Final

Question 0

Produced by physicians (drug caused disease, dispensing/administration)

Answer 0

Iatrogenic Disease

Question 1

Uncommon drug response resulting from genetic predisposition. (we dont know they occur until they happen)

Answer 1

Idiosyncratic Effect

Question 2

birth defects/ ability to produce birth defects.

Answer 2

teratogenic

Question 3

unavoidable secondary drug effect produced by a therapeutic dose

Answer 3

side effects

Question 4

any severe advanced drug action regardless of dose

Answer 4

toxicity

Question 5

the study of the biochemical and physiological effects of drugs on the body

Answer 5

pharmacodynamics

Question 6

the study of the absorption, distribution, metabolism, and excretion of drugs

Answer 6

pharmacokinetics

Question 7

the study of drugs and their interactions with living organisms

Answer 7

pharmacology

Question 8

the use of drugs in the treatment and prevention of disease or conditions (also called therapeutics)

Answer 8

pharmacotherapy

Question 9

List the FDA Drug Schedule: I-V

Answer 9

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

Question 10

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.

Answer 10

controlled substance act

Question 11

Phases of Drug Trials in Clinical Testing:

Phase I?

Answer 11

normal volunteers (ex: nursing students, pharmacy students).
Tests metabolism and biologic effects.

Question 12

Phases of Drug Trials in Clinical Testing:

Phase II?

Answer 12

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.

Question 13

Phases of Drug Trials in Clinical Testing:

Phase III?

Answer 13

Application for New Drug Application (big trials, randomized controls, blinded, the real deal, 5-40 thousand people).
Tests safety and effectiveness.

Question 14

Conditional approval of New Drug Status is…

Answer 14

New Drug Status

Question 15

Phases of Drug Trials in Clinical Testing:

Phase IV?

Answer 15

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.

Question 16

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.

Answer 16

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.

Question 17

Factors that affect the volume of distribution:

albumin primary protein. Higher protein binding–>lower Volume of distribution

Answer 17

plasma protein binding

Question 18

Factors that affect the volume of distribution:

Lipid soluble pass membranes easily.

Answer 18

solubility

Question 19

Factors that affect the volume of distribution:

lipid soluble, non-ionized, small size, non-protein bound– pass easier

Answer 19

placental transfer

Question 20

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.

Answer 20

blood brain barrier

Question 21

Define Drug Half-life.

Answer 21

T 1/2 time required for amount of drug in the body to decline by 50%

Question 22

Explain Longer Dosing Interval.

Answer 22

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.

Question 23

Decreased responsiveness to a drug as a result of repeated drug administration.

Answer 23

Tolerance

Question 24

What the drug does to your body (type of tolerance) is called...

Answer 24

Pharmacodynamic tolerance

Question 25

this type of tolerance is due to accelerated drug metabolism (ex, auto inducer)

Answer 25

metabolic tolerance

Question 26

this tolerance is described as repeating dose over short period of time. Ex. Nitroglycerine

Answer 26

Tachyphyslaxis

Question 27

The component of the drug response that is cause by psychologic factors and not by the biochemical or physical properties of the drug.

Answer 27

Placebo effect

Question 28

____ is what happens to the mind; "not real" is NOT necessarily true.

Answer 28

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.

Question 29

FDA Pregnancy Categories of Risk and Classifications: | Category ____ is Safe drug (proven in humans and animals)

Answer 29

Category A

Question 30

FDA Pregnancy Categories of Risk and Classifications: | Category __ is thought to be safe (animals, ex: Benadryl, Claritin)

Answer 30

Category B

Question 31

FDA Pregnancy Categories of Risk and Classifications: | Category __ is very high risk for teratogenicity

Answer 31

Category X

Question 32

Narrow therapeutic range versus wide therapeutic range. wider=safer.

Answer 32

therapeutic index- the bigger the number, the safer it is. 3 vs 30--> 30 is safer.

Question 33

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.

Answer 33

blood brain barrier

Question 34

process of action potential (burst) being delivered down the axon.

Answer 34

axonal conduction

Question 35

information is shared between the nerve terminal and the target

Answer 35

synaptic transmission

Question 36

neurotransmitter diffuses across the synapse and undergoes reversible binding to get target

Answer 36

receptor binding

Question 37

Explain the goal of Parkinson's disease

Answer 37

there is no cure; the goal is to improve abilities of daily life, to feel as normal as possible

Question 38

The force of ventricular contraction is proportional to the stretch

Answer 38

Frank Starling's Law

Question 39

The biggest determinant of venous dilation/ venous constriction

Answer 39

Cardiac preload: SV

Question 40

Force against what the heart has to pump, what the heart must overcome, arterial vasoconstriction/vasodilation

Answer 40

cardiac afterload:SV

Question 41

``` Therapeutic Uses for ACE1 Inhibitors: HTN--? HF--? MI--? Diabetic and nondiabetic nephropathy--? ```

Answer 41

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.

Question 42

What is the primary intracellular ion?

Answer 42

potassium

Question 43

What is the primary extracellular ion?

Answer 43

sodium

Question 44

Explain how loope diurectics work.

Answer 44

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

Question 45

How do thiazides work?

Answer 45

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.

Question 46

What are three factors for blood flow and which is the most important determinant?

Answer 46

Vessel diameter (most important determinant) vessel length blood viscosity

Question 47

sodium and water lost in equal proportions is called

Answer 47

isotonic contraction (NS 0.9%)

Question 48

Loss of water is greater than sodium. excessive sweating, burn victims, uncontrolled diabetes.

Answer 48

hypertonic contraction-->give hypotonic solution

Question 49

Losing more sodium than water. Caused by kidney probs, lack of aldosterone, excessive use of diuretics.

Answer 49

hypotonic-->treat with hypertonic solutions (3%). This isnt used very much, be very careful. Lots of side effects, sometimes NS and a diuretic, too.

Question 50

Formula for Cardiac output?

Answer 50

CO=HRxSV: cardiac output= heart rate (sns, pns, beta increase, muscarinic decreases)x SV (myocardial contractility, cardiac afterload, cardiac output, starling's law)

Question 51

Formula for Arterial BP

Answer 51

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

Question 52

MOA: Depletion of the formation of NE from postganglionic sympathetic neurons. It lowers BP and wipes out CNS (lysis SNS)

Answer 52

Resperpine

Question 53

ACE1 inhibitor side effects

Answer 53

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)

Question 54

endocrine issues=gynecomastia, menstrual irregularities, excessive hair growth, sensitive nipples, hypercholemia..these are side effects for what?

Answer 54

spironolactone side effects. | **if you take spironolactone and ACE1, it'll result in severe hyperkalemia

Question 55

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+

Answer 55

role of triamterene

Question 56

Hyperventilation; deep and rapid breathing

Answer 56

repiratory alkalosis; lowers CO2 levels in the blood

Question 57

Retention of CO2 with hypoventilation. Can be a brain issue or a lung issue (COPD)

Answer 57

Respiratory acidosis

Question 58

increase in serum bicarb (increasing pH). Excessive vomiting or excessive suctioning

Answer 58

metabolic alkalosis

Question 59

Chronic renal failure; really bad diarrhea, drinking methanol, increased doses of aspirin.

Answer 59

metabolic acidosis

Question 60

list the normal values for pH, bicard, co2

Answer 60

pH 7.35-7.45 HCO3 22-26 CO2 35-45

Question 61

How do ACE1 work?

Answer 61

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.

Question 62

What does ATII do in our body normally?

Answer 62

it's a blood vessel constrictor and makes it harder for blood to flow through the arteries.

Question 63

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

Answer 63

ACE1 inhibitors

Question 64

These are the "sartans". These work identically to ACE1's with LESS cough and LESS angioedema.

Answer 64

ARB (angiotensin II receptor blocker)

Question 65

Atypicals have the same effects on positive symptoms but are superior on cognitive and negative symptoms. Atypicals also produce little to no tardive dyskinesthesia.

Answer 65

side effects for traditional versus atypical antopsychotics

Question 66

metabolism is saturated; this is very unique for phenytoin; very high levels-->toxicity. a small dosage can make increasing levels shoot through the roof.

Answer 66

michaelis menten

Question 67

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

Answer 67

auto-induction

Question 68

molecules which activate receptors

Answer 68

agonist

Question 69

molecules which prevent receptor activation by endogenous regulatory

Answer 69

antagonist

Question 70

can act as both an agonist and antagonist

Answer 70

partial agonist

Question 71

A _____ is a compound that is pharmacologically inactive as administered as then undergoes conversion to its active form within the body.

Answer 71

prodrug example: levadopa

Question 72

Receptors that mediate responses to epinephrine (adrenaline) and norepinephrine.

Answer 72

adrenergic

Question 73

4 receptor sites: __,__,__,&__ and then dopamine may be seen as an adrenergic receptor.

Answer 73

alpha 1, alpha 2, beta 1, beta 2

Question 74

Receptors that mediate responses to acetylcholine

Answer 74

Cholinergic

Question 75

cholinergic receptor sites

Answer 75

nicotinic N, nicotinic M, and muscarinic

Question 76

performs 7 regulatory functions that have particular relevance to drugs

Answer 76

parasympathetic

Question 77

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.

Answer 77

parasympathetic

Question 78

performs 3 main functions; regulating the cardiovascular system, regulating body temperature, implementing the "fight-or-flight" reaction.

Answer 78

sympathetic

Question 79

muscle relaxation during surgery (used when they fight the ventilator) facilitation of mechanical ventilation, endotracheal intubation.

Answer 79

Blockade of Nicotinic N Consciousness: if patient is paralyzed, they can still hear everything

Question 80

Epinephrine receptors:

Answer 80

alpha 1, alpha 2, beta 1, beta 2

Question 81

norepinephrine receptors:

Answer 81

alpha 1, alpha 2, beta 1

Question 82

what response would you expect if given a acetylcholinesterase inhibitor?

Answer 82

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.