lysosomal membranes. Makes the cells strong and stable. Histamines and kinases stay inside the cell.
3. Decreases antibody formation
4. Decreases phagocytosis. Decreases WBC
5. Inhibits collagen deposits
6. Inhibits capillary dilation and permeability -- vasoconstriction, decreased blood flow, contents won't leak out.
Dosage - Gluco

Individual
May not get complete relief; controls s/s. Dosage is highly individual. Not life threatening - start with a low dose and step dose upward (titrate). Life threatening - large initial doses, no reposnse X2 or X3.
Dosage - Gluco

Alternate day therapy
Given a dose every other morning; usually prior to 9AM, mimicing the body's steroid production.

This is a good method because it:
1. Reduces risk of adrenal insuff.
2. Reduces risk of s/e.
3. In children reduces risk of bone retardation.
(May have flare-up or symptoms on day 2)
Dosage - Gluco

Step dosing
Must be weaned off drug before discontinuing. Gradually dcrease dose. Stopping dosage abruptly can cause adrenal insuff., decreased b/p, decreased glucose, hypotension, muscle ache, joint pain (myalgia, athralgia)
(Gluco)

Uses
Patient with inflammatory disease: rheum. arthritis, lung disease, COPD, inflamm. bowel, bursitis, tendinitis.
(Gluco)

S/E
1. Adrenal insuff.
2. Infection
3. PUD
4. Osteoporosis
5. Growth retardation
6. Glucose intol.
7. Myopathy
8. Cataracts
9. Psychological
10. Cutaneous changes
11. Neg. Nit. Balance
12. Iatrogenic cushings syndrome
13. Fluid and lyte imbalances
(Gluco S/E)

Infection
Because it suppresses the immune system. Masks the s/s of infection. Need to monitor for infection.
(Gluco S/E)

PUD
Peptic ulcer disease because we block prostaglandins which decrease acid and increases mucus, increases blood flow; they mediate pain.
(Gluco S/E)

Osteoporosis
Related to chronic use. Ribs and vertebrae are the most affected. Occurs because of decreased osteoblasts and decreased intestinal absorption of Ca.
(Gluco S/E)

Growth retardation
Related to catabolism. Seen primarily in children. Monitor height and weight.
(Gluco S/E)

Glucose intolerance
Causes hypoglycemia. Monitor insulin.
(Gluco S/E)

Myopathy
Muscle weakness related to protein catabolism. More often seen with increased doses, upper arms and legs; reversible.
(Gluco S/E)

Cataracts
related to long-term use and CHO and protein metabolism.
(Gluco S/E)

Psychological
Mood changes, hallucinations
(Gluco S/E)

Cutaneous changes
skin, related to protein catabolism; atrophy of the skin; changes in hair and nails
(Gluco S/E)

Neg. Nitro. balance
From the breakdown of protein. Patient breaks down more protein than takes in.
(Gluco S/E)

Iatrogenic cushings syndrome
Mimics cushings syndrome which is an adrenal disorder. Results from chronic/excessive use of steroids.
Symptoms include: rapid weight gain especially in trunk and face with sparing of the limbs, moon face, excessive sweating, dilation of capillaries, atrophy of the skin.
(Gluco)

NI
Careful admin. with diabetics, hypertensive patients, children, patients with PUD, anyone with a systemic fungal or blood infection should not get this because it decreases the immune system.
Mineralcorticoids
A class of steroids characterized by their similarity to aldosterone and their influence on salt and water metabolism.
Aldosterone
Acts on the kidneys to provide active reabsorption of Na and an associated passive reabsorption of water.
Drugs for treating UTI
1. Sulfonamides
2. Unrinary Tract Anagesic (Pyridium)
3. Nitrofurantoin (macrodantin)
Sulfonamides - MOA & Spectrum
MOA: Inhibits the synthesis of folic acid, which is needed for DNA & RNA in bacteria. (PABA is the precursor to folic acid. PABA & protein = folic acid).

Spectrum: Broad spectrum, + and -. Good for UTI because drug levels remain high and active in urine.
Sulfonamides - S/E & NI
1. Hypersensitivity (rash)
2. Photosensitivity
3. Hematologic, action on bone marrow.
4. Can cause renal damage due to crystal formation (in acidic acid)

NI: Increase hydration, alkalize urine, mult. drug interactions.
Nitrofurantoin (Macrodantin) - MOA & Spectrum
MOA: Not fully understood. Interferes with carbohydrate metabolism. Blocks acetyl Coenzyme A. Needed for CHO metabolism.

Spectrum: Broad. Increasedeffectiveness against E. Coli. Therapeutic levels/effects only found in urine, local effect. Increases excretion rate.
Nitrofurantoin - S/E & NI
S/E: GI, superinfection, peripheral neuropathy - demyelination - muscle weakness and tingling, irreversible.

NI: Monitor BUN and Creatine, monitor neuro, changes urine to a brown color. Admin with food and milk. It can stain the teeth.
Urinary Tract Analgesic (Pyridium)
MOA: Unknown
Uses: Treats pain and irritation assoc. with UTI.

S/E: GI, turns urine orange/red.

NI: Used for pain response, tell patient about color; no systemic effect.
Bacitracin
Polypeptide antimicrobial used for skin/eye infection.

MOA: Inhibits cell wall synthesis. Works agains gram +.

S/E: Topical, skin/eye, can cause vision to blur.
What are some Antifungal Agents and what are their MOA?
1. Fluconazole
2. Amphotericin B
3. Nystatin

They alter/increase cell permeability and allow the cell contents to leak out.
Nystatin
Uses: Treat local fungal infection (local effect only). Can be used topically and orally (Kids with thrush).

S/E: Local irritation, GI upset

NI: Keep in mouth for a while. Swish and spit/swallow - adults. Tastes awful. 12 - 72 hrs.
Amphotericin B - uses & S/E
Uses: Severe symptoms of fungal infections. It's the **DOC for systemic mycoses (resistant to treatment).

S/E: Highly nephrotoxic, anemia, hypokalemia, chills, nausea, head ache, severe phlebitis if it infiltrates, Dose related, damages renal cells. Decreases erythropoeitine.
Amphotericin B - NI
Caution with patients with renal disease and other nephro drugs. Monitor BUN and creatine, check I/O. Patient is given a test dose first. Admin IV slowly. Can't mix with other drugs and needs a filter and good line.

Best absorbed IV (can cause chills, nausea, and head ache, poorly absorbed through GI.
Fluconazole
Uses: Treat esophageal/oropharyngeal infections, **drug of choice for this; systemic.

S/E: n/v/abd pain, can increase hepatic enzymes which discontinue after drug is stopped. PO or IV.
NI: Monitor hepatic enzymes. Can be given with food.
Influenza
Caused by the influenza virus, which spreads from infected persons to the nose or throat of others.
2 types of influenza vaccine
1. An inactivated (killed) vaccine, given as a shot.

2. A live, weakened vaccine was licensed in 2003. It's sprayed into the nostrils.
How long does it take for protection to develop for the flu vaccine?
2 weeks and lasts up to one year.
How is the flu vaccine administered?
Admin in deltoid, 1-inch needle.
What is the flu season?
November to April
People at risk for complications from influenza.
- People who will be preganant during season.
- all children 6 - 23 months.
- People 65 yrs and older
- Residents of long-term care facilities with chronic medication conditions.
- People with certain muscle or nerve disorders.
- People with weakened immune systems (HIV, AIDS, long-term treatment with steroids, cance treatment.)
-People 6 mos. to 18 yrs. on aspirin treatment.
What is the best time to get the influenza vaccine?
Oct or Nov
How many flu shots should people get? Why would you get 2?
Most people need only one flu shot.

Children younger than 9yrs of age getting the flu shot for the first time should get 2 doses, given at least one month apart.
What are the risks from the flu vaccine (inactivated)?
- Severe allergic reactions

Mild problems include: soreness, fever, aches
Who should not get the flu shot?
- the flu vaccine is grown in eggs. People with a severe egg allergy should not get it.
- Those with GBS should ask their dr.
- People who are moderately or severely ill.
- Those with latex allergy
Pneumococcal disease
Leads to serious infections of the lungs (pneumonia), the blood (bacteremia), and the covering of the brain (Meningitis).
What does the Pneumococcal polysaccharide vaccine (PPV) protect against?
23 types of pneumococcal bacteria
Who develops protection with the PPV and how long does it take?
Most healthy adults.

Develop protection within 2 to 3 weeks.
**Who should get the PPV?
- All adults 65yrs+
- Anyone 2yrs+ who has a long-term health problem.
- Anyone over 2 yrs who has a disease or condition that decreases the body's resistance to infection.
- Alaskan natives/native americans
How effective is the PPV?
50 - 60%
How many doses of PPV is needed? Why would you need a second dose?
- One dose

- A 2nd dose for those 65+ who got their 1st shot when they were under 65, if 5+ yrs have passed since that dose.
How is the PPV administered?
SC or IM in deltoid.
What should be done after admin. of PPV?
- Have patient wait 30 min.
- Document bottle number and exp. date.
Reglan
GI stimulant
Zofran
SSR Antagonist
Zantac
H2 Blocker
Pepcid
H2 Blocker
Metamucil
Bulk forming laxative
Colace
Emollient laxative
What kind of agent is Carafate?
cytoprotective agent
Prevacid
Proton Pump Inhibitor
Prilosec
Proton Pump Inhibitor
Dantrolene
a direct acting skeletal muscle relaxant
Cox2 Inhibitors
MOA: inhibits Cox2 prostaglandin synthesis.
Uses: Reduces p/f/inflamm. Keep protective effect in the GI tract.
S/E: Decreases GI S/E, less problems with bleeding, risk of cardiotoxicity.
NI: Mult. drug interactions, d/g to history of cardio problems or stroke. Can increase effects of anticoagulants.
Celebrex
Cox2 Inhibitor
NSAIDS
MOA: Inhibits prostaglandin synthesis.
Uses: anti inflammatory, antipyretic (fever), analgesic (pain), platelet suppressant.
S/E: GI bleed, upset, increased risk for PUD. Decreased renal blood flow.
NI: Cautious use with elderly; patients with renal disease. Long-term use can cause hepatic change; watch drug interaction with clotting drugs; GI upset, give with food.
What is the antidote for tylenol overdose?
Mucomyst

Works within 24 hrs.
Acetaminophin
Para amino phenol drug
MOA: Selective prostaglandin inhibition in the CNS (only)
Uses: helps to reduce pain, treat fever, no anti inflammatory effects. Not on platelet aggregation. No GI distress.
S/E: Rare at therapeutic doses
NI: Large doses over 4000mg can cause liver damage. It overloads the liver, causing hepatic necrosis, then liver failure. Different non-steroidals block at different points.
Salicylism
Toxic levels of aspirin. 1st sign is ringing in the ears (tinitis), tendency to bleed, CNS effects, dizziness.
Salicylates (aspirin)
MOA: inhibits cyclooxygenase and throboxane A in the CNS and peripheral NS. Patient won't get prostaglandins because they are blocked. They are non-selective inhibitors of Cox1 and Cox2 (blocks both).
Uses:
1. Decrease inflammation (need higher doses)
2. analgesic (pain reief for mild to moderate). Best on joints, muscle, headache.
3. Decreased fever caused by infection.
4. Decreased platelet aggregation at lower doses. Lasts lifetime of platelet (4-7 days)
Salicylates - S/E & NI
S/E: Gi is the most common due to blocking Cox1; GI ulceration, heartburn, nausea, bleeding, can cause renal problems, Reyes syndrome.
NI: Take with food to decrease GI S/E.
Name the medications to treat pain
1. Opiate agonists
2. salicylates
3. acetaminophin
4. NSAIDS
5. Cox2 Inhibitors (Celebrex)
Opiate Agonists - MOA and Uses
Capability to relieve mod. to severe pain without loss of consciousness.
MOA: Stimulation of opiate receptors in the CNS (binds to it). Changes patient's perception of pain. Decreases transmission of the pain response. Drecreases production and release of Substance P - mediator of pain (the messenger).
Uses:
1. Relieve acute and chronic pain
2. decrease anxiety
3. Increase sedation (increase effectiveness of anathesia)
4. Vasodilation around the heart.
5. decrease cough reflex/center.
For what conditions are opiate agonists used with?
CHF and pulmonary edema. Reduces venous return.
What is the OD remedy for opiate agonists?
Narcan; a competitive antagonist.
What are the 4 types of opiate receptors?
Mu, Kappa, Delta, and sigma.

Mu, Kappa, Delta deal with pain response and euphoria. Sigma deal with mood.
What are the largest opiate receptors?
Mu
What are some opiate agonist drugs?
Morphine and demerol.
(Opiate Agonist)

S/E
1. Respiratory depression
2. Orthostatic Hypotension
3. Cough Suppression
4. Constipation
5. Urinary retention
6. Emesis
7. Euphoria/sedation
8. Miosis
(Opiate Agonist - S/E)

Orthostatic hypotension
caused by dilation of arteries and veins. More likely with ambulatory patients.
(Opiate Agonist - S/E)

Cough suppression
Suppresses the cough reflex in the medulla (helps patients to sleep at night). At risk for aspiration, pneumonia, and infection.
(Opiate Agonist - S/E)

Constipation
Suppresses motility/peristalsis. Decreases secretion of fluids into the intestine.
NI: Increase fluids, increase fiber, give colace.
(Opiate Agonist - S/E)

Urinary retention
Can cause urinary urgency and hesitancy. Increase sphincter tone of the bladder, increase tone of detrusor muscle (bladder) feels like you have to pee. Suppresses awareness of voiding. Decreases renal blood flow and decreases urine production. Increases ADH release. Patient at risk for UTI. Palpate bladder, monitor I&O.
(Opiate Agonist - S/E)

Emesis
(vomiting) Stimulates CTZ. More frequency in ambulatory patients. Greatest with first dose. Pre-treat with antiemetic.
(Opiate Agonist - S/E)

Euphoria/Sedation
Due to the stimulation of Mu. Kappa, and Delta receptors, causes euphoria and sedation. Can increase anxiety in some patients.
(Opiate Agonist - S/E)

Miosis
(pupillary constriction) Safety concerns, can cause blurred vision.
(Opiate Agonist)

N/I
Cautious use with patients with decreased respiratory rates (less than 12) and those taking other respiratory depressants, the elderly. Can cause hypotension; use caution with patients that have liver disease or head injury. Hold it if resp. below 12. Assess VS.
Parkinson's Disease
Def: A progressive neurological disorder caused by loss of dopamine containing neurons in the substantia nigra.

There needs to be a balance of dopamine and Ach for smooth motor coordinated movement. Imbalance between lack of dopamine and Ach results in s/s of Parkinson's. Unopposed Ach stimulation. GABA - rigidity, akinesia, tremors at rest.
First s/s of Parkinson's Disease
Nonspecific - slowness, fatigue, disturbances in speech.
4 classic traits of Parkinson's Disease
1. Tremors at rest
2. Akinesia - Bradykinesia
3. Rigidity - cogwheel rigidity
4. Disturbances of balance - increased fall risk
Treatments of Parkinson's Disease
1. Anticholinergics
2. Dopaminergics
3. COMT Inhibitors
4. Antiviral
What are some examples of cholinergic drugs?
Congentin, Artane, Benedryl.
Dopaminergic Drugs - Def & MOA
Def: It's a combination drug, carbidopa-levodopa.

MOA: It diffuses levodopa into the CNS, where it is converted into dopamine. It balances dopamine and Ach.
3 Dopaminergic Drugs
1. Levodopa
2. Sinemet
3. Mirapex
Levodopa
Part of the drug sinemet. Helps get dopamine to the brain. Inactive until it crosses the b/b barrier (converted by enzymes). Replaces doapmine in the CNS. Dopamine is in the basal ganglia.
S/E: Increased anxiety, confusion, n/v/c, nightmares, difficulty urinating, orthostatic hypotension, cardiac dysrythmia. After 3 - 5 years it loses its effectiveness.
Food interactions with Levodopa
Vitamin B6 cannot be ingested because it stimulates the breakdown of levodopa.

MAO inhibit. can cause hypertensive crises.
**Sinemet
DOC. Has levodopa in it as well as carbidopa, which inhibits decarboxylases in periphery. By suppressing decarb. in periphery it makes more levodopa available in the CNS. Can give less levodopa with this combination. Carbidopa doesn't cross the b/b barrier.
S/E: Similar to levodopa. Advantage to sinemet dose of levodopa is smaller, single dose, increased compliance, lower s/e, better balance between dopamine & Ach.
NI: There are different strengths.
Mirapex
Carbidopa-levodopa is converted in the brain into dopamine. A selective agonist at D2 and D3 receptors in the brain.
COMT Inhibitors
COMT is an enzyme that makes more dopamine available by blocking the COMT enzyme.
One example of a COMT Inhibitor & S/E
Tasmar

S/E: dyskinesia and CNS s/e
Antiviral medication example and S/E
An example is Amantadine, not sure how it works; works with the re-uptake of dopamine in the neurons.

S/E: CNS s/e
Basal ganglia
Where dopamine is made and stored.
Drug holiday
Time off drug to re-establish sensitivity to the drug.
Cogwheel rigidity
rigidity in the extremities
Akinesia
Loss of muscle movement
Bradykinesia
slowing of movement
Dyskinesia
movement with pain or difficulty
What are the 2 neurotransmitters within the neurons of the striatum of the brain that have opposing effects?
Dopamine and Ach

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