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232 Cards in this Set
- Front
- Back
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rank the strengths of the following drug trials
-open-uncontrolled...controlled trial lacking blinding or randomization....blind randomized controlled.....cohort, case-control analytic |
blind randomized controlled > controlled no blinding > open uncontrolled > cohort/case-control analytic
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look at the summary of Ferguson's paper! "skeptical of efficacy" etc etc
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ok.
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t/f it's cool to accept info from newspaper and magazine articles written by scientific reporters.
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false.
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what's are examples of primary, secondary, and tertiary sources for drug information?
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p-journal articles (.2 - 2 years old)
s-indexers (medline, VIN) .5-3 years t-textbooks, reference works (.5-10 years) |
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what are the 3 considerations you should take for drug information sources?
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age, validity, accessibility
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what's the basic path of a one-compartment model?
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admin->body->elimination
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what is first order?
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elimination is constantly proportional to the concentration at that moment.
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the idea of half-life only works with what type of elimination?
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1st order.
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Vd is expressed in what type of units?
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volume.
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half life is ______ related to Vd and ________ related to clearance.
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directly, inversely
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define bioavailability.
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the fraction of a dose which is absorbed.
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what are the drug schedules again....?
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C1 = high abuse potential, no use at all
C2 = high abuse but legally accepted use. C3-C5 = decreasing abuse potential |
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what are 3 big abuse drugs right now?
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tramadol
propofol pentobarbital |
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what's the assisted suicide drug?
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pentobarbital
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T/F ALL controlled substances must be in a securely locked, strong cabinet.
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true.
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what are the 4 record keeping requirements?
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acquisition
invoices inventory medical record |
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what's the special form for a C2?
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222 form.
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how long do you have to keep invoices at a minimum?
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2 years.
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what are the 8 prescription requirements?
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drug name
dosage form directions date written signature dr. name and DEA# patient name number of refills |
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what's special about C2 prescriptions, how long are they good and what's the max # of refills?
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must be on separate prescription
expires in 7 days NO REFILLS |
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T/F you can combine C3-C5s
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true!
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for C3-C5s, what's the expiration date and how many refills max?
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6 months
5 refills |
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what's the expiration for legend and OTC prescriptions?
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12 months.
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T/F for labeling requirements, state requirements are MINIMUM
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false. federal are minimum
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T/F you shouldn't use SID
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true.
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What 3 things are also required for a University prescription?
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Client name + stickers
Client status (in, out, home) supervising clinician |
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T/F a DEA# signature is always needed when writing a controlled med script
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false. only if it's going home.
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hydromorphone, morphone, fentanyl are all examples of what?
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C2s
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what is the 3 line script format?
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Drug name + strength
Sig Quantity Tramadol 50mg 1 tab PO Q8H #30 |
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T/F younger animals have less % H20 as body weight
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false. higher
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what provides hydrostatic vs. osmotic forces?
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HS - heart/vasc tone
osmotic - solutes |
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osmolarity vs. osmolality
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larity = particles/liter
lality = particles/kg |
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what's the osmolarity equation?
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mosmoles/l = 2[Na] + 2 [K] + glucose (mmol/l)
NOTE: if glucose is in mg/dl need to divide it by 18. |
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define one milliosmole
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one millimole of an undissociable solution.
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what is the major determinant of plasma osmolality? (it's an ion)
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Na+
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what is the normal plasma osmolality range? (UNITS TOO)
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280-310 mOsm/kg
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T/F the osmotic effect is mostly dependant on the weight of the particles involved.
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false. ONLY on the number. nothing else matters.
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what is the osmotic effect of a solute dependant on?
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the membrane surrounding the compartment.
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what do you call the effective osmotic pressure of a solution and what does it mean?
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tonicity....how much membranes are expanded from drawing water in.
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will hypertonic solutions increase or decrease vascular space?
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increase. puts pressure on the vascular membranes.
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T/F urea and potassium have no tonic effect, while glucose and sodium do.
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true.
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crystalloids are solutes of (high/low) mol wt. that can enter (some/all) body fluid compartments
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low
all |
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animals with ascites have [low/high] oncotic pressure in the vascular space
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LOW.
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colloids are solutes of [high/low] molecular weight that can enter [some/all] fluid compartments
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high
restricted to plasma compartment |
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T/F all body spaces are isotonic with one another
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true.
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which electrolyte gets lost in addison's disease?
glucose, sodium, or potassium? |
Na.
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what are 6 signs of ECF volume depletion
(temp, pulse, MMs, CRT, skin, extremities) |
higher temp, weak fast pulse, pale/dry MM, slow CRT, poor elasticity, cool distal extremities
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what are 4 things you use to monitor hydration?
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skin turgor
thoracic auscultation weight hematocrit |
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look at L6 S30.
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ok.
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how do you do replacement volume? how about for an 8% dehydrated 10kg dog?
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% dehydration x body weight (kg)
so 10kg dog 8% dehydrated: .08 x 10 = .8 liters |
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what is the amount of normal maintenance fluids for a NON DEHYDRATED dog (daily)?
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40-60 ml/kg/day
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evaporation and sweating are examples of (insensible/sensible) losses?
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insensible
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what route should you give hypertonic fluids with?
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oral.
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when and what kind of fluids do you give sub Q?
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mild dehydration
isotonic fluids |
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what 4 things do you need to consider for type of fluid replacement?
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type of loss (ECF tonicity)
acid-base energy special ions |
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what has the highest NaCl of all solutions given for therapy?
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saline
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what is the only non-isotonic solution given for therapy (hypotonic...)
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D5W
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LRS is a balanced or unbalanced e- solution?
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balanced
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what's to worry about giving fluids with calcium?
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they can combine with drugs.
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T/F plain sterile water is a decent fluid preparation
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false. never use it alone it's hypotonic.
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T/F .9% (normal) saline is a safe choice when e- status is unknown.
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true
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when you combine dextrose with saline what is the animal actually getting? what does this mean?
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the dextrose gets metabolized so the saline is what is actually working ie if you start isotonic it will NOT end up that way.
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T/F for maintenance the amount of K+ is correct in Normosol R/M
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false. you need to add a lot if the animal is not eating.
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what is the MAX rate for parenteral K+ administration?
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.5 meq/kg/hr
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T/F you can use glucose for long-term energy replacement
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FALSE.
you need IV nutrition. |
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T/F glucose overdose can lead to H20 and sodium retention!
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FALSE.
causes h20 and Na+ loss. |
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T/F 5% dextrose should not be used as maint. fluid.
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true.
will give e- depletion. |
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when would you give bicarb?
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severe metabolic acidosis only.
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when do you give colloid?
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shock or hypoproteinemia
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plasma protein and dextran are examples of what?
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colloids
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what can acidosis do to K+ levels?
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make them look falsely high.
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check out L6S56ish for case examples
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ok.
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what are the 4 determinants of cardiac performance?
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preload
cardiac output contractility afterload |
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what is the main cause of congestive heart failure in dogs? the 2nd?
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mitral disease
2nd is DCM |
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what is the equation for CO?
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HR x SV
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what do you call the degree to which the myocardium is stretched prior to the onset of systole?
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preload.
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what do you call the force that resists ventricular ejection of blood?
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afterload
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T.F. afterload is pretty much equal to arterial blood pressure
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false.
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what is the frank-starling relationship?
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preload is related to EDV
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CO (SV) is generally maintained at the expense of what 2 things?
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EDV and EDP
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what is the major goal of CHF treatment?
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to maintain CO (SV) at a lower EDP
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for CHF treatment, what do you want to do to the following values?
preload, contractility, afterload |
decrease preload and afterload
increase contractility |
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what should you do regarding dietary sodium in a CHF patient?
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lowwwwwwwww
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what kind of diuretic do you want to use with CHRONIC CHF management?
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a K-sparing like spironolactone
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what are 2 benefits of preload reduction?
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diminished pulmonary edema/congestion
reduction in cardiac size |
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T/F preload reduction can have ADVERSE effects on SV
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true! vigorous reduction.
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what are 2 ways to reduce intravascular volume?
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low dietary salt
promote excretion of salt and water |
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what are 2 ways of redistributing vascular fluid?
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venodilation
afterload reduction |
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what is by far the most common CHF drug?
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DIGOXIN!!!!!
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what are 4 effects of digitalis?
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decrease sinus rate
slow AV conduction increase PS tone and decrease sympathetic tone increased CO |
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HOW does digoxin increase PS tone and decrease sympathetic tone?
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inhibit na/k atpase in the baroreceptors.
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how does digoxin increase CO?
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when you block that atpase it indirectly makes more calcium go into the cardiac cell which increases contractility!
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what's special about dosing digoxin and also its excretion?
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it's based on LEAN BODY WEIGHT!!!! so fat animals should not get more! also dose AWAY from eating or giving other drugs.
also it's renally excreted so be careful in patients with renal failure |
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digoxin has a wide/narrow TI
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narrow!
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GI upset/vomiting and ECG changes are indications of what?
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digitalis toxicity
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what are some predisposing conditions to digitalis toxicity?
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renal failure, thyroid issues, obesity, hypo K/Mg, hyper Ca
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what exactly are you reducing when you have "afterload reduction"?
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the forces opposing myocardial fiber shortening this reducing the resistance to ventricular ejection
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what is the main driving force that governs tissue perfusion?
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ABP
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what kind of drugs do you use to reduce afterload?
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arterial vasodilators
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what does afterload reduction do to EDP?
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lowers it.
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decline in vasc resistance --> rise in SV --> ABP?
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ABP is usually only slightly reduced
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what are the 2 classes of non-digitalis positive inotropes?
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B1 agonists
phosphodiesterase inhibitors |
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botutamine and dopamine are examples of what class of meds?
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B1 agonists
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when do you use B1 agonists?
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acute CHF when waiting for digitalis steady state levels.
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T/F B1 agonists can predispose one to cardiac arrhythmias
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true.
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T/F B1 agonists increase contractility and o2 consumption but decrease heart rate
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false. all three are increased.
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Adenosine is a(n) ________ receptor agonist that has a (+/-) effect on heart rate.
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A1
inhibitory/tonic effect |
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what is pimobendan?
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the only widely used PDE inhibitor.
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what is the strongest indication for pimobendan?
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treat advanced canine DCM
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what is the mechanism behind pimobendan as an inotrope?
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PDE3 inhibitor--> increases ventricular contractility by increasing sensitivity to intracellular Ca by increasing the affinity of troponin C for Ca2+.
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what are 2 advantages of pimobendan compared to other inotropes?
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modest increase in intracell. calcium and little increase in o2 demand
reduced arrhythmia potential |
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what is the mechanism behind pimobendan as a vasodilator?
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PDE3 inhibitor --> increased cAMP--> decrease Ca binding to myosin
this opens ATP dependant K channels which has vasodilating effects |
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which of the following is NOT vasodilated by pimobendan?
peripheral arterioles, pulmonary arterioles, pulmonary venules, coronary arteries, peripheral veins |
NOT pulmonary venules
the rest are true. |
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Beta antagonists have (+/-) inotropic effects
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negative
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HOW do B1 antagonists help with DCM?
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by reversing sympathetic stimulation.
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Ca channel blockers are (+/-) inotropes
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negative
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what are 3 mechanisms for vasodilation?
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direct action on smooth muscle cells
interaction with ANS/Angio2 action Ca channel blockers |
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A1 antagonists, parasympathetic agonists and Beta agonists all do what to blood vessels?
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vasodilate.
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T/F you want to use vasodilators to treat cushing's
|
true!
because it helps hypertension which is often secondary |
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which of the following do you NOT want to use vasodilators with?
hyperthyroid, renal failure, cushings |
use them with ALL of those because those all cause hypertension
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what are 3 general uses for vasodilators?
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hypertension
CHF preload/afterload local vasoconstriction ie laminitis |
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what do nitrates/nitrites specifically do?
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VENOdilate
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what do you need to keep in mind givine oral nitrates?
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very high 1st pass hepatic metabolism.
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what is an example of an oral, transdermal, and an IV nitrate?
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oral - nitroglycerine
transderm - nitroglycerine IV- nitroprusside |
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see S6 of vasodilators lecture.
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ok.
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skin rash, hypotension, cyanide tox and tolerance are all side fx of what drugs?
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nitrates.
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what happens to the heart if you have both an A1 and an A2 blockade?
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tachycardia
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what does hydralazine do and how?
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direct acting arteriodilator by essentially being an afterload reducer
don't really know mech |
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T/F B1 agonism is inotropic.
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true.
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what are aminophylline and pimobendan? how do they work?
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PDE inhibitors.
inhibit cAMP breakdown resulting in smooth muscle relaxation. |
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what effect do cholinergics, beta adrenergics and A1 antagonists have on the vasculature?
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autonomic vasodilaters!
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what class is dopamine and where does it mainly affect? how does it work?
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B1 agonist.
renal vasculature. so with low/no urine output even after fluids. LOW doses. |
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what class is prazosin? when is it used?
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A1 antagonist.
used in CHF. |
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what do A1 antagonists do both to vaso system and the heart overall.
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arteriolar AND venous dilatation
decreases afterload. |
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why would you want to use A1 (specific) vs. a nonspecific A1 antagonist?
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avoid tachycardia!
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what is the DOC for CHF?
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prazosin, an A1 antagonist
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what do you need to watch out for with the 1st dose of an A1 antagonist?
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striking arteriolar and venous dilitation leading to hypotension and maybe passing out.
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what is the main use of ACE inhibitors?
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heart failure and mitral insufficiency (esp. early)
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what do ACE inhibitors do to aldosterone secretion?
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reduction.
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if a drug name ends in "pril" what does it do?
|
ACE inhibitors.
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what's the big benefit of enalapril?
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increased exercise tolerance
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T/F ACE inhibitors are prodrugs.
|
true.
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what is special about benazepril compared to the other ACE inhibitors?
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doesn't have a sulfhydryl group which can lead to AI reactions.
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what is losartan?
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an angiotensin II receptor antagonist.
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T/F the afferent arteriole is more sensitive to the effects of ATII than the efferent arteriole.
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false. thats backwards.
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what 3 things affect the amount of glomerular filtrate?
|
systemic BP
renal bloodflow state of Aff/Eff arterioles |
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in CHF there is a (higher/lower) amount of circulating AT II.
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higher.
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HOW does AT II keep the kidney happy?
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by constricting the efferent arteriole MORE which increases back pressure and keeps normal filtration going.
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what do ACE inhibitors do to GFR?
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increase it.
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T/F you should be careful when using ACE inhibitors because you can cause prerenal azotemia.
|
true.
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what do calcium channel blockers do to the vasc system?
|
dilate!
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what's the big side effect of Ca channel blockers?
|
negative inotropic
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what Ca blocker is mainly just vasodilitative?
|
nifedipine
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what Ca channel blocker is has vasodilitating and cardiac effects?
|
diltiazem
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what Ca channel blocker mainly affects the heart?
|
verapamil
|
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review: what class are straight arteriodilators, combined art-veno dilators and just venodilators?
|
arterio - hydralazine
arterio/veno - prazosin, ACE inhi, Ca blockers veno - nitrates |
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what are the 2 biggest drugs used for mitral disease in dogs?
|
ACE inh
furosemide (loop diuretic) |
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as far as treating arrhythmias goes...you want to do what to automaticity, refractory period,AV conduction and spontaneous discharge.
|
reduce automaticity
increase refractory slow AV conduction reduce spontaneous discharge |
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what does the QRS look like with a supraventricular arrhythmia?
|
normal.
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what is the important electrolyte for each phase of the cardiac electrical cycle?
|
sodium then calcium then potassium
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what phase of the cardiac e- cycle do a lot of the ANS drugs work on?
|
4
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what does isoproterenol do to phase 4 of the e- cycle?
|
increases the slope so increases heart rate.
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look at L9 S7 very important
|
ok.
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class 2 antiarrhythmics are essentially what ANS drug type? what phase do they affect?
|
beta blockers. phase 4.
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class 4 antiarrhythmics are essentially doing what? how do they affect phase 4?
|
calcium blocking. they push the phase 4 plateau down.
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class 1s work via what mechanism?
|
Na blockers
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class 3s work via what mechanism?
|
K channel blockers
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what phase do class 1s work on and what do they do overall and to the refractory period and AP duration?
|
reduce phase 0 depole so delay it....prolong ERP and APD.
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when do you NOT want to use Class 1s?
|
complete heart block or w/ sinus bradycardia or AV blocks.
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what kind of antiarrhythmic can cause seizures?
|
Class 1s. note they can also cause cardiovascular collapse.
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what are quinidine, procainamide and lidocaine classified as?
|
class 1s?
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what are a few oral versions of lidocaine?
|
tocainamide
mexilitine phenytoin |
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what is the adverse cardiac effect of quinidine the class 1?
|
indirect antimuscarinic! can increase sinus rate and AV conduction.
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what are the 2 extracardiac side fx of quinidine the class 1?
|
GI - vomiting/diarrhea etc.
CNS - issues horse allergies! |
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what's the DOC for ventricular arrhythmias, premature ventricular contractions, and re-entry arrhythmia?
|
quinidine.
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procainamide is basically weakass quinidine EXCEPT in what respect?
|
it's a more potent negative inotrope.
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how are class 1Bs like lidocaine different than class 1s like quinidine as far as ERP and APD go?
|
shorten them so accelerate repolarization.
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what are class 1bs selective for?
|
arrhythmogenic tissue NOT normal tissue!
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whats the administration for lidocaine the class 1b?
|
IV b/c oral bioavailability is 30%ish.
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what is the IV DOC for ventricular arrhythmias and ventricular premature complexes?
|
lidocaine.
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T/F lidocaine is a pretty good choice for atrial problems.
|
false better go with procainamide and quinidine.
|
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what are the 2 ORAL class 1B drugs (lidocaine-ish)?
|
tocainide and mexiletine
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which class 1b is more likely to cause toxicity: IV or oral?
|
oral
|
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what do you use for supraventricular arrhythmia...
-with CHF -w/o CHF |
with CHF = digitalis
w/o CHF = C2 (beta blockers) and C4 (Ca blockers) |
|
|
see L9 S37 very important
|
ok.
|
|
|
which part of the EKG do Class 2 work on? what do they do in general?
|
prolong phase 4!
reduce everything! including airway space. |
|
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what are the first letters for the nonspecific beta blockers? the specific?
|
nonspecific = T-P-N + olol
B1 specific = M - E -A |
|
|
what drug do you use for: supraventricular tachyarrhythmias (atrial flutter + fibrillation, sinus tachytardia) and ventricular tachycardia?
|
beta blockers! Class 2!
|
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when do you NOT want to use beta blockers? there's 5 sitcheations
|
AV block
asthma CHF hypotension Diabetes |
|
|
what are amiodarone and sotalol?
|
Class 3 ie K blockers!
|
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what do you use to suppress life-threatening arrytthmias like ventricular tachycardia and DCM in dogs?
|
K blockers! class 3
|
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T/F K blockers like amiodarone are slow onset and you should use a loading dose
|
true.
|
|
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what are 2 big side fx of class 3s like amiodarone?
|
liver dz
GI problems |
|
|
what are verapamil, diltiazem, and the 2 dipines?
|
class 4! Ca blockers!
|
|
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which class 4 has mainly cardiac action?
|
verapamil
|
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which C4 has mixed cardiac/vascular action?
|
diltiazem
|
|
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which 2 C4s have primarily vascular action?
|
the dipines
|
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which part of the EKG do C4s affect and how?
|
lengthens repolarization!
phase 1 and 2. |
|
|
what part of the heart do C4s have the greatest effect on?
|
AV node
|
|
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what's the DOC for cat hypotension?
|
amlodipine the C4
|
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|
T/F C4s are good for supraventricular tachyarrhythmias and hypertension in dogs AND cats by slowing AVN conduction.
|
true.
|
|
|
see L9 S37
|
ok.
|
|
|
so what kind of drug do you want to give if you have pulmonary edema AND CHF? why?
|
IV furosemide.
because it is selective for pulmonary veins only. |
|
|
which positive inotropic drug do you want to give in an emergency and why? what is the major side effect of this drug?
|
NOT digoxin b/c oral takes too long
NOT nonspecific B agonists b/c too risky you want SPECIFIC beta agonist dobutamine. the major side effect is tachycardia. |
|
|
which oral drug has been shown to extend lifespan in CHF?
|
pimobendan.
|
|
|
what is the mechanism of pimobendan?
|
PDE3 inhibitor.
|
|
|
T/F digoxin directly decreases aldosterone?
|
false.
|
|
|
what type of arrhythmias do you use digoxin for specifically?
|
supraventricular.
|
|
|
what's the standard deal for monitoring for digoxin toxicity?
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measure right after the 2 hour peak and just before giving the next pill (12 hour trough)
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what drug best manages preload: nitrates or A1 antagonists? why?
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nitrates! because its only a venodilator and A1 antagonists manage pre and afterload.
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what is the mechanism of furosemide?
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selective dilation of the pulmonary veins
stimulates prostacyclin release = enhanced fluid reabsorption from the pulmonary interstitium |
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what is the STRONGEST indication of pimobendan?
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treatment of advanced DCM
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what are 2 advantages to pimobendan compared to other inotropes?
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modest increase in Ca and little increase in 02 demand
fewer arrhythmias |
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what are 3 signs of digoxin toxicity?
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vomiting, extended PR interval, tachyarrhythmias
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what two classes of drugs reduce preload AND afterload? give an example of each?
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A1 antagonists (PRAZOSIN!), ACE inhibitors
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what are the big 2 side effects of prazosin the A1 antagonist?
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hypotension and secondary syncope.
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what 2 drugs do you use IV for ventricular arrhythmias if digoxin is already being used?
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quinidine and lidocaine!
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what are the primo examples of Class 1A and Class 1B (Na blockers)?
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1A - quinidine
1B - lidocaine |
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what is the DOC for atrial fibrillation in horses?
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quinidine
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what drug is good in ALL species for ventricular arrythmias, premature ventricular contractions and re-entry arrhythmias?
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quinidine!
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what is important to note about the interaction between digoxin and quinidine?
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quinidine decreases digoxin elimination!
so 1/2 dose only when giving quinidine too. |
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what are the 4 big side effects of quinidine (1 is in horses only)
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1)indirect antimuscarinic = inc. sinus rate, AV conduction causing supravent. tachyarrythmias
2) GI 3) CNS 4) allergic rxns in horses only. |
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what does it mean if you use quinidine and you note a widening of the QRS on the ECG?
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serious toxicity!
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T/F lidocaine is a common choice for use in dogs with CHF
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false! bad idea.
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Is it OK to give fluids to CHF patients?
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yes just be careful.
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what are 3 complicating factors to drug distribution in cancer patients?
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3rd spacing
aberrant blood vessels high interstitial pressures. |
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what are 2 examples of polymorphisms that cause variability in drug metabolism?
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impaired detox (enzymes expression)
altered activation (C450) |
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T/F a lot of cancer patients come in hypocalcemic.
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false. HYPERcalcemic.
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T/F chemo can be a very selective agent.
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false! it attacks very rapidly dividing cells
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what 3 types of cells does chemo really go after?
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Bone Marrow, Hair in anaphase, GI
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how does chemo kill cells?
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DNA damage (unfixable)
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chemo has a wide/narrow TI
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very narrow.
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