Final Flashcards
Produced by physicians (drug caused disease, dispensing/administration)
Iatrogenic Disease
Uncommon drug response resulting from genetic predisposition. (we dont know they occur until they happen)
Idiosyncratic Effect
birth defects/ ability to produce birth defects.
teratogenic
unavoidable secondary drug effect produced by a therapeutic dose
side effects
any severe advanced drug action regardless of dose
toxicity
the study of the biochemical and physiological effects of drugs on the body
pharmacodynamics
the study of the absorption, distribution, metabolism, and excretion of drugs
pharmacokinetics
the study of drugs and their interactions with living organisms
pharmacology
the use of drugs in the treatment and prevention of disease or conditions (also called therapeutics)
pharmacotherapy
List the FDA Drug Schedule: I-V
I: has no medicinal value/very addictive, highest risk for abuse (–>meth, LSD)
II: tightly regulated, some medicinal value,high risk for abuse (addicted)–>cocaine, morphine, oxycodone
V: Medicinal value, non-addictive–>cough syrup
New drugs must undergo testing for toxicity reviewed by the FDA (1938). In 1970, the _______ states that drugs with potential for abuse must be tightly regulated, hence the drug schedule.
controlled substance act
Phases of Drug Trials in Clinical Testing:
Phase I?
normal volunteers (ex: nursing students, pharmacy students). Tests metabolism and biologic effects.
Phases of Drug Trials in Clinical Testing:
Phase II?
Testing in patients (ex: HTN and take 10 mg and take BP and Tomorrow take 20 mg and take BP, etc).
Tests Therapeutic utility and dosage range.
Phases of Drug Trials in Clinical Testing:
Phase III?
Application for New Drug Application (big trials, randomized controls, blinded, the real deal, 5-40 thousand people).
Tests safety and effectiveness.
Conditional approval of New Drug Status is…
New Drug Status
Phases of Drug Trials in Clinical Testing:
Phase IV?
Post marketing surveillance (still under investigation—still on “trial”).
HCP’s evaluate closely and report finding because they are still under investigation. RN’s and Pharmacists need to monitor these.
A numerical parameter that indicates extent of drug distribution in the body. The higher the number, the more penetration outside the vascular system moving into tissues. Give example.
Volume of Distribution
Ex: 12 liters and we give Digoxin, ionic penetration– goes to heart tissue– large volume of distribution. Check the serum plasma level– its not there– it took off and went into system.
Factors that affect the volume of distribution:
albumin primary protein. Higher protein binding–>lower Volume of distribution
plasma protein binding
Factors that affect the volume of distribution:
Lipid soluble pass membranes easily.
solubility
Factors that affect the volume of distribution:
lipid soluble, non-ionized, small size, non-protein bound– pass easier
placental transfer
Factors that affect the volume of distribution:
Drugs which are lipid soluble and have a transport system pass easier. Non-polar, Non-ionized penetrate blood brain barrier. Keeps toxic substances out but very difficult to get drugs in there too.
blood brain barrier
Define Drug Half-life.
T 1/2 time required for amount of drug in the body to decline by 50%
Explain Longer Dosing Interval.
Dosing interval corresponds to T 1/2 longer T1/2.
The longer the half life, the longer the dosing interval.
Ex. Morphine 1/2 life every 3 hrs wears down. Warfarin has 1/2 life of 24 hrs, so take it daily.
Decreased responsiveness to a drug as a result of repeated drug administration.
Tolerance
What the drug does to your body (type of tolerance) is called…
Pharmacodynamic tolerance
this type of tolerance is due to accelerated drug metabolism (ex, auto inducer)
metabolic tolerance
this tolerance is described as repeating dose over short period of time. Ex. Nitroglycerine
Tachyphyslaxis
The component of the drug response that is cause by psychologic factors and not by the biochemical or physical properties of the drug.
Placebo effect
____ is what happens to the mind; “not real” is NOT necessarily true.
Placebo; let them have their placebo. it is real. placebo can be positive or negative. Depression has a strong placebo effect. YOU CAN THINK YOURSELF BETTER.
FDA Pregnancy Categories of Risk and Classifications:
Category ____ is Safe drug (proven in humans and animals)
Category A
FDA Pregnancy Categories of Risk and Classifications:
Category __ is thought to be safe (animals, ex: Benadryl, Claritin)
Category B
FDA Pregnancy Categories of Risk and Classifications:
Category __ is very high risk for teratogenicity
Category X
Narrow therapeutic range versus wide therapeutic range. wider=safer.
therapeutic index- the bigger the number, the safer it is. 3 vs 30–> 30 is safer.
Drugs which are lipid soluble and have a transport system pass easier. Non-polar and non-ionized penetrate it. It keeps toxic substances out but its also very difficult to get drugs in when needed.
blood brain barrier
process of action potential (burst) being delivered down the axon.
axonal conduction
information is shared between the nerve terminal and the target
synaptic transmission
neurotransmitter diffuses across the synapse and undergoes reversible binding to get target
receptor binding
Explain the goal of Parkinson’s disease
there is no cure; the goal is to improve abilities of daily life, to feel as normal as possible
The force of ventricular contraction is proportional to the stretch
Frank Starling’s Law
The biggest determinant of venous dilation/ venous constriction
Cardiac preload: SV
Force against what the heart has to pump, what the heart must overcome, arterial vasoconstriction/vasodilation
cardiac afterload:SV
Therapeutic Uses for ACE1 Inhibitors: HTN--? HF--? MI--? Diabetic and nondiabetic nephropathy--?
HTN-through vasodilation of arteries and veins and reduces volume
HF-decreases the CO;fluid overload,volume issues.
MI-reduces risk of HF.
D&NN-protein in urine issues, reducing pressure.
What is the primary intracellular ion?
potassium
What is the primary extracellular ion?
sodium
Explain how loope diurectics work.
act on the ascending loop of henle, block reabsorption there (20%) significant diaphoresis. Give loops to move fluid. S/E: hyponatremia, hypochloremia, potential dehydration, hypotension, hypokalemia, ototoxicity, hypocalcemia, hyperglycemia,hyperuricemia
How do thiazides work?
block reabsorption of sodium and calcium in the early distal tubule (10%). Must have a GFR greater than 30. This is the drug of choice for HTN. It dilates the arteries and lowers BP other than fluid loss.
S/E: same as loops except but to a lesser degree with a huge diff being thiazides INCREASE calcium levels.
What are three factors for blood flow and which is the most important determinant?
Vessel diameter (most important determinant)
vessel length
blood viscosity
sodium and water lost in equal proportions is called
isotonic contraction (NS 0.9%)
Loss of water is greater than sodium. excessive sweating, burn victims, uncontrolled diabetes.
hypertonic contraction–>give hypotonic solution
Losing more sodium than water. Caused by kidney probs, lack of aldosterone, excessive use of diuretics.
hypotonic–>treat with hypertonic solutions (3%). This isnt used very much, be very careful. Lots of side effects, sometimes NS and a diuretic, too.
Formula for Cardiac output?
CO=HRxSV:
cardiac output= heart rate (sns, pns, beta increase, muscarinic decreases)x SV (myocardial contractility, cardiac afterload, cardiac output, starling’s law)
Formula for Arterial BP
AP=PVRxCO
Arterial BP=peripheral vascular resistance (afterload) x cardiac output autonomic nervous system (can kick in in seconds)
CO=parasympathetic, sympathetic, baroreceptor reflex RAAS, kidneys, orthostasis
MOA: Depletion of the formation of NE from postganglionic sympathetic neurons. It lowers BP and wipes out CNS (lysis SNS)
Resperpine
ACE1 inhibitor side effects
drugs with “pril” in their name. Hypotension, cough (5-10% of the time, tickling, irritating because increase in bradykinin), hyperkalemia (because of blocking of ATII), renal failure (stenosis), fetal injury (especially in 2nd and 3rd trimesters), angioedema (big fat lips/tongue)
endocrine issues=gynecomastia, menstrual irregularities, excessive hair growth, sensitive nipples, hypercholemia..these are side effects for what?
spironolactone side effects.
**if you take spironolactone and ACE1, it’ll result in severe hyperkalemia
Used in conjunction with a Thiazide or a loop as an addictive effects. It increased diuretic but can lead to dehydration so watch closely. it helps reduce the loss of K+
role of triamterene
Hyperventilation; deep and rapid breathing
repiratory alkalosis; lowers CO2 levels in the blood
Retention of CO2 with hypoventilation. Can be a brain issue or a lung issue (COPD)
Respiratory acidosis
increase in serum bicarb (increasing pH). Excessive vomiting or excessive suctioning
metabolic alkalosis
Chronic renal failure; really bad diarrhea, drinking methanol, increased doses of aspirin.
metabolic acidosis
list the normal values for pH, bicard, co2
pH 7.35-7.45
HCO3 22-26
CO2 35-45
How do ACE1 work?
They decrease levels of circulating ATII and increase levels of bradykinin. This leads to vasodilation of arteries and veins (reduces preload and afterload); reduces blood volume.
What does ATII do in our body normally?
it’s a blood vessel constrictor and makes it harder for blood to flow through the arteries.
The drug of choice of HF; Can cause a cough because of increased level bradykinin; the cough will be a tickly/irritating cough;this condition happens about 10% of the time;can also cause angioedema, which is potentially a life-threatening condition; you may experience fat lips&tongue due to bradykinin;happens 1% of time
ACE1 inhibitors
These are the “sartans”. These work identically to ACE1’s with LESS cough and LESS angioedema.
ARB (angiotensin II receptor blocker)
Atypicals have the same effects on positive symptoms but are superior on cognitive and negative symptoms. Atypicals also produce little to no tardive dyskinesthesia.
side effects for traditional versus atypical antopsychotics
metabolism is saturated; this is very unique for phenytoin; very high levels–>toxicity. a small dosage can make increasing levels shoot through the roof.
michaelis menten
pharmacokinetics where levels can drop on their own. over time, it induces its own induction and we will have to increase the dose at some point
auto-induction
molecules which activate receptors
agonist
molecules which prevent receptor activation by endogenous regulatory
antagonist
can act as both an agonist and antagonist
partial agonist
A _____ is a compound that is pharmacologically inactive as administered as then undergoes conversion to its active form within the body.
prodrug
example: levadopa
Receptors that mediate responses to epinephrine (adrenaline) and norepinephrine.
adrenergic
4 receptor sites: __,__,__,&__ and then dopamine may be seen as an adrenergic receptor.
alpha 1, alpha 2, beta 1, beta 2
Receptors that mediate responses to acetylcholine
Cholinergic
cholinergic receptor sites
nicotinic N, nicotinic M, and muscarinic
performs 7 regulatory functions that have particular relevance to drugs
parasympathetic
Slowing in heart rate, increased gastric secretion, emptying the bladder, emptying of the bowels, focusing the eye for near vision, constricting the pupil, contracting bronchial smooth muscle.
parasympathetic
performs 3 main functions; regulating the cardiovascular system, regulating body temperature, implementing the “fight-or-flight” reaction.
sympathetic
muscle relaxation during surgery (used when they fight the ventilator) facilitation of mechanical ventilation, endotracheal intubation.
Blockade of Nicotinic N
Consciousness: if patient is paralyzed, they can still hear everything
Epinephrine receptors:
alpha 1, alpha 2, beta 1, beta 2
norepinephrine receptors:
alpha 1, alpha 2, beta 1
what response would you expect if given a acetylcholinesterase inhibitor?
you would give an Acetylcholinesterase inhibitor (aka cholinesterase inhib) to reverse nondepolarized drugs.MOA:increase the acetylcholine in the synapse allowing the receptors to attract and attach to acetylcholinesterase. Effects:exactly the same muscarinic agonist (man in the ally)& enhances Nic M, Nic N. ADR:look like man in ally. Toxicity:reverse w/ atrophine drugs-inhibit muscarinic drugs.
