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Pharmacology 1 > Final Review > Flashcards

Final Review Flashcards

1
Q

Adverse Drug Reactions ADR

A

any noxious, unintended, and undesired effect that occurs at a normal drug dose

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2
Q

side effect

A

unavoidable secondary drug effect produces at therapeutic doses

Example- NSAIDS cause ulcers

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3
Q

toxicity

A

any severe ADR regardless of the dose

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4
Q

excretion

A

removal of drug from the body

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5
Q

idiosyncratic effect

A

uncommon drug response resulting from genetic predisposition

example succetylcholine is supposed to last 4-5 min, instead, it would last hours

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6
Q

Iatrogenic Disease

A

disease produced by drugs (our fault)

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7
Q

teratogenic

A

causing malformations of an embryo or fetus.

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8
Q

Med Errors

A

any preventable event that may cause or lead to inappropriate medication use or patient harm, while the medication is in the control of the health care professional, patient, or consumer

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9
Q

tolerance

A

decrease responsiveness to drug as a result of repeated drug administration

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10
Q

pharmacodynamic tolerance

A

patient requires increase drug levels to produce effects that could formerly be produced at decreased drug levels

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11
Q

tachyphylaxis

A

reduction in responsiveness brought on by repeated dosing over a short period of time

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12
Q

Enzyme inducer

A

Decrease levels of object drug by double pac man

Tells enzymes to metabolize drug faster

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13
Q

Pharmacodynamics

A

The study of the biochemical and physiological effects of drugs and the molecular mechanisms by which those effects are produced

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14
Q

Relative potency

A

Refers to the amount of drug needed to elicit an effect

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15
Q

pharmacology

A

the study of drugs and their interactions with living systems

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16
Q

pharmacotherapy

A

use of drugs in the treatment and prevention of disease or conditions

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17
Q

therapeutic objective

A

provide maximum benefit with minimum harm

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18
Q

what are the 9 characteristics of the ideal drug?

A 
effective MOST IMPORTANT
safety
selective-perfect drug is 100% effective
reversibility
predictable
easily administered
void of drug interactions
inexpensive
chemically stable
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19
Q

Enzyme inhibitor

A

Stop the breakdown of other drugs

Increase the level of the object drug
by distracting the pac man with another drug

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20
Q

What characteristics does a drug need to have for it to be able to pass freely though membranes

A

nonpolar
nonionized
lipophilic
minimal protein bound

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21
Q

carcinogenic effect

A

drugs cause cancer

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22
Q

Drug

A

any chemical agent that affects the processes of living

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23
Q

pharmacokinetics

A

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

the effects of the body on the drug

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24
Q

How are controlled substances scheduled?

A

I-worse; no medicinal value and greatest potential for abuse (heroine, meth)

II-medicinal abuse and greatest potential for abuse (dilaudid, percocet, ritalin, morphine)

III-
IV-
V-cough syrup, steroids

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25
Q

Half life

A

time required for amount of drug in the body to decline by 50%

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26
Q

Steady state

A

Point at which the amount of drug eliminated between doses equals the amount of drug administered

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27
Q

Minimum effective concentration

A

the minimum amount of a drug needed to produce a therapeutic effect

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28
Q

The randomized, controlled, tiral (BCT) is the

A

most reliable way to evaluate all drugs

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29
Q

Preclinical Testing

A

usually done on animals,
measures: toxicity, Kinetics, possible therapeutic uses.

Investigational new drug status allows the drug to be tested in humans

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30
Q

Clinical testing

A

happens after preclinical testing

occurs in humans

has three phases

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31
Q

Phase 1 clinical testing

A

before the drug has a name,

tested in normal volunteers

tests for metabolism and biologic effects

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32
Q

Phase 2 clinical testing

A

testing in patients

may not be healthy people

tests therapeutic utility and dosage range

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33
Q

Phase 3 clinical testing

A

tests safety and effectiveness

large multisite trials

after completion may file for new drug application if the data comes out good

if approved granted new drug status and given a name by the FDA

marketing starts

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34
Q

Phase 4 Clinical testing

A

Post marketing survalence

release the drug to the masses, need monitoring, may pull off the market and send out a warning if the drug gets bad post market survalence

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35
Q

volume of distribution

A

numerical parameter which indicates the extent of the distribution of the drug within the body. The measuring of the apparent space in the body that is able to contain the drug

example

if the VOD is 5, there is 5 liters of blood in the body, so the drug will stay within the bloodstream,. if greater then 5, it will travel into the tissues,.

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36
Q

With highly bound protein drugs, you have to worry about protein displacement.

A

Volume of distribution can be effected by protein binding.

example, 99% of warfarin is albumin bound and only 1% is active. If you give another drug that is also protein binding, it can cause the active level of warfarin to rise because they get displaced from the albumin. this can cause the patient harm

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37
Q

agonists

A

molecules which activate receptors (stimulate)

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38
Q

antagonist

A

molecules that prevent receptor activation (blocker)

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39
Q

partial agonist

A

can act as both an agonist and an antagonist

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40
Q

therapeutic index

A

the therapeutic range is the toxic level and the minimum effective concentration.

the more narrow the therapeutic index, the less safe the drug.

the larger the therapeutic index, the more safe the drug.

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41
Q

drug category x

A

never consume while prego

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42
Q

drug category a

A

safe

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43
Q

drug category b

A

safe in animals

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44
Q

an acid in acid is

A

nonionized

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45
Q

Name the only Non sulfa loop diuretic

A

Ethacrynic acid

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46
Q

Dehydration symptoms (one ADRs of diuretics)

A 
orthostasis
dry mouth
dizzy
skin turger
BUN ratio (normal 10-1) when it gets wider it means dehydrated
thirst
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47
Q

ADR of loop diuretics

A 
*****hypokalemia most dangerous
dehydration
hypernatremia
hypochloremia
Hypotention
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48
Q

IV loop diuretics can cause damage to the ears

True or false

A

true

usually transient ototoxicity
can also increase blood suger

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49
Q

Hyperuricemia can be caused by loop diuretics. Why is this important

A

because it increases uric acid which can cause gout

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50
Q

Where do Thiazide and Thiazide like diuretics work and what percentage of sodium do they block from getting reabsorbed

A

they work at the distal convoluted tubule

they block 10% of sodium and water from being reabsorbed

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51
Q

ADR’s for Thiazides

A

the same as loop diuretics except for it increased serum CALCIUM

*****hypokalemia most dangerous
dehydration
hypernatremia
hypochloremia
Hypotention
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52
Q

Isotonic contraction

A

volume contraction- dehydrated, but serum osmo is 270

causes: vomiting diarrhea, misuse of diuretics

Treatment: normal saline

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53
Q

Hypertonic contraction

A

loss of H2O exceeds the loss of Na

Causes: excessive sweating, burns
Treatment: Hypotonic Fluid (.45%NS or D5W)

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54
Q

Name 2 aldosterone antagonists

A

spironolactone (more hormonal)

eplerenone (less hormonal)

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55
Q

ADR’s of Potassium sparing diuretics (aldosterone antagonists)

A 
hyperkalemia
menstrual irregularities
deepening of the voice
excessive hair growth in girls
gynomastia in men
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56
Q

__________ is the hormone that is a stimulant for the production of the sodium-potassium exchange pumps

A

Aldosterone

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57
Q

After the Sodium Potassium pumps within the collecting ducts are stimulated by aldosterone, what will they do?

A

after stimulation, these pumps will pull in sodium in exchange for potassium. (potassium wasting)

(they spit out potassium to be excreted in the urine and absorb sodium back into the ECF)

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58
Q

The more __________ your body produces, the more sodium potassium pump action you will have within your collecting ducts.

A

Aldosterone

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59
Q

What is ADH?

A

Anti Diuretic Hormone

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60
Q

What does ADH do?

A

ADH is a hormone within the body that causes the membranes in the collecting ducts to be more permeable to water.

This allows free water to be pulled into the body and thus concentrates the urine.

This is independent of solute.

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61
Q

When you are running a marathon, and your body needs to conserve free water ______ is released and it causes free water to be absorbed which darkens the urine.

A

ADH

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62
Q

There is not a diuretic that works at the Proximal Convoluted Tubule. Why?

A

because you would lose 65% of your ECF at once and you would shrivel up and die.

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63
Q

In the Loop of Henle, ______% of NaCl gets reabsorbed at the ascending loop.

A

20%

remember that water follows solute.. so 20% of water will be PASSIVELY reabsorbed here.

64
Q

Loop Diuretic work in the ________ loop in the Loop of Henle.

A

Ascending

65
Q

The Distal Convoluted Tubule is where _____% of NaCl is actively reabsorbed into the ECF.

A

10

remember that water follows solute.. so 10% of water will be PASSIVELY reabsorbed here.

66
Q

In the collecting ducts, you have ________ exchange pumps…

A

Sodium Potassium

67
Q

The collecting ducts are where _____% of NaCl is actively reabsorbed.

A

5

remember that water follows solute.. so 5% of water will be PASSIVELY reabsorbed here.

68
Q

Respiratory Alkalosis

A

produced by hyperventilation

69
Q

Respiratory Acidosis

A

retention of co2 secondary to hypoventilation COPD patients

70
Q

Metabolic Alkalosis

A

increase in serum bicarb levels thus increasing pH

vomiting, excessive gastric acid suctioning

71
Q

Metabolic Acidosis

A

chronic reanal failure, Diabetes Mellitus, ketoacidosis, asprin overdose

72
Q

Hyperkalemia

A

typically defined as a K level greater than 5 meq/L

Causes: excessive K administration, spironolactone, epleronone *** Renal Failure

**Treatment: if the heart is irritated infuse CA Salt, insulin with D5W, kxelate (sodium polystyrene sulfonate

73
Q

Hypokalemia (most important)

A

when serum sodium levels drop below 3.5 meq/L

Causes: acidotic state, diuretics, vomiting, diarrhea, laxitive use, severe acidosis

Significance: weakness, paralysis, arrhythmias

Treatment: Give K

74
Q

potassium

A

the most abundant intracellular cation

75
Q

lower the preload

A

lower the cardiac output

76
Q

vasodilater

A

is an afterload reducer

77
Q

Myocardial contractility

A

the force of contraction of the ventricals - beta 1 vs. muscarinic stimulation + more stretch

78
Q

cardiac afterload (arteries):

A

he force that the heart has to overcome to pump blood

the greatest determinant is arteriole vasoconstriction and vasodilation

79
Q

Starlings law

A

force of ventricular contraction is proportional to the stretch

soggy boggy- ends up not pumping as well

the greater the stretch the greater the contraction

80
Q

Cardiac preload (veins)

A

how much volume gets to the heart

reduced preload: over diuresis, dehydrated,vasodilater

81
Q

natriuretic peptides

A

protectors of volume overload

82
Q

Atrial Natriuretic Peptide

A

released from stretching in the atria

83
Q

Brain Natriuretic Peptide

A

released from stretching in the ventricals

84
Q

C natriuretic Peptide

A

released from stretching in the veins and the arteries

85
Q

What are the therapeutic uses for Potassium sparing diuretics (aldosterone antagonists)

A

cirrosis of the liver
CHF
primary hyperaldosteronism

86
Q

Angiotension II

A

stimulates the release of aldosterone

actions:
vasoconstriction, - most potent vasoconstrictor in the body.

aldosterone- Na retention, K wasting

alterations of cardiac output and vascular structure

AT2 + aldost = heart to change shape and fail

87
Q

Aldosterone agonists cause you to retain K, this is the reason that it cannot be combined with

A

Ace inhibitors. Because ace inhibitors also increase K.

88
Q

ACE inhibitors cause a build up of bradykinin. The effects of an increase in bradykinin is

A

a cough and angioedema

89
Q

Therapeutic implications of ACE

A

HTN- dilation of A+V+ decreased blood vol + decreased Cardiac output

Heart Failure- drug of choice

Heart Attack-

diabetic and non diabetic nephropathy

reduce risk of MI, stroke, and death in high risk heart patients

90
Q

ACE side effects

A 
hypotension
cough
hyperkalemia
renal failure
fetal injury
angioedema
91
Q

any drug ending in ‘pril

A

is an ace inhibitor

92
Q

Epinephrine stimulates

A

Alpha 1
Alpha 2
Beta 1
Beta 2

93
Q

Norepinephrine stimulates

A

Alpha 1
Alpha 2
Beta 1

94
Q

Norepinephrine is

A

Recycled in the nerve terminal

Or broken down by monoaminoxydase

95
Q

Epi

A

Disassociates and floats away and is metabolized by the liver

96
Q

Atropine

A

The antidote to muscarinic overdose

97
Q

Acetylcholine is broken down by

A

Acetylcholinesterase

98
Q

Atropine is anticholinergic

A

Used for pre-anesthesia

99
Q

Tubocurarine and atracurium

A

Block nic m receptors

Does not effect cns

Antidote is physostigmine

100
Q

Physostigmine

A

Antidote give atropine

101
Q

RAAS

A

Angiotensinogen stimulates release of renin -> AT1 -> AT2 -> stimulates release of aldosterone -> AT3

102
Q

Hemoglobin A1C- _______% or greater is diagnostic

A

6.5%

103
Q

Glycosylated Hemoglobin (HBA1)

A

glucose control over last 2-3 months (report card) Avg of glucoses over 2-3 mo.

Goal 7%

Best test for DM- AVG BG for 120 days. If its elevated- that’s bad! Long term elevation is what we worry about.

104
Q

What are the consequences of COX 1 and 2 inhibition

A

COX 1 – gastric erosion, ulceration, bleeding, renal impairment, MI/CVA protection

COX2- suppression of inflammation, pain relief, decreased fever, renal impairment.

105
Q

What are the two forms of COX

A

COX 1- good one- promotes housekeeping chores- renal blood flow- protects gastric mucosa

COX 2- bad one- produced mainly at sites of tissue injury- the one we want to wipe out

106
Q

Latent Auto immune Diabetes of Adulthood (Diabetes 1 and ½- LADA)

A

Typically manifests between 3rd and 4th decade of life-

Looks more like type 1 diabetes- very thin- they need insulin very quickly.

is autoimmune, so attacks the beta islet cells

oral therapy helps at first, but usually have to go to insulin very quickly (within about a year)

107
Q

List symptoms of hyperthyroidism

A

skin- warm, moist

cardiac- tachycardia, arrhythmias (afib)

CNS excitation- insomnia, excitable rapid speech, weak muscles

metabolism- increases- wt loss

thermoregulation- increased temp, always feel hot

Exophthalmos (eyeball protrusion)

108
Q

List symptoms of hypothyroidism

A

skin— cold,dry—always cold

hair- brittle and possible alopecia

cardiac- bradycardia

body temp-lowered

psyche-depression, lethargy, AMS, malaise

metabolism-low-unexplained wt gain

Infants- (creatinism) mental retardation, short dwarf-like stature, large protruding tongue, potbelly

109
Q

What is the MOA of acetaminophen

A

Moa unlike other NSAIDS, limited to CNS- good for pain and fever.—not for inflammation

110
Q

ADE of acetaminophen

A

liver injury in over dosage,

does not cause GI issues, renal impapirment does not promote bleeding, no link to reyes syndrome

111
Q

LIVER DAMAGE pertaining to acetaminophen

A

produces metabolites that eats liver

saturable pathway- non toxic metabolite

alternative pathways- toxic metabolites

***Glutathione- our bodys own antidote

acetylcysteine (mucomyst) replaces depleted glutathione levels, spares liver

112
Q

What is Glutathione-

A

our bodys own antidote for acetaminophen poisoning

113
Q

acetylcysteine (mucomyst) helps reduce tylenol overdose by

A

Acetylcysteine may protect against acetaminophen overdose-induced hepatotoxicity by maintaining or restoring hepatic concentrations of glutathione.

114
Q

What drug is used for hypothyroidism?

A

Levothyroxine- (T4) (Synthroid)-

makes more sensitive to warfin

Uses- hypothyroidism, previously used at wt loss agent- causes arrhythmias,

7day ½ life, 28 day steady state.

Adverse effects- if overdosed sxs of thyroid toxicosis

Therapeutic interchange- narrow

Goal- to become euthroid

115
Q

Pre-Diabetes-

A

IGT (OGTT with 2 hr. PP at 140-199 mg/dl) and/or IFG (FPG b/w 100 and 125).

116
Q

Diabetes control and complications trial (DCCT)-

A

Type 1 diabetic population.

one group kept 9% on A1C and sugars less than 200 (less controlled)

other group kept 70-100 blood sugars and 7% A1C (tightly controlled)

results were:

were able to substantially reduce microvascular complications, but were NOT able to reduce heart attacks or strokes

117
Q

UKPDS

A

type 2 population- loosely controlled( A1C 7.9%) and tightly controlled A1C 7%. Cannot reduce the risks of macrovascular (heart attacks and strokes)

118
Q

Random plasma glucose more >______ mg/dl (with symptoms)- thirsty, polyuria is used to diagnose diabetes.

A

200

119
Q

Another diagnostic tool is a FPG level > or = _______mg/dl (repeat on separate day)

A

126

120
Q

2 hour OGTT> __________ mg/dl (repeat on separate day) Pregnant women have to do this

A

200

121
Q

Extravasation of adrenergic agonists. What happens? How to reverse

A

If extravasation of adrenergic agonist, tissue necrosis and gangrene will occur unless you administer a ADRENERGIC ANTAGONIST such as PHENTOLAMINE.

122
Q

BPH and Treatment

A

Adrenergic Antagonist-

Alpha Antagonist (Blocker)

Alpha 1 causes restriction in arteries and veins.

Therapeutic Applications:

  • Essential HTN
  • Alpha 1 Agonist Toxicity
  • BPH

Example of an Alpha Blocker is Tamulosin (Flomax)

123
Q

Therapeutic uses for exogenous Epinephrine

A

Used in Anaphalectic Shock

Epi-Pen

124
Q

Why are Beta Blockers Contraindicated for Diabetics

A

Takes away hypoglycemia Indicators such as increased Heart Rate.

Patient wont realize their sugars are low.

125
Q

Autonomic Control

A

Parasympathetic and sympathetic are in opposition of each other, and can also complement each other.

Autonomic Tone- is when you are at rest (just chillin), Parasympathetic is in control.

126
Q

Erection is caused by the

A

parasympathetic

127
Q

Ejaculation and prostate contraction is caused by the

A

sympathetic

128
Q

Which nervous system solely innervates the vascular system.

A

sympathetic

129
Q

Rebound HTN

A

CLONIDINE - Central Acting Alpha 2 Agonists

works by stimulation of alpha 2 in CNS, whoas NE Stimulation w/o depleting Receptor

uses: 
HTN
Cancer pain
Decreased Heart rate
Decreased BP
Side effects:
Sleepy
Dry Mouth
ED
Dizzy
Rebound HTN
130
Q

First Dose Phenomenon

A

Bad orthostasis on the first dose, not after

Seen with Alpha Blockers

Example:
Prazosin
Terazosin
Doxazosin
Tamulosin
Phentolamine
131
Q

Pre-Term Labor. How to abate? By What Mechanism? What Drugs.

A

Beta 2 stimulation ,

causes bronchodilation, Relaxation of Smooth Muscle, skeletal muscle contraction, increase blood glucose

Drugs:
Terbutaline
Isoproterenol
Epinepherine

132
Q

IV Dopamine and Concentration Dependent receptor activity

A

Low Dose- Stimulates Dopamine Receptors Only

Medium Dose- Stimulates Dopamine and Beta 1 Receptors

High Doses- Stimulates Dopamine, Beta 1, and Alpha 1 Receptors

133
Q

Hypothalamus produces TRH (thyrotropin releasing hormone)-> which stimulates the__________

A

Pituitary->

134
Q

The Pituitary produces

A

THS (thyroid stimulating hormone)—–>

135
Q

THS (thyroid stimulating hormone) stimulates the ________

A

thyroid gland—–>to produce t3 and t4 and synthesized by iodide

So, Hypothalamus produces TRH (thyrotropin releasing hormone)-> which stimulates the Pituitary-> which stimulates THS (thyroid stimulating hormone)> thyroid gland> t3 and t4 and synthesized by iodide

136
Q

Hypothalamus sends Corticotropin Releasing Hormone (CRH) to

A

Anterior Pituitary which stimulates ACTH which goes to the adrenal cortex and causes release of cortisol

so CRH->ACTH->Cortisol

137
Q

Basal

A

24 hours a day constantly produced

138
Q

Bolus

A

Insulin that is released when high glucose parameter is sensed. such as after you eat.

139
Q

Mix insulin Clear before Cloudy

A

These Insulins cannot be mixed:
Insulin Detmir
Insulin Glargine
Pramlinitide (Symlin)

140
Q

What are the three types of cholinergic receptors

A

Nicotinic N- nerves- pns and sns

Nicotinic M- muscles. Somatic

Muscarinic. On target organs. The locks. Key is acetylcholine.

141
Q

Agenergic receptors

A

Sympathetic

Alpha 1
Alpha 2
Beta 1
Beta 2
Dopamine
142
Q

Alpha 1 Stimulation

A

Vaso constriction, pupil dilating

MEDS- Afrin, Epi, NE, Phenylephrine, dopamine, ephedrine

Therapeutic Applications:
To stop Bleeding
Nasal Decongestants
Adjunct to Local Anesthesia
Increase BP during shock
Dilate Puplil (Mydriasis)

Adverse Effects:
HTN
Necrosis
Bradycardia

143
Q

Whoa receptor

A

Alpha 2

Shuts Down additional release of neurotransmitters

stimulation of alpha 2 in CNS reduces sympathetic outflow.

can cause vasodilation

Used for HTN, pain, some psych issues

ADE-
hypotension
bradycardia
dry mouth
sedation

Examples: Clonidine, methyldopa

144
Q

Beta 1 Stimulation

A

On heart.

Increases conduction, contraction, rate

Therapeutic Applications; 
Cardiac Arrest
Heart Failure
Shock
AV Heart Block

ADE-
Dysrhythmias
Tachycardia
angina

Ex- Epi, NE, isoproterenol, dopamine, dobutamine, ephedrine

145
Q

Beta 2 Stimulation

A

Arteries. Dilation

Sympathetic

Lungs- cause bronchi dilation- albuterol

Liver- glycogen breakdown

Skeletal muscle- enhances contraction

146
Q

Epinephrine stimulates

A

Alpha 1
Alpha 2
Beta 1
Beta 2

147
Q

Norepinephrine stimulates

A

Alpha 1
Alpha 2
Beta 1

148
Q

Dopamine stimulates

A

Alpha 1
Beta 1
Dopamine

149
Q

Cholinergic receptors are stimulated by

A

Acetylcholine

Primarily pns

150
Q

Dopamine Stimulation

A

Effects: Dilation of the vasculature of the kidney, heart, Increases BP

Therapeutic Applications:
maintain renal perfusion during shock
enhance cardiac performance (CHF, shock)
pressure agent when hypotensive

151
Q

Alpha Blockade (Alpha Antagonist)

A

Dilates arteries and Veins; preload and afterload reducer; urinary retention ;

Therapeutic Applications; BPH, Essiential HTN; Alpha 2 agonist toxicity; Raynauds; pheochromocytoma

ADE: Orthostatic Hypotension, Reflex Tachycardia, nasal congestion; inhibition of ejaculation; sodium and water retention

Examples: Prazosin, Terazosin, doxazosin, tamulosin, Phentolamine

152
Q

Beta Blockade (Beta antagonist)

A

effects of blockade:
reduced heart rate, reduced force of contraction, reduced AV node, reduced SA node conduction, decreases demand of blood for <3.

Therapeutic Applications:
Hypertension, Angina, Dysrhythmias, MI, Hyperthyroidism, Migraine, Stage Fright, Pheochromocytoma, Glaucoma, CHF

Adverse Effects:
Beta 1: bradycardia, decreased cardiac output, heart failure, AV heart block

Beta 2: Bronchoconstriction, Inhibition of Glycogenolysis

Agents: Propranolol, Metoprolol, Caredilol,Labetalol

153
Q

Metoprolol is a better beta blocker for people that have

A

asthma because it is more selective (Beta 1) than Propranolol (beta 1-2)

154
Q

Arterial Blood Pressure

A

(Afterload)

= Peripheral Vascular Resistance x Cardiac Output

155
Q

Sulfa Allergic

A

cant take

celebrex

Loop Diuretics:
Furosemide
Bumetamide
Torsemide

sulfonylureas:
Glipizide
Glyburide
Glimepiride

156
Q

Creatinine Clearance

A

Measures decreased renal function

CrCl = [(140-age) x (weight kg)] / (Scr) x (72kg)

x0.85 if female

Drug excretion decreases with age due to decrease in renal blood flow so the GFR goes down.

Pharmacology 1 (6 decks)

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