• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/156

Click to flip

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;

156 Cards in this Set

  • Front
  • Back
Introduction to Narcotics (Opiates):
-what is pain
-what is endorphans
pain
- is an unpleasant sensation disturbing patient's comfort, thought sleep or normal daily activity and is symptomatic of an underlying disease process
- is the 5th vital sign

Endorphans are the body's own internal analgesic.
When opiates stimulate the endorphan receptors the perception of pain is blocked.
Narcotics (Opiates) Mechanism of Action
Endorphans --> blocks perception of pain when stimulated.

people's endorphan varies, some produce more, some less. so pain threshold varies b/w individuals

the more endorphans the less pain
therapeutic uses of Narcotics
analgesia (moderate to severe)

antitussive - blocks cough reflex

antidiarrheal - side effect of narcotic is constipation. it slows down the GI. not good for Bacterial diarrhea.
Pharmacology of Narcotic (Opiates): CNS
-analgesia without loss of consciousness (moderate to sever)
-drowsiness
-behavioral changes (euphoria with Heroin IV, and dysphoria)
-depress cough reflex
-nauseant and emetic (esp. injectible ones. makes the patient nauseous so the solution is add another drug) **BUT THIS ONLY WORKS FOR NO MORE THAN 3 DAYS**
Pharmacology of Narcotic (Opiates): CNS
-toxicities
-head injury
-toxic effects:
respiratory depression and miosis (pupil constriction) this indicates that the pt. od'ed on Narcotics

-head injury:
pts. who had head injury should not be given narcotics because or the already low resp. drive.
Pharmacology of Narcotics: Cardio
SPECIFIC FOR IV MORPHINE

-orthostatic hypotension -bp goes down when pt. moves

-Morphine effects: IV administration decrease cardiac workload during MI ...good property or bad?


GOOOD!! during heart attack (MI) we want to decrease heart workload to decrease the demand of O2 in the heart
Pharmacology of Narcotics: Gastrointestinal
-decrease peristalsis = stomach and intestines = decrease diarrhea, increase constipation

-increases biliary pressure. good or bad property of narcotics for pts. with gall stones? -----> BAD! why? because narcotics INCREASES biliary pressure.
Pharmacology of Narcotics MISC.
Uterus - prolongs labor - do not give high doses ..it can stop labor.
Narcotic Analgesics:
-3 drugs and what they do.
MORPHINE - intermediate action, but can be given sustained release. decreases cardiac workload (IV). long acting sustained release narcotics for terminal pts.

MEPERIDINE - short acting. used after surgery

FENTANYL - extremely potent. dose in mcg because of resp. depression. patch form is available for terminal pts. --> patch is 72 hours.
NARCOTIC ANTAGONIST
-Blocks opiate receptor --works IMMEDIATELY -- pulls narcotic and replaces and blocks it.

-Short acting (45 min.) --> pts. who OD on long acting narcotics goes back and OD again.

-precipitates withdrawal. no use for addicts. severe withdrawal immediately

- Naloxone (Narcan)
Narcotic Agonist/Antagonist
-stimulates or blocks receptors -- no surge to the brain (100% stimulation) only 50% is being stimulated
-not effective in severe pain
-advantages : decrease abuse potential, and decrease addictive potential. less change of causing problems in labor and gall stone pts.
-drawback : not for severe pain
Narcotic (Opiates): Antidiarrheal
-effective in non-infectious diarrhea
-decreases GI motility to decrease diarrhea - but will retain toxins and bacteria
Narcotic (Opiates): Antitussive
-why we give antitussive to pt.?
1. so they can sleep, 2. for people with chronic dry unproductive cough.
-decreases cough reflex
-decreases sternal pain to encourage deep breathing
Narcotic (Opiates): Pain control concepts
-pt controlled analgesia - leads to less use

-chronic terminal pain - addiction is not a concern

-post-operative use is a recommendation - not adequately utilized to promote healing --should not be used more than 3 days (addiction potential)
Name 9 Narcotic Analgesics (Sched. II)
-Morphine Sulfate (MS Contin)
-Meperidine (Demerol) is very short acting
-Hydromorphone (Dilaudid)
-Codeine -also found in combination (eg. Tylenol/Codeine Sched. III)
-Hydrocodone (Vicodin) in combo with acetaminophen -sched III
-Fentanyl (Sublimaze, Duragesic) inj., patch --use very low dose
-Methadone (Dolophine)
-Oxycodone (Percodan, Percocet, Tylox, Oxycontin)
-Propoxyphene (Darvon) Sched IV
Name 3 Narcotic Agonist/Antagonist Analgesics
-Pentazocine (Talwin) ---why sched. IV? --> Talwin Nx

-Butorphanol (Stadol) - not sched.

-Nalbuphine (Nubain) - not sched.
Name 1 Narcotic Antagonists
-Naloxone (Narcan) pure antagonist **CANNOT BE TAKEN ORALLY. only works for IV.
Name 2 Narcotic Antidiarrheals
-Diphenoxylate with Atropine (Lomotil) Sched. V --> Atropine is an anticholinergic= slow down GI

-Loperamide (Imodium) no abuse potential. OTC
Name 4 Narcotic Cough Preparations
-Hydromorphone (Dilaudid) Sched II

-Hydrocodone (Hycodan) Sched III

-Codeine (Robitussin AC) Sched V

-Dextromethorphan (Robitussin DM) OTC no abuse potential (only one on this list)
Name 5 Non-Narcotic Analgesics (eg. Salicylates)
4 SALICYLATES:
-Acetylsalicylic Acid - Aspirin (Bayer, Anacin, Alka Seltzer)
-Enteric Coated Aspirin (Ecotrin)
-Salsalate (Disalcid)
-Choline Salicylate (Arthropan) liquid

-Acetaminophen (Tylenol, Anacin III) -*NOT A SALICYLATE
Salicylates Therapeutic Properties - all salicylates have these properties
-Analgesia =mild to moderate pain
-Antipyretic =lowers febrile temperature for fever
-Anti-inflammatory =arthritis
-Anti-platelet =**Acetylsalicylate only
Salicylate: Antiplatelet properties
-acetylsalicylate only
-transient ischemic attacs (TIA)
-post heart attack - lowers possibility of having a second MI
-cardiac valve replacement (CVR)=thrombosis. --aspirin = less clotting **that's the new use of baby aspirin. it's now for adults, it's never used for children. and use only in VERY LOW dose of Aspirin
Salicylates: GI Effects
-nausea/vomiting

-Ulcerations -enteric coating to bypass stomach
Salicylates: Toxicities
-tinnitus= early warning- salicylate in the blood is too high

-metabolic acidosis

-dehydration
Salicylates: Uricosuric Properties
-higher doses =uricosuric
-uric acid is pushed from the blood to the urine = helpful for gout pts.
-retains uric acid at LOW DOSES
note to remember about the doses for Salicylates
LOW DOSES = retain uric acid

HIGH DOSES = uricosuric
Salicylates: Hypersensitivity
-higher incidence in women
-higher incidence in asthmatics
-cross sensitivity with some NSAIDs (pts. may also be allergic to Motrin, Aleve)...
Salicylates: Doses
LOW DOSE for Antiplatelet

HIGH DOSE for Anti-inflammatory

LOW DOSE to retain uric acid

HIGH DOSE for uricosuric
Salicylates: Other Uses
-topical use
1. keratolytic =dissolve on top layer of skin. treatment of warts
2. counter irritant for muscle pain = sports cream --no lactic acid before pain
Salicylates: Products
-Acetylsalicylate =possesses antiplatelet properties

-Salsalate =low incidence of GI irritation (remember its side effects? ulcerations)

-Methylsalicylate =extremely TOXIC -your sports creams

-NO liquid form of Aspirin -must use Alka Seltzer -liquid aspirin
Acetaminophen (not a Salicylate) Properties
-Analgesic
-Antipyretic
-do not have anti inflammatory and platelet properties

-dont exceed more than 4g/day
-why cough adult syrups are not used for toddlers now?
Acetaminophen Toxicities
-Hepatotoxicities : fatal doses at 25 grams (or 50 strong Tylenol)

-Antidote - must be within 6 hours of OD. --> Acetylcysteine (Mucomyst) have also been used for resp. therapy
Rheumatoid Arthritis Intro
-Auto-immune disease
-progressive
-destruction and deformities of joints
-juvenile to adult onset
-Step therapy (less toxic to more toxic): --> salicylate, NSAIDs. progressively more toxic
NSAIDs Properties (Antiarthritic)
-Analgesic, antipyretic, anti-inflammatory

-has a little bit of antiplatelet property but not used for that, like Aspirin, it can make a pt. bleed
NSAIDs Side effects (Antiarthritic)
-GI effects : nausea, ulcerations

-Na & H2O retention = NSAIDs can increase BP

-Decreased renal function

-Anti-Platelet = must discontinue prior to a procedure
NSAIDs : Indomethacin, Ketorolac, Sulindac (Antiarthritic)
-Indomethacin =side effects of severe frontal headaches

-Ketorolac =inj. for acute pain, no abuse potential.

-Sulindac =low incidence of decreasing renal function (least used)
what is the only inj. analgesic in the market that is NOT controlled substance?
KETOROLAC

no more than 5 days of drug therapy = renal damage also used for drug abusers
Cox 2 Inhibitors -Cyclooxygenase 2 receptors) Cox 1 and Cox 2 (Antiarthritic)
-Properties
**not always prescribed for ulcer pts. because its too expensive only prescribed when 1. severe ulcer 2 no other drug works

PROPERTIES
-decreases inflammation with lesser effects on GI tract
-specifically inhibits cyclo-oxygenase 2 receptors
Cox 1 and Cox 2?
Cox 1 =production of a muco-protective coating in the intestinal tract (against ulcers) --side effect of pts using this for arthritis?. but less.

Cox 2 =causes inflammation of joints
Hydroxychloroquine (Antiarthritic)
-onset of action
-misc.
-side effects
-onset of action : 3 months ...add another drug

-also possesses anti-malarial properties (what its originally used for)

-side effects: 1.reversible coreal opacity -like cataract
2. irreversible retinal damage -destroys the nerve of the eye, pt. can lose their vision so they have to go to eye exams when on this drug.
Intra-Articular Steroids (Antiarthritic)
-useful if only a few joints involved

-biggest risk is infection and antibiotics don't go to joints easily.

-limit on how many joints
Systemic Steroids (Antiarthritic)
-consequences of prolonged use:
adrenal suppression, cataracts, ulcers, depression
Gold Therapy (Antiarthritic)
-inj. =1/month. pill= 1/day but with greater risks of adverse reactions

-gold sodium thiomalate and auranofin

-onset of action is 3 moths =add another drug

-may slow progression of Rheumatoid arthritis

-Adverse reactions : renal damage, and bone marrow depression
MISC. Disease modifying antirheumatic drugs (DMARD's)
-all may slow disease progression
-the following drugs increases the risk of lymphoma and leukemia

-Anakinra (Kineret) =inhibits interleukin1 inflammation
-Etanercept (Enbrel) =inhibits tumor necrosis factor (TNF) inflammation
-Leflunamide (Arava)=inhibits immune modulator inflammation
Chemotherapeutic Agents for Rheumatoid Arthritis
examples: Azathioprine, Methotrexate, Cyclophosphamide

-inhibits immune response- what we want for RA
-adverse reactions : carcinogenic (can cause cancer), bone marrow depression, low immune response
Gouty Arthritis
-in-born metabolic error
-over production of urates
-under excretion of urates through kidneys

-extra uric acid cristalizes in the joint where immune system tries to attack it.

-may be secondary to other disease or drug therapy: 1. sickle cell anemia --> (destruction of RBC realease RNA=purines =uric acid) 2. thiazide and loop diuretics can increase uric acid
Acute therapy for Gouty Arthritis
Colchicine (0.6mg)

-blocks migration of granulocytes to inflamed area, causing less urate deposits
-side effects: (toxicity) severe diarrhea
-dose: is every hour until symptomatic relief or side effects.
Prophylactic Therapy for Gouty Arthritis
-diet-low purine/high carbs: avoid beans, pease, spinach, mushrooms.... restrict meat, fish, seafood, and alcohol....increase intake of H2O.

-Allopurinol (Zyloprim) =decrease metabolic formation of uric acid for over producers

-Probenecid (Benemid) or Sulfinpyrazone (Anturane) =uricosuric agents where uric acid is pushed to the urine for under excreters
Migraine
-recurrent headache with N/V
-contraction of intracranial vessels lead to an aura
-serotonin causes a compensatory vasodilations that impinges on nerves
-contributing factors : 1 tension, 2 medications (birth control pills), 3 food (chocolate, milk)
Acute therapy for Migraine
-medications cause severe vasoconstriction--> not specific for blood vessels in the brain = heart attack

-Ergotamine (Caffergot)= 2dose/24hours

-Triptans= warning is no more than 2 dose/24 hours
Prophylactic Therapy for Migraine
-Propranol (Inderal) - beta blocker
-everyday use
mechanism is still unknown
Name 12 NSAIDs/Antiarthritic/Cox1&2 Inhibitors
-Indomethacin (Indocin)
-Ibuprofen (Motrin, Advil, Nuprin)
-Tolmetin (Tolectin)
-Naproxen (Naprosyn, Aleve)
-Diclofenac (Voltaren)
-Ketorolac (Toradol)
-Fenoprofen (Nalfon)
-Sulindac (Clinoril)
-Etodolac (Lodine)
-Piroxicam (Feldene)
-Ketoprofen (Orudis)
-Meclofenamate (Meclomen)
Why do pts. in NSAIDs get ulcers?
because it blocks Cox 1
Name 1 Cox 2 Inhibitor
Celocoxib (Celebrex)

-given to pts. with higher risk of ulcers. very expensive
Name 7 DMADs

-slows progression of the disease but are MORE toxic
-Hydroxychloroquine (Plaquenil)
-Gold Sodium Thiomalate (Myochrisine)
-Auranofin (Ridaura)
-Etanercept (Enbrel)
-Anakinra (Kineret)
-Methotrexate (Rheumatrex) chemo drug
-Leflunomide (Arava)
Name 4 Gout Therapy Drugs
-Colchicine
-Allopurinol (Zyloprim)
-Probenecid (Benemid)
-Sulfinpyrazone (Anturane)
Name 4 Acute Migraine Drugs
-Ergotamine (Caffergot)

-Sumatriptan (Imitrex)
-Rizatriptan (Maxalt)
-Zolmitriptan (Zomig)
What are the warnings when using Migraine Therapy Agents?
make cause heart attack

...drug mechanism = non specific vasoconstriction = increase cardiac workload = heart attack
1 Prophylactic Migraine Drug
Propranolol (Inderal)

-taken every day
-taken before aura/migraine
Autonomic Nervous System Intro
-Purpose/primary function
-maintain stable internal environment by coordinating, adjusting, and regulating the body's visceral activity

-examples include: digestion, body temperature, heart reate
-primary function is to maintain homeostasis.
ANS Parasympathetic division
-cranio-sacral system
-conserve and restore energy

increase GI and sweat
decrease BP
ANS Sympathetic Division
-Thoraco-lumbar system
-Prepares body for stress and emergency
-also non-stress regulation

increase BP and sweat
decreases GI
Neurofiber Anatomy
-Pre-ganglionic and post-ganglionic fibers
-neurotransmitter vesicles
-junctional spaces
-receptors
Parasympathetic Fiber
-post-ganglionic neurotransmitter: Acetylcholine

-receptor site: Muscarinic

-Activity stopped by Acetylcholine esterase
Sympathetic Fiber
-Post-ganglionic neurotransmitter: Norepinephrine (Catecholamine)

-Receptor Site: alpha, beta1, beta 2

-Activity stopped by: Reuptake (primary mechanism) and Mono amine oxidase (MAO) destroys NE
Neurohormonal Transmission: Acetylcholine
-released by all pre-ganglionic fibers (stimulates nicotinic receptors)

-post ganglionic parasympathetic fibers (stimulates muscarinic receptors)
Neurohormonal Transmission:
Norepinephrine
-post ganglionic sympathetic fibers (stimulates alpha, beta 1 and beta 2 receptors)
Parasympathetic effects in the Eye
-miosis (pupil constriction)
-lacrimation (tear secretion)
-accommodate for near vision (fixed for reading)
-decreased intra-ocular pressure (decrease symptoms of glaucoma)
Parasympathetic effects in the Digestion
-increase saliva secretion
-increase stomach acid = ulcer
-increase peristalsis = diarrhea
Parasympathetic effects: cardio, lungs, and bladder
-decrease heart rate

-bronchial constriction (asthmatics) =bad property--> muscarinic receptor stimulates this--> antiasthmatic drugs = blocks muscarinic =anticholinergic = asthma

-Enhances urination: bladder contraction, and sphincter relaxation
Parasympathomimetic Agents
-Bethanechol =stimulates GI motility and bladder (specific for GI & bladder contraction) - for pts who came out of surgery and to stimulate them

-Pilocarpine =ophthalmic - lowers intra-ocular pressure =gluacoma pts.
Parasympathomimetic Agents Contraindications
-asthma
-cardiac insufficiency
-peptic ulcer
-eye drps may still be used with precaution (make sure it does not drain and get in the blood stream)
Acetylcholine Esterase Inhibitors
-blocks acetylcholine esterase enzyme from breaking down acetylcholine

-pharmacology will be similar to parasympathomimetic agents, just mechanism of action differs
Edrophonium
-Acetylcholine Esterase Inhibitor
-short acting reversible = minutes. only used for diagnosis.
-diagnose myasthenia gravis -muscle weakness. theory is body does not produce enough Ach
Intermediate acting reversible agents
-Neostigmine and Pyridostigmine:
treatment of myasthenia gravis

-Physostigmine: ophthalmic agent -lower intra-ocular pressure (glaucoma)

-Donepezil, Galantamine, Rivastigmine: temporarily lessen symptoms of Alzheimer's Disease - theory is the body not producing enough Ach.
Long Acting Irreversible Agents
Echothiophate and Isofluorphate:

-Organophosphate (used in pesticides, bannned in US) toxic agents --powerful treatment for glaucoma but cant go to blood stream
-Must use precaution when administering by placing pressure on the corner of the eye
-only utilized as an ophthalmic agent
Anticholinergics
-blocks muscarinic receptor so that acetylcholine cannot bind and stimulate
Anticholinergic effect on the eye
-dry eye
-accommodate for far vision
-mydriasis -dilate pupil
-increase intra-ocular pressure
Anticholinergic effect on digestion
-decreased saliva production
-decreased acid production = decrease ulcer
-decreased peristalsis =constipation
Anticholinergic effect: cardio, pulmonary, and urinary
-increased heart rate (good for bradycardia)

-urinary retention especially in BPH (esp. prostatic pts)

-bronchodilation (asthmatics)
Anticholinergic order of sensitivity (by dose)
-secretory (saliva, sweat, stomach acid)
-eye
-heart
-GI motility (highest dose, but more side effects and secretory, eye, heart, are being affected)
Anticholinergic Therapeutic Use
1. Natural Alkaloids

-prior to procedure (decrease aspiration) to avoid secretions and infection during procedure
-sinus bradycardia
-motion sickness
-GI cramping to slow down peristalsis

2. Antispasmodic (bladder/GI)
3. Mydriatic (dilates eyes) and Cycloplegic (far vision) -opthalmic exam (eye drops for testing)
Anticholinergic Contraindications
-Myasthenia gravis b/c body does not make enough Ach so we wanna save s many Ach as possible

-Narrow angle glaucoma : most have wide angle

-unstable cardiovascular system: we don't want to keep stimulating the heart

-intestinal atony: don't have bowel sounds= no peristalsis
Sympathetic (Adrenergic)
Alpha, Beta 1, Beta 2 properties
Alpha
-vasoconstriction= increase BP = good for shock
-stimulate sweat and salivary gland
-decrease intra-ocular pressure

Beta 1
-increase heart rate and force of contraction= shock pts = increase cardiac output

Beta 2
-bronchodilation, smooth muscle relaxation for asthmatics and for uterus to relax. used for premature labor to slow/delay it.
Epinephrine: Alpha, Beta 1, 2
Alpha
-decrease IOP
-prolong action of local anesthetics and decrease bleeding (very small amount for its alpha properties)

Beta 1
-increase blood pressure in shock

Beta 2
-relieve bronchospasm
-status asthma -non-stop asthma and anaphelactic shock (ex. "epipen")
Advantages of Alpha properties of Epinephrine?
1. constricts BV = no bleeding

2. constricts BV =anesthetic stays in that area
Levarterenol
Alpha
-very strong vasoconstriction --too strong that it can cause heart failure
-reversed by Alpha blocker so no strain on the heart. alpha property of Levarterenol is not wanted so we add another drug to block it.

Beta 1
-increases blood pressure in shock
Isoproterenol
Beta 1
-increase blood pressure = shock

Beta 2
-bronchodilation =asthma (inhaled or injected)
Dopamine
Dopamine (outside CNS)
-Renal Artery Dilation for shock pts. =urine output is decreased during shock

Beta 1
-increase blood pressure =shock

Alpha
-very strong vasocontriction (dose rate dependent) =decrease infusion rate of Dopamine so it does not reach alpha level
Dobutamine
Beta 1
-cardiogenic shock
Bronchodilators
Beta 2 Stimulation

Beta 1 Spill over can increase heart rate, sweat, solution=inhalation*
-best avoided by giving via inhaled route and utilizing a beta 2 specific agent (ex. Albuterol )
Alpha Stimulants
Opthalmic Decongestants
-getting congestant out of eye =getting red eye out =Visine
warning*: do not use moe than 3 days--> autonomic rebound effect and eyes will get redder than ever

Nasal Decongestant
-oral products may also increase BP
-topical nasal sprays should not be used for more than 3 days - can cause addiction
Alpha blocking agents
Pheochromocytoma
-disease/tumor in the adrenal gland
-secretes NE that increases BP

Reverse Alpha properties of Levarterenol
-Phentolamine
Beta Blockers
-Utilized to block beta 1 receptors
-all will have beta 2 spill over, some more than others (asthmatic will have problem with this -->blocking B2 = bronchoconstriction)
Beta Blockers Use
-Arrythmia (tachycardia) =B1 blockade slows BP
-Hypertension (decrease renin release) high renin hypertension = block or decrease release of renin
-angina = blocker decrease 02 demand = B1 blocked = decrease HR = decrease O2 demand diminishes
-post MI = beta blocker increases survival (used prophylactically)
-migraine also used prophylactically
Beta blocker caution
-Asthma =use Beta 1 specific

-insulin dependent diabetic = masks symptoms of hypoglycemia

-peripheral vascular disease = poor blood flow to the lower extremities
Hypertension Intro
-afflicts over 60 million americans
-diagnosis
-diastolic > 90 systolic > 140
-age, # of readings (best taken in the morning)
-etiology: essential (primary), and secondary (high renin, Cushing's, drugs)
Hypertension long term consequences
-renal, cardiac, vascular
-non-pharmacologic therapy
-diet = decrease weight, decrease Na, decrease alcohol, decrease fats
-decrease smoking
-increased exercise
-relaxation techniques
Hypertension: Pharmacologic Therapy
short term benefits versus long term
-VHA Coop Study = benefits demonstrated
-mortality and morbidity consequences
Causes of Therapeutic failures : coop study
-compliance = drug side effects
-insufficient dose
-non-compliance to diet/exercise
-drug interactions
-acquired resistance
step approach : hypertension step 1
-diuretic
-beta blocker
-alpha adrenergic blocker
-ace inhibitor
-calcium channel blocker
step approach : hypertension step 2
-sympatholytic
-beta blocker
-alpha adrenergic blocker
-ace inhibitor
-calcium channel blocker
step approach : hypertension step 3
-vasodilator
step approach : hypertension step 4
-sympatholytic --> Guanethidine
Diuretics
-Definition
-Use
Definition = increases formation of urine

Use =
-management of edema (worse lungs) - CHF, cranial, ascites (fluid build up in the abdominal area)
-hypertension
-maintain urine flow -shock
-protect from nephrotoxic agent
-glaucoma
Osmotic Diuretics (1st category)
-non -electrolyte
-freely filterable at glomerulus
-pharmacologically inert = no receptors = no side effects
-osmotically pull active particles into blood stream and into uring
-no effect on serum electrolyte balance
Osmotic Diuretics
-toxicities
-use
toxicities
-increased cardiac work load

use
-maintain urine volume during shock/renal failure
-protect against nephrotoxic agents
-glaucoma -intraocular pressure decreased
-cerebral edema - often trauma
Carbonic Anhydrase Inhibitors (2nd category)
Pharmacology
-increases loss of bicarbonate in urine and loss of sodium
-diuretic effects works for only 3 days (short term)
-decrease intraocular pressure effects continues indefinitely

if used more than 3 days can cause metabolic acidosis and resp. complications
Carbonic Anhydrase Inhibitors
-toxicities
-use
toxicities
-drowsiness
-metabolic acidosis

therapeutic use
-short term diuretic
-glaucoma
Thiazide Diuretics
pharmacology
-blocks reabsorption of Na and H20 in distal tubule of kidney

-Metolazone also blocks reabsorption in the proximal tubule of kidney

-increases secretion of K into urine
Thiazide Diuretics other metabolic effects
-increases blood uric acid (gout pts), sugar, cholesterol, and triglyceride
-increases blood Ca
-decreases blood K, and Magnesium
Thiazide Diuretics
-Use
-hypertension
-management of Edema (Metolazone with or without a loop diuretic)
-contraindication: hypercalcemia
Loop Diuretics (4th Category)
pharmacology
-blocks reabsorption of Na and H2O in ascending loop of henle (more powerful diuretic)
-increases secretion of K into urine
Loop Diuretics
-toxicities
-other metabolic effects
toxicities
-Ototoxicity, nephrotoxicity

other metabolic effects
-increases blood uric acid, sugar, cholesterol, and triglyceride
-decreases blood Ca *
-decreases blood K and Magnesium
Loop Diuretics
-Use
-hypertension
-management of Edema
-treatment of hypercalcemia
Potassium Sparing Diuretics (5th Category)
-direct acting
-indirect acting
direct acting
-Triamterene
-Amiloride
-blocks reabsorption of Na and H2O in collecting duct of nephron

indirect acting
-Spironolactone
-competetive inhibitor of Aldosterone
Potassium sparing diuretics
-pharmacology
-minimal diuretic effects
-decreases secretion of K into urine
Potassium sparing diuretics
-use and therapeutic alternatives
therapeutic use
-spare K loss of diuretics
-additional uses of Spironolactone (block aldosterone) =edema with liever failure and congestive heart failure

therapeutic alternatives
-foods high in K
-K supplement - caution with IV administration
Potassium sparing diuretics
-toxicities
-hyperkalemia = therefore K is not administered concurrently
Sympatholytics (6th category)
Step 2 therapy

Side effects
-Na and H2O retention
-postural hypotension
-constipation
-dry mouth
-impotency
Sympatholytic Agents
Clonidine
- rebound hypertension if not compliant
-patch alternative
-may be used for acute high BP

Methyldopa

Reserpine
-noted to cause breast CA

Guanethidine
-4th step due to diarrhea
Hypertension : Beta Blockers
-blocks renin release

-caution: diabetics (masks hypoglycemia) and asthmatics (effect of Beta 2)
Hypertension : Alpha Adrenergic Blockers
-Dual mechanism = blocks alpha receptor and directly causes vascular smooth muscle vasodilation

-no rebound tachycardia

-first dose effect = caution for syncope
Hypertension : Alpha Adrenergic Blockers

-uses
-hypertension
-prostate hyperthropy -shrinks prostate
Hypertension : Vasodilator (Step 3)
-direct relaxation of vascular smooth muscle
-rebound tachycardia (beta blocker 1)
-Na and H2O retention
Hypertension :Vasodilator Agents
Hydralazine
-side effect= lupus like syndrome= affects joints and skin. dose related

Minoxidil
-side effect = hair growth

Nitroprusside (used for hypertensive emergency)
-dilates arterioles and venules
-therapy cannot exceed 3 days or leads to thiocyanate poisoning (muscle spasm, stupor)

Diazoxide
-side effect =hyperglycemia
-very poor control of the lowering of blood pressure
Hypertension : Angiotensin Converting Enzyme Inhibitor
-blocks conversion of angiotensin 1 to angiotensin 2
-side effects = non productive cough
-use = hypertension, congestive heart failure, diabetic renal sparing
Hypertension: Angiotensin Receptor Blocker
-utilized for pts. that cannot tolerate side effects of ACE inhibitors
-examples: Losartan, Irbesartan
Hypertension: Calcium Channel Blocker
-blocks entry of Ca into cells
-prevents contraction of vascular smooth muscles

use
-hypertension
-angina
-arrhythmia
Name 2 Parasympathomimetic Agents (cholinergic drugs)
-Bethanechol (Urecholine) = stimulate GI motility and bladder

-Pilocarpine (Pilocar) = short acting glaucoma drug
Name 7 Anticholinesterase agents (Acetylchilinesterase inhibitors)
-Edrophonium (Tensilon) = diagnosis for myasthenia gravis
-Neostigmine (Prostigmin) = treatment for myasthenia gravis
-Physostigmine (Eserine)
-Pyridostigmine (Mestinon) =treatment for myasthenia gravis
-Donepezil (Aricept) -treatment for Alzheimer's disease
-Galantamine (Reminyl) -treatment for Alzheimer's disease
-Rivastigmine (Exelon) =treatment for Alzheimer's disease
Name 4 Anticholinergic drugs : Natural Alkaloids
-Atropine = used before surgery to dry up secretion. found in crash carts for bradycardia

-Belladonna =dilates eyes. intestinal cramping

-Hyoscyamine =for intestinal cramping

-Scopolamine (Hyoscine) =before procedure to dry out secretions. patch form is used for motion sickness
Name 3 Synthetic Antispasmodic Drugs (anticholinergic)
-Dicyclomine (Bentyl) =specific for intestinal cramping

-Oxybutynin (Ditropan) =specific for bladder contractions/incontinence

-Tolterodine (Detrol) =specific for bladder contractions/incontinence
Name 3 Synthetic Anticholinergic drugs
-Glycopyrrolate (Robinul) =use before surgery to dry secretions

-Propantheline (Pro-Banthine) =not commonly used because of its too many side effects. but some still used for ulcers

-Ipratropium (Atrovent) =inhaler for asthma
Name 5 Mydriatics and Cycloplegics
-Atropine =long acting m&c

-Cyclopentolate (Cyclogyl) =short acting m&c

-Homatropine (Homatrocel) =short acting m&c

-Scopolamine (Hyoscine) =short acting m&c

-Tropicamide (Mydriacyl) =mydriasis only
Name 5 drugs used in shock (Sympathomimetic/Adrenergic)
-Epinephrine (Adrenalin)

-Isoproterenol (Isuprel)

-Levarterenol (Levophed)

-Dopamine (Intropin)

-Dobutamine (Dobutex)
Name 5 Adrenergic Bronchodilatros/ Beta 2 bronchodilators
-Metaproterenol (Alupent)

-Pirbuterol (Maxair)

-Albuterol (Ventolin, Proventil) = "rescue inhalers" for acute =draw back is it can't be over use = beta 1 spill over =heart attack

-Terbutaline (Brethine, Bricanyl)

-Salmeterol (Serevent) =Prophilactic and sometimes mixed with steroids, Advair. should only be inhaled 2/day
Name 3 Nasal Decongestant
-Phenylephrine (Neo-Synephrine)

-Oxymetazoline (Afrin)

-Pseudoephedrine (Sudafed) =long term pts. with high BP cannot use this
Name 2 Alpha blocking agents
-Phenoxybenzamine (Dibenzyline) =Pheochromocytoma disease

-Phentolamine (Regitine) =reverese Alpha properties of Levarterenol
Name 5 Beta Blocking Agents (Beta1/2 non selective)
-Propranolol (Inderal)

-Nadolol (Corgard)

-Timolol (Blocadren)

-Pindolol (Visken) =also ISA activity

-Labetalol (Normodyne, Trandate) =also alpha blocking activity
Name 3 Beta Blocking agents (Primarily Beta 1 activity)
-Atenolol (Tenormin)

-Metoprolol (Lopresor)

-Acebutolol (Sectral) =also ISA activity
Name 3 Opthalmic (Topical) Sympathetic Blocking Agents
-Timolol (Timoptic)

-Betaxolol (Betoptic)

-Levobunolol (Betagan) =primarily beta 1
Name 3 Osmotic Diuretics
-Mannitol =can be used for glaucoma, shock and nephrotoxic kidneys

-Hetastarch (Hespan) =shock

-Albumin =naturally occurring protein in our blood stream
Name 3 Carbonic Anhydrase Inhibitor
-Acetazolamide (Diamox)

-Methazolamide (Neptazine)

-Dorzolamide (Trusopt) =ophth drop =less potential for side effects if use for glaucoma
Name 4 Thiazide Diuretics
-Chlorthiazide (Diuril)

-Hydrochlorthiazide (Hydrodiuril)

-Metolazone (Zaroxolyn) = **works on both proximal/distal tubule making it synergistic with the loop diuretics
Name 4 High ceiling loop diuretics
-Ethacrynic Acid (Edecrin)

-Furosemide (Lasix)

-Bumetanide (Bumex)

-Torsemide (Demadex)
Name 3 Potassium sparing diuretics
-Spironolactone (Aldactone)

-Triamterene (Dyrenium)

-Amiloride (Midamor)
Name 5 Sympatholitic Antihypertensives
-Methyldopa (Aldomet)

-Clonidine (Catapres) -also topical

-Reserpine (Serpasil)

-Guanabenz (Wytensin)

-Guanethidine (Ismelin) =4th step drug
Name 8 Beta blocking Antihypertensive Agents
-Propranolol (Inderal)
-Metoprolol (Lopresor, Toprol XL)
-Nadolol (Corgard)
-Timolol (Blocadren)
-Atenolol (Tenormin)
-Pindolol (Visken)
-Acebutol (Sectral)
-Labetalol (Normodyne)
Name 3 Alpha Adrenergic Blocking Agents
-Prazosin (Minipres)

-Terazosin (Hytrin)

-Doxazosin (Cardura)
Name 4 Vasodilators
-Hydralazine (Apresoline)

-Minoxidil (Loniten)

-Diazoxide (Hyperstat)

-Nitroprusside (Nipride)
Name 7 Angiotensin Converting Enzyme Inhibitor
-Captopril (Capoten)
-Enalapril (Vasote)
-Lisinopril (Zestril, Prinivil)
-Benazepril (Lotensin)
-Fosinopril (Monopril)
-Quinapril (Accupril)
-Ramipril (Altace)
Name 5 Angiotensin receptor blocker
-Irbesartan (Avapro)

-Losartan (Cozaar)

-Valsartan (Diovan)

-Candesartan (Atacand)

-Telmisartan (Micardis)
Name 9 Calcium Channel Blocking Agents
-Diltiazem (Cardizem)
-Diltiazem SR (Cardizem SR)
-Diltiazem Long Acting (Cardizem CD, Dilitrate XR)
-Felodipine (Plendil)
-Nicardipine (Cardene)
-Nifedipine (Procardia, Adalat)
-Nifedipine XL (Procardia XL, Adalat CC)
-Verapamil (Calan, Isoptin)
-Verapamil SR (Calan SR, Isoptin SR)
What is the receptor site in a parasympathetic fiber?
muscarinic
What is the receptor site in a sympathetic fiber?
Alpha, beta 1, and beta 2