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Pharmacology Final-LindseyVersion > Final > Flashcards

Final Flashcards

0
Q

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

A

Iatrogenic Disease

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1
Q

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

A

Idiosyncratic Effect

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2
Q

birth defects/ ability to produce birth defects.

A

teratogenic

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3
Q

unavoidable secondary drug effect produced by a therapeutic dose

A

side effects

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4
Q

any severe advanced drug action regardless of dose

A

toxicity

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5
Q

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

A

pharmacodynamics

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6
Q

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

A

pharmacokinetics

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7
Q

the study of drugs and their interactions with living organisms

A

pharmacology

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8
Q

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

A

pharmacotherapy

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9
Q

List the FDA Drug Schedule: I-V

A

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

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10
Q

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.

A

controlled substance act

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11
Q

Phases of Drug Trials in Clinical Testing:

Phase I?

A 
normal volunteers (ex: nursing students, pharmacy students).
Tests metabolism and biologic effects.
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12
Q

Phases of Drug Trials in Clinical Testing:

Phase II?

A

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.

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13
Q

Phases of Drug Trials in Clinical Testing:

Phase III?

A

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

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14
Q

Conditional approval of New Drug Status is…

A

New Drug Status

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15
Q

Phases of Drug Trials in Clinical Testing:

Phase IV?

A

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.

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16
Q

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.

A

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.

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17
Q

Factors that affect the volume of distribution:

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

A

plasma protein binding

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18
Q

Factors that affect the volume of distribution:

Lipid soluble pass membranes easily.

A

solubility

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19
Q

Factors that affect the volume of distribution:

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

A

placental transfer

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20
Q

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.

A

blood brain barrier

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21
Q

Define Drug Half-life.

A

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

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22
Q

Explain Longer Dosing Interval.

A

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.

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23
Q

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

A

Tolerance

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24
Q

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

A

Pharmacodynamic tolerance

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25
Q

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

A

metabolic tolerance

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26
Q

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

A

Tachyphyslaxis

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27
Q

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

A

Placebo effect

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28
Q

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

A

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.

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29
Q

FDA Pregnancy Categories of Risk and Classifications:

Category ____ is Safe drug (proven in humans and animals)

A

Category A

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30
Q

FDA Pregnancy Categories of Risk and Classifications:

Category __ is thought to be safe (animals, ex: Benadryl, Claritin)

A

Category B

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31
Q

FDA Pregnancy Categories of Risk and Classifications:

Category __ is very high risk for teratogenicity

A

Category X

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32
Q

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

A

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

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33
Q

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.

A

blood brain barrier

34
Q

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

A

axonal conduction

35
Q

information is shared between the nerve terminal and the target

A

synaptic transmission

36
Q

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

A

receptor binding

37
Q

Explain the goal of Parkinson’s disease

A

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

38
Q

The force of ventricular contraction is proportional to the stretch

A

Frank Starling’s Law

39
Q

The biggest determinant of venous dilation/ venous constriction

A

Cardiac preload: SV

40
Q

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

A

cardiac afterload:SV

41
Q 
Therapeutic Uses for ACE1 Inhibitors:
HTN--?
HF--?
MI--?
Diabetic and nondiabetic nephropathy--?
A

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.

42
Q

What is the primary intracellular ion?

A

potassium

43
Q

What is the primary extracellular ion?

A

sodium

44
Q

Explain how loope diurectics work.

A

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

45
Q

How do thiazides work?

A

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.

46
Q

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

A

Vessel diameter (most important determinant)
vessel length
blood viscosity

47
Q

sodium and water lost in equal proportions is called

A

isotonic contraction (NS 0.9%)

48
Q

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

A

hypertonic contraction–>give hypotonic solution

49
Q

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

A

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

50
Q

Formula for Cardiac output?

A

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

51
Q

Formula for Arterial BP

A

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

52
Q

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

A

Resperpine

53
Q

ACE1 inhibitor side effects

A

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)

54
Q

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

A

spironolactone side effects.

**if you take spironolactone and ACE1, it’ll result in severe hyperkalemia

55
Q

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+

A

role of triamterene

56
Q

Hyperventilation; deep and rapid breathing

A

repiratory alkalosis; lowers CO2 levels in the blood

57
Q

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

A

Respiratory acidosis

58
Q

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

A

metabolic alkalosis

59
Q

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

A

metabolic acidosis

60
Q

list the normal values for pH, bicard, co2

A

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

61
Q

How do ACE1 work?

A

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.

62
Q

What does ATII do in our body normally?

A

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

63
Q

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

A

ACE1 inhibitors

64
Q

These are the “sartans”. These work identically to ACE1’s with LESS cough and LESS angioedema.

A

ARB (angiotensin II receptor blocker)

65
Q

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

A

side effects for traditional versus atypical antopsychotics

66
Q

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

A

michaelis menten

67
Q

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

A

auto-induction

68
Q

molecules which activate receptors

A

agonist

69
Q

molecules which prevent receptor activation by endogenous regulatory

A

antagonist

70
Q

can act as both an agonist and antagonist

A

partial agonist

71
Q

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

A

prodrug

example: levadopa

72
Q

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

A

adrenergic

73
Q

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

A

alpha 1, alpha 2, beta 1, beta 2

74
Q

Receptors that mediate responses to acetylcholine

A

Cholinergic

75
Q

cholinergic receptor sites

A

nicotinic N, nicotinic M, and muscarinic

76
Q

performs 7 regulatory functions that have particular relevance to drugs

A

parasympathetic

77
Q

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.

A

parasympathetic

78
Q

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

A

sympathetic

79
Q

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

A

Blockade of Nicotinic N

Consciousness: if patient is paralyzed, they can still hear everything

80
Q

Epinephrine receptors:

A

alpha 1, alpha 2, beta 1, beta 2

81
Q

norepinephrine receptors:

A

alpha 1, alpha 2, beta 1

82
Q

what response would you expect if given a acetylcholinesterase inhibitor?

A

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.

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