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151 Cards in this Set

  • Front
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CHF Agents:
Heart Failure Drugs
Antianginals
Improve cardiac blood flow
Diuretics
Reduce blood volume (1st prescribed for high blood pressure)
Antidysrhthymics
Control heart rhythm
Anticoagulants
Reduce blood clotting
Antilipidemics
Reduce lipids
Systole
Contraction of the heart
Diastole
resting of the heart
Where does the electrical impulse originate?
SA Node
The product of cardiac output (CO) and peripheral vascular resistance (PVR)
Blood Pressure
What is the pressure with which blood is pushed from the heart?
Systolic pressure (CO mainly determines systolic BP)
What is the pressure when the heart relaxes between contractions?
Diastolic pressure (PVR mainly determines diastolic BP)
What is the amount of stretch applied to a muscle before contraction?
Preload (determined by the force of venous return)

Diuretics effect preload
What is the force of ventricular contraction?
Contractility
What is the load the heart must overcome in order to contract?
Afterload
Where the impulse is slowed so the atria and ventricles don't contract at the same time.
AV Node
Pacemaker rate 60-100, impulse to atria and AV Node
SA Node
Also called the AV Node
Junctional Area
Drugs with an inotropic effect
affect the force of contraction
Positive inotropics
-used for heart failure
-increase the force of contraction
Negative inotropics
-slow the force of contraction
Drugs with chronotropic effect
affect the heart rate
Positive chronotropics
increase the rate
Negative chronotropics
decrease the rate
Drugs with a dromotropic effect
affect the conduction of the electrical impulses through the heart
Positive dromotropic
enhance the conduction of electrical impulses in the heart
Negative dromotropic
decrease the conduction of electrical impulses in the heart
The amount of volume the heart ejects with each contraction (should be 65%)
ejection fraction
A major contractile element that must be moved into cells for contraction to occur
Calcium!
A condition that exists when the right, left, or both ventricles lose the ability to pump enough blood to meet the body's needs (usually due to chronic high blood pressure)
Heart Failure
Cardiac Glycosides
-Increase the force of the contraction and thus increase CO
-Positive inotropic drugs and negative chronotropic and negative dromotropic
-must take apical pulse for 1 minute and can not give if under 50 bpm
-oldest and most effective group of drugs
-originally derived from the digitalis lanta plant
Phosphodiesterase inhibitors
-Positive Inotropics that inhibit the enzyme phosphodiesterase whih increases force of contraction by increasing the amount of Ca+ available.
-ONLY USED IN HEART FAILURE
-Vasodilator
Not used much an more
-must be on monitor because causes dysrhythmias
Digoxin (Cardiac Glycoside)
-Used for CHF and dysrhythmias
-Adverse effects due to narrow therapeutic window (Bradycardia, vision changes, n/v)
-Therapeutic level is 0.5 to 2 mg/dl
-Long half-life (up to 3 days)
NUMEROUS DRUG INTERACTIONS
ACE Inhibitors, ARB's, Aldosterone antagonists, renin inhibitors (All affect the RAAS)
The renin system casues the release of aldosterone to cause vasoconstriction and Sodium retention and Potassium excretion to cause increased blood volume BUT intervening causes no release of aldosterone and no vasoconstriction to keep BP low!!!
ACE Inhibitors
-blocks enzyme involved in conversion of angiotension 1 to angiotensin 2
-inhibits aldosterone secretion (vasoconstrictor) and inhibits breakdown of bradykinin (vasodilator)
-these drugs end in -RIL
-40% develop DRY COUGH that is releated to the inhibition of bradykinin breakdown
ARB's
-Angiotensin 2 Receptor Blockers
-similar to ACE but dont cause cough
-end in -SARTAN
Aldosterone Blockers
-blocks aldosterone receptors in the heart and blood vessels
-used in heart failure
Renin Inhibitors
-blocks renin release from the kidneys
-very new and possibyl not used much due to price
Nitrate Vasodilators: Antianginals
-drugs used in the management of angina
-Dilate vessels and thereby increase supply of oxygen to the heart
-decrease the workload of the heart to decrease the demand for oxygen
-CHF related angina treated with the same drugs
Chest pain that is the result of cardiac tissue beign deficient in oxygen and nutrients
Angina
caused by atherosclerosis and triggered by exertion of stress
Chronic stable angina
seen in the early stages of coronary disease and ends with MI
Unstable angina (preinfartion angina)
caused by spasms of the smooth muscle surrounding the atherosclerotic coronary vessels.
Vasospastic angina
Therapeutic purpose of antianginals
-minimize frequency of attacks and decrease duration and intensity
-improve patients functional capacity with few side effects
-prevent or delay worst possible outcome
Classes of drugs used in angina
-nitrates/nitrites
-beta blockers
-calcium channel blockers
Nitrates/Nitrites
-dilate all blood vessels, especially coronary arteries
-adverse effect: reflex tachycardia, severe hypotension
-prototype: Nitroglycerin which is rapid acting and has large first-pass effect so given SL
Beta blockers
-decrease myocardial oxygen demand by decreasing heart rate and contractility
-protects heart from SNS and dysrhythmias
-decreases contractility
-Adverse effects: bronchial constriction if not cardioselective
-prototype: metaprolol (cardioselective)
Calcium channel blockers
Vasodilation and increased blood flow=decrease demand for oxygen
-types: heart and vessel specific
Adverse Effects: decreased bp, and bradycardia
-new designer calcium channel blocker targeted specifically for vasculature in the brain (lipophilic to cross BBB and good for migraines)
Human Brain Natriuretic Peptide
-newest drug developed by DNA technology
-short term, IV for severe heart failure ONLY
Natriuretic Peptides
-three peptides that provide protection to the CV system in overload.
-Action: released when blood volume is excessive
-lowers pressure by reducing blood volume and shifts fluid to the intravascular compartment (edema)
-lab tests for: elevated suggest too much fluid or says how treatment is going.
Drugs used to treat defects in the electrical system of the heart
Antidysrhythmic drugs
-not used much anymore because they can worsen an exsisting dysrhythmia and generate new ones.
A disturbance of impulse formation
Dysrhythmias
Antidysrhythmic Classifications
-Class I or sodium channel blockers
-Class II or beta blockers
-Class III or potassium channel blockers
-Class IV or calcium channel blockers
Class I: Sodium Channel Blockers
-inhibit movement of sodium
-Divided into Ia, Ib, and Ic
Class Ia
-fast sodium channel blockers
-slows conduction and prolongs repolarization
-use: atrial fib is example
-Prototype: quinidine
Class Ib
-used for premature ventricular contractions ONLY
-Action: slows conduction and shortens repolarization
-Prototype: Lidocaine
Class Ic
-most potent
-slow the conduction rate through the atria and ventricles with no effect on repolarization
-use: severe ventricular dysrhythmias
-prototypes: Encainide
Class II:
-beta blockers
-action: prevent stimulation of beta cells of the SNS of the heart; reduces calcium entry
-use: ventricular dysrhythmias
Class III
-potassium channel blockers
-Action: slows the rate of electrical conduction and prolongs repolarization
-use: life threatening
ventricular tachycardia or fibrillation
-limited use due to side effects (damage lungs)
Class IV
-calcium channel blockers
-action: blocks Ca+ channels, slows conduction through the AV node to slow heart rate
-use: supraventricular tachycardia
-SE: hypotension, dizzimess
Diuretic
-Drug that promotes the excretion of urine
-increase the removal of sodium and water from the body
-used for the treatment of hypertension and heart failure (decrease Extracellular volume), intraocular pressure
-most are safe but can cause electrolyte/fluid imbalance
-many times combined with antihypertensive drugs in one pill
Diuretic Classifications
1. Carbonic anhhydrase inhibitors
2. Loop Diuretics
3. Osmotic diuretics
4. Potassium Sparing diuretics
5. Thiazide and Thiazide-like diuretics
Carbonic Anhydrase Inhibitors (CAI's)
-sulfonamide antibiotic derivatives-weak and not used often because better ones have been developed
-Action: inhibits enzyme carbonic anhydrase in the proximal tube (enzyme responsible for reabsorption of sodium and bicarbonate)
-main use is in the treatment of glaucoma
-Adverse effect: Acidosis
Loop Diuretics
-work in the Loop of Henle
-must watch potassium levels
-Action: inhibit reabsorption of sodium and cholride in teh ascending loop of henle
-use: edema associated with CHF
-Adverse effects: dizziness, n/v, HYPOKALEMIA
-Prototype: furosemide (Lasix)
Osmotic diuretics
Action: Proximal tubule action. Pull water into blood vessels and nephrons and ultimately increases urine production.
-NOT FOR CHF patients!!
-Use: intracranial edema, intraocular pressure (used for head injuries)
Potassium-sparing diuretics
-Aldosterone antagonists: block aldosterone action in distal nephron so K+ is retained and sodium excreted. Used for CHF in children and reversal of K+ loss produced by other diuretics
Adverse effects: HYPERKALEMIA
-Non aldosterone antagonists: disrupts sodium potassium exchange by directly blocking exchange.
-use: hypertension and edema
Thiazide and thiazide-like diuretics
-derivatives of sulfonamides
-action: Inhibit Na+, water, Cl-and K+ reabsorption in the ascending loop of henle and early distal tubule
-have a ceiling effect
-used widely for hypertension
-Adverse effects: hypokalemia
Coined the term antibiotics and predicted that substances derived from microbes would be used to treat infections
Louis Pasteur
Won the nobel prize in 1908 for a formula to treat sleeping sickness, "magic bullet", and in 1909 salvarsan for the treatment of syphillis (led to sulfonamides)
Paul Erlich
Discovered Penicillin (widely used in WWII for staph and strep cases
Sir Alexander Fleming
Drug used to treat diseases caused by bacteria
Antibacterial
Antibacterial drugs obtained from chemical synthesis and not other microorganisms
Antimicrobial
Chemical compounds produced by living microorganisms capable of inhibiting or killing growth or other microbes.
Antibiotic
A drug used to prevent or treat infections
Anti-infective
Slows growth so body's natural defenses can dispose of the bacteria. Does not kill the bacteria
Bacteriostatic
Kills bacteria
Bacteriocidal
Classifications
-by organism
-by use
-by chemical structure
-by mechanism of action
Classifications: By organism
-Antibacterial (narrow spectrum, broad spectrum, mycobacteria, extended spectrum)
-Antivial (drugs for HIV, drugs for influenza, other)
-Antifungal
-Antiparasitic
-Antihelmintic (for worms)
Classifications: By use
-treat illness
-prevent illness
Classifications: By mechanism of action
-cell wall inhibitors
-protein synthesis inhibitors
-inhibitors of synthesis of DNA or RNA
-Antimetabolites
Current Problem?....
Overuse of antibiotics causing resistance
Ways microbes become resistant?
-produce an enzyme to deactivate the drug
-change cellular permeability to prevent entry or alternating of transport system
-alter binging sites on membranes so they no longer accept drug
-produce drug antagonist chemical
Common resistant microbes
-methicillin resistant staphylococcus aureus (MRSA)
-Methicillin resistant staphylococcus epidermis (MRSE)
-Penicillin resistant streptococcus pneumoniae
-Vancomycin resistant enterococci (VRE)
-Multiple drug resistant Tuberculosis (MDR-TB)
Preventing antibiotic resistance
-limit use to agents specific for pathogen
-highest does for longest period of time
-COMPLETE THE DRUG!!
-education!
-DO NOT use a more powerful drug when a less powerful drug is just as effective
Other issues with antimicrobial...
-Culture and Sensitivity done before starting antibiotic
-keeping levels up (keep doses on time, peak and trough levels)
Peak
drawn minutes after IV antibiotic completed to prevent toxicity
Trough
drawn immediately prior to the next IV given to measure elimination
Antibiotic Host Factors
-Age groups (infant/children-early exposure leads to sensitivity; pregnancy-most category B and C; elderly)
-Drug interactions
-Toxicity
-Allergies (hypersensitivity and cross sensitivity)
-Superinfections
Cell wall Inhibitors
-All are bacteriocidal
-Beta-Lactam Antibiotics (beta lactam ring)
-Vancomycin
-Isoniazid
-Betalactamase (penicilinase) inhibitors (betalactamase is an enzyme produced by some bacteria that break down the beta lactam ring and is always paired with penicillin)
Beta-Lactam Antibiotics
-Penicillin
-Cephalosporins
-Carbapenems
-Monobactams
Penicillins
-weaken bacterial cell wall, water enters, organism dies
-generally bacteriocidal
-some are penicillinase resistant
-one of the safest
-braod, narrow, or extended spectrum
-Use: prevention and treatment of wide range of bacterial infections (DONT CROSS BBB)
-Nursing care: take with water 2 hours before or after eating and monitor for 30 minutes after
Cephalosporins
-largest class with over 20 drugs
-four generations: first generation beta-lactamase bacteria will be resistant and 3rd and 4th generation cross BBB to treat CNS infections
-very safe
-broad spectrum
-same uses as penicilin (dont give if allergic to penicilin)
-Nursing Care: oral forms should be given with food to decrease GI upset but will delay absorption
Carbapenems
-"last resort" for very serious infections
-can cause seizures
-no cross sensitivity with penicillin
Monobactams
-no cross sensitivity with penicillin
-narrow spectrum to gram negative
-bacteriocidal
-use: systemic infection, UTI
-ADVERSE EFFECTS: NEPHROTOXIC
-IM or IV only
-Nursing care: look at kidney function labs before being on drug
Vancomycin
-narrow spectrum
-binds to cell wall and alters permeability results in death
-use: DOC in MRSA, gm + microbes, c diff, staph, strep.
-some bacteria resistant (VRE)
-IV administration too rapid=red man syndrome
Protein synthesis Inhibitors
-generally bacteriostatic
-Action: inhibit protein synthesis by binding to ribosomal unit in the cell and bacterial stops growth
-Tetracyclines
-Macrolides
-Aminglycosides
-Lincosamides
-Cloramphenicol
-Oxazolidinones
Tetracycline
-used when allergy to penicillin
-made from strep
-broad spectrum
-use: pneumonia, acne, H pylori
-CANT USE IN CHILDREN
-Adverse effects: teeth dicoloration in unborn an dkids, photosensitivity (sunburn)
-Interactions: bind to Ca+ and Mg- (NO ANTACIDS, DAIRY PRODUCTS, IRON)
-Nursing care: take with 6 to oz of fluid, avoid milk products, iron supplements, antacids, and the sun
Macrolides
-large
-broad spectrum
-use: upper respiratory and lower resp. tract infection, strep throat
-Adverse effects: GI, many drug interactions
-EX: erythromycin
-NOT CONTRAINDICATED WITH MILK
-Nursig Care: take with a meal or snack to avoid GI upset
Aminoglycosides
-narrow spectrum (gm-)
-derived from strep
-rarely oral due to poor absorption
-use: serious life-threatening infections
-ADVERSE EFFECTS: NEPHROTOXIC AND OTOTOXIC
-not used much anymore because better drugs are available
-Nursing Care: monitor peak and trough levels and BUN and serum creatinine levels
Lincosamides
-broad spectrum
-bacteriostatic or cidal
-VERY TOXIC!!!! (high association with c diff)
-use: bone, abdominal infections (life-threatening)
-does not cross BBB
Chloramphenicol
-only used in severe infections
-crossed BBB
-ADVERSE EFFECTS: SEVERE BONE DEPRESSION AND GRAY BABY SYNDROME IN NEWBORNS
-Nursing Care: DONT GO IN SUN
Oxazolidinones (designer drug)
-developed for MDR gm + orangisms (very specific infections)
-bacteriostatic
Streptogramins (designer drug)
-newest and also only for super bugs
-bactericidal
-need central line
Inhibit an enzyme (gyrase) inside the bacterial cell that is needed for DNA replication so the bacteria can not multiply
DNA Synthesis Inhbitors
DNA Synthesis Inhibitors: Fluoroquinolones/quinolones
-four generations (first narrow spectrum fro gm - and used ONLY for UTI; 2nd-4th are wider spectrum)
-bactericidal
-use: resp, GI, anthrax
-well absorbed in GI and only qd or bid dosing
-adverse effects: risk of tendon rupture, photosensitivity, NOT WITH ANTACIDS, MILK/DAIRY, VITAMINS, MINERALS
Nursing Care: intake of dairy, vitamins, minerals, antacids should be minimal; avoid the sun, achilles tendon rupture
Act by blocking a step in the synthesis of folic acid which is needed for bacteria to synthesize RNA, DNA and proteins
Antimetabolites (sulfonamides)
Antimetabolites: Sulfonamides
-old so lots of bacterial resistance
-use: UTI, ear infection
-Adverse effects: GI, photosensitivity, common cause of allergic reaction, crystaluria, highly protein bound and may displace other protein bound drugs
-Nursing Care: avoid sunlight and tannign beds, birth control decreases, and take with food or milk if PO
Drugs that destroy viruses by inhibitign the ability of viruses to replicate
Antivirals
Who is at risk for a viral infection?...
-innumocompromised patients (AIDS, HIV, cancer patients, transplant patients)
What are the two categories of antiviral meds?...
-Antiviral agents (non HIV)
-Antiretroviral agents (only for HIV/AIDS)
Antiviral MEds (NON HIV)
-Block enzyme necessary for symthesis of new viruses so virus can not replicate
-Adverse effects: vary with drug, generally well tolerated and safe
Antiretrovirals
-act by blocking different phase of the replication cycle
-use HAART therapy (drugs from four different categories to treat)
Five categories of antiretroviral drugs:
-nucleotide/nucleoside reverse transcriptase inhibitors (NRTI): in DNA and blocks enzyme
-nonnucleosides reverse transcriptase inhibitors (NNRTI): bonds directly to enzyme to inhibit it
-Protease inhibitors (PI's): work in last stage of replication so virus isnt released from CD4 cell
-Fusion inhibitor (newest): WORKS OUTSIDE THE CD4 CELL to stop the c=virus from entering
-Integrase Inhibitors: work inside the cell to integrate and prevent HIV DNA from entering healthy cell DNA
Drugs used in the treatment of systemic and cutaneous fungal (mycosis) infections
Antifungals
-Topical agents most common
-small group of drugs because fungal infections are hard to kill
-usually require prolonged therapy
Superficial Fungal Infections
-Candida (yeast): mucous membranes
-Dermatophytes: skin, hair, and nails (ex. ringworm, onchomycosis)
FIve main groups of fungal drugs
-polyenes
-imidazoles or "azoles"
-antimetabolite flucytosine
-echinocadins (newest)
-others (allylamine and griseofulvin)
Polyenes: Amphotericin B
-DOC for most systemic mycoses
-6-8 weeks of therapy
-very toxic ("shake and bake", nephrotoxic in 80%, ototoxic)
-only given slowly IV
-may pretreat with ASA or benadryl
-black box warning for use only in life threatening infections
Polyenes: Nystatin
-only for candida
-no systemic absorption so no SE(sometimes ordered swish and swallow)
-DOC for chemo related candida
"Azoles"
-most commonly used
-can be used systemically or superficially
-all interfere with ergosterol
-most 'azoles' have lots of drug reations
-Ketaconazole is hepatotoxic--alternative to amphotericin B
Antimetabolite flucytosine
-interrupts RNA and protein synthesis of fungus
-bone marrow suppression (not used alot now)
Echinocadins (newest)
-cancidas given slow IV and metabolized by liver
-anidulafungin is not metabolized by the liver (no DRUG INTERACTIONS)
-best safety profile of all drugs in this group
-phlebitis risk---give central line
Allylamine
-not for systemic
-treatment of onychomycosis
Griseofulvin
-treatment of superficial dermatophyte infections
-product of penicillin
-not for systemic use
Over the Counter fungal infections
-tinactin
-desenex
-lamisil
Tuberculosis
-mycobacterium tuberculosis bacteria
-affects 1/3 of the world population
-carried by droplets from infected person to host
-located in the lungs
-drug resistance is a HUGE problem (MDR-TB)...why?...No COMPLIANCE IS HIGH
-duration of treatment varies
Mechanism of action of TB drugs
-Inhibit pprotein synthesis
-inhibit cell wall synthesis
-other
-mot people with TB will be on 2 to 3 different antibiotics (ususllay 1 or 2 primary with 1 or 2 secondary)
Primary agents (first line)
-Isoniazid (INH): used alone or in combinations (MOST COMMONLY USED)
-Rifampin
-others
INH
-DOC due to efficacy, low toxicity, and affordability
-bacteriocidal to actively dividing bacilli and bacteriostatic to dormant bacilli
-used alone in prevention and in combination for treatment
-Adverse effects: peripheral neuropathy-prevent with concurrent B6 and HEPATOXICITY (esp. with alcohol or rifampin)
Rifampin
-bancteriocidal
-always in combination due to high risk for resistance
-also DOC in Hansen's Disease
-STAINS BODY FLUIDS RED-ORANGE
Others: Ethambutol
-used in combination
-only used in TB
-used if resistant to INH and rifampin
-opti-neuritis (must have eye exam to be put on it)
Secondary (second line ) agents
-usually less effective and more toxic
-used in combination with first line agents
Parasitic infection in gut and tissue-includes protozoa and helminths
Endoparasitic Infection
Parasitic infection on skin or hair
Ectoparasitic infections
used to kill parasitic aorganisms of the Plasmodium species
Antimalarial agents
Antimalarial Drugs
-affect parasite during the sexual cycle
-The "quines"
Quines
-quinine
-causes severe diarrhea and cinchonism (halluncinations)
-used for years but now out due to resistance
Drugs to treat other protozoal infections
-metronidazole
-binds to DNA
-many parasitic infections have a specific drugs used for it
Agents to treat lice, crabs/mites, scabies
-lindane: (NEUROTOXIC to INFANTS) not indicated for children under 2
-permethrin: safer and made from mums
-THESE ARE BUG KILLERS BE SURE TO FOLLOW INSTRUCTIONS
Drugs used in the elimination of worms and most are derivatives of antimony
Antihelmintics
Antihelmintics
-some are specific for a particular worm so need to ID worm
-mebendazole (Vermox): DOC for most intestinal worms
-invermectin: treat nematodes and heartworms in dogs, along with scabies
-short course of therapy (1 to 3 days) so SE rare
Drugs for UTI
-four antiseptics only used fo UTI
-Nalidixic acid (Negram): 1st generation fluoroquinolone (risk for shoulder tendon rupture)
-Cinoxacin: same as nalidixic acid
-Methenamine: only for chronic UTI
-Nitrofurantion: most serious SE is neuropathy, broad spectrum
Dermatologic agents
-meds applied to the skin
-Antibacterial and antiinfectives
-acne agents
-antifungal
-antivirals for herpes simplex 1 and 2
-topical anesthetics
-pediculicides and scabicides
Open angle
-drain is plugged
-gradual
-chronic
Closed Angle
-occludes drain
-emergency
Open angle drugs: First line
-beta blockers: nonselective and beta-1 selective DONT AFFECT PUPIL but lower pressure by reducing production of aqueous humor
-Alpha 2 agonists: decrease aqueous humor formation
-prostaglandin analogs: increases drainage of aqueous humor (increase fluid flow)
Open Angle drugs: Second line
-change pupil
-parasympathomimetics: Increase outflow through trabecular network; miotics
-carbonic anhydrase inhibitors: diuretic that blocks enzyme involved in production of aqueous humor
-nonselective adrenergics: dilate pupil, decreases rate of production and increase outflow, causes conjuctival pigmentation
Drugs for closed angle:
-osmotic diuretics: pull fluid from eye and pressure decreases
Otic Agents
-antibacterial and antifungal
-antibiotic and steroid combinations
-local anesthetics
-cerumenolytics
Topical Antimicrobial
agents used to reduce the risk of nosocomial infection
skin and mucous membrans can not be sterilized but the number of bacteria can be reduced (bacteriostatic)
-antiseptics
used on inanimate objects that may harbor bacteria (bacteriocidal). Toxic if ingested or absorbed through skin
disinfectants