Final Review Flashcards
(156 cards)
1
Q
Adverse Drug Reactions ADR
A
any noxious, unintended, and undesired effect that occurs at a normal drug dose
2
Q
side effect
A
unavoidable secondary drug effect produces at therapeutic doses
Example- NSAIDS cause ulcers
3
Q
toxicity
A
any severe ADR regardless of the dose
4
Q
excretion
A
removal of drug from the body
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
6
Q
Iatrogenic Disease
A
disease produced by drugs (our fault)
7
Q
teratogenic
A
causing malformations of an embryo or fetus.
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
9
Q
tolerance
A
decrease responsiveness to drug as a result of repeated drug administration
10
Q
pharmacodynamic tolerance
A
patient requires increase drug levels to produce effects that could formerly be produced at decreased drug levels
11
Q
tachyphylaxis
A
reduction in responsiveness brought on by repeated dosing over a short period of time
12
Q
Enzyme inducer
A
Decrease levels of object drug by double pac man
Tells enzymes to metabolize drug faster
13
Q
Pharmacodynamics
A
The study of the biochemical and physiological effects of drugs and the molecular mechanisms by which those effects are produced
14
Q
Relative potency
A
Refers to the amount of drug needed to elicit an effect
15
Q
pharmacology
A
the study of drugs and their interactions with living systems
16
Q
pharmacotherapy
A
use of drugs in the treatment and prevention of disease or conditions
17
Q
therapeutic objective
A
provide maximum benefit with minimum harm
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
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
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
21
Q
carcinogenic effect
A
drugs cause cancer
22
Q
Drug
A
any chemical agent that affects the processes of living
23
Q
pharmacokinetics
A
the study of the absorption, distribution, metabolism, and excretion of drugs
the effects of the body on the drug
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
25
Half life
time required for amount of drug in the body to decline by 50%
26
Steady state
Point at which the amount of drug eliminated between doses equals the amount of drug administered
27
Minimum effective concentration
the minimum amount of a drug needed to produce a therapeutic effect
28
The randomized, controlled, tiral (BCT) is the
most reliable way to evaluate all drugs
29
Preclinical Testing
usually done on animals,
measures: toxicity, Kinetics, possible therapeutic uses.
Investigational new drug status allows the drug to be tested in humans
30
Clinical testing
happens after preclinical testing
occurs in humans
has three phases
31
Phase 1 clinical testing
before the drug has a name,
tested in normal volunteers
tests for metabolism and biologic effects
32
Phase 2 clinical testing
testing in patients
may not be healthy people
tests therapeutic utility and dosage range
33
Phase 3 clinical testing
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
34
Phase 4 Clinical testing
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
35
volume of distribution
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,.
36
With highly bound protein drugs, you have to worry about protein displacement.
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
37
agonists
molecules which activate receptors (stimulate)
38
antagonist
molecules that prevent receptor activation (blocker)
39
partial agonist
can act as both an agonist and an antagonist
40
therapeutic index
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.
41
drug category x
never consume while prego
42
drug category a
safe
43
drug category b
safe in animals
44
an acid in acid is
nonionized
45
Name the only Non sulfa loop diuretic
Ethacrynic acid
46
Dehydration symptoms (one ADRs of diuretics)
```
orthostasis
dry mouth
dizzy
skin turger
BUN ratio (normal 10-1) when it gets wider it means dehydrated
thirst
```
47
ADR of loop diuretics
```
*****hypokalemia most dangerous
dehydration
hypernatremia
hypochloremia
Hypotention
```
48
IV loop diuretics can cause damage to the ears
True or false
true
usually transient ototoxicity
can also increase blood suger
49
Hyperuricemia can be caused by loop diuretics. Why is this important
because it increases uric acid which can cause gout
50
Where do Thiazide and Thiazide like diuretics work and what percentage of sodium do they block from getting reabsorbed
they work at the distal convoluted tubule
they block 10% of sodium and water from being reabsorbed
51
ADR's for Thiazides
the same as loop diuretics except for it increased serum CALCIUM
```
*****hypokalemia most dangerous
dehydration
hypernatremia
hypochloremia
Hypotention
```
52
Isotonic contraction
volume contraction- dehydrated, but serum osmo is 270
causes: vomiting diarrhea, misuse of diuretics
Treatment: normal saline
53
Hypertonic contraction
loss of H2O exceeds the loss of Na
Causes: excessive sweating, burns
Treatment: Hypotonic Fluid (.45%NS or D5W)
54
Name 2 aldosterone antagonists
spironolactone (more hormonal)
eplerenone (less hormonal)
55
ADR's of Potassium sparing diuretics (aldosterone antagonists)
```
hyperkalemia
menstrual irregularities
deepening of the voice
excessive hair growth in girls
gynomastia in men
```
56
__________ is the hormone that is a stimulant for the production of the sodium-potassium exchange pumps
Aldosterone
57
After the Sodium Potassium pumps within the collecting ducts are stimulated by aldosterone, what will they do?
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)
58
The more __________ your body produces, the more sodium potassium pump action you will have within your collecting ducts.
Aldosterone
59
What is ADH?
Anti Diuretic Hormone
60
What does ADH do?
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.
61
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.
ADH
62
There is not a diuretic that works at the Proximal Convoluted Tubule. Why?
because you would lose 65% of your ECF at once and you would shrivel up and die.
63
In the Loop of Henle, ______% of NaCl gets reabsorbed at the ascending loop.
20%
remember that water follows solute.. so 20% of water will be PASSIVELY reabsorbed here.
64
Loop Diuretic work in the ________ loop in the Loop of Henle.
Ascending
65
The Distal Convoluted Tubule is where _____% of NaCl is actively reabsorbed into the ECF.
10
remember that water follows solute.. so 10% of water will be PASSIVELY reabsorbed here.
66
In the collecting ducts, you have ________ exchange pumps...
Sodium Potassium
67
The collecting ducts are where _____% of NaCl is actively reabsorbed.
5
remember that water follows solute.. so 5% of water will be PASSIVELY reabsorbed here.
68
Respiratory Alkalosis
produced by hyperventilation
69
Respiratory Acidosis
retention of co2 secondary to hypoventilation COPD patients
70
Metabolic Alkalosis
increase in serum bicarb levels thus increasing pH
vomiting, excessive gastric acid suctioning
71
Metabolic Acidosis
chronic reanal failure, Diabetes Mellitus, ketoacidosis, asprin overdose
72
Hyperkalemia
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
Hypokalemia (most important)
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
potassium
the most abundant intracellular cation
75
lower the preload
lower the cardiac output
76
vasodilater
is an afterload reducer
77
Myocardial contractility
the force of contraction of the ventricals - beta 1 vs. muscarinic stimulation + more stretch
78
cardiac afterload (arteries):
he force that the heart has to overcome to pump blood
the greatest determinant is arteriole vasoconstriction and vasodilation
79
Starlings law
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
Cardiac preload (veins)
how much volume gets to the heart
reduced preload: over diuresis, dehydrated,vasodilater
81
natriuretic peptides
protectors of volume overload
82
Atrial Natriuretic Peptide
released from stretching in the atria
83
Brain Natriuretic Peptide
released from stretching in the ventricals
84
C natriuretic Peptide
released from stretching in the veins and the arteries
85
What are the therapeutic uses for Potassium sparing diuretics (aldosterone antagonists)
cirrosis of the liver
CHF
primary hyperaldosteronism
86
Angiotension II
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
Aldosterone agonists cause you to retain K, this is the reason that it cannot be combined with
Ace inhibitors. Because ace inhibitors also increase K.
88
ACE inhibitors cause a build up of bradykinin. The effects of an increase in bradykinin is
a cough and angioedema
89
Therapeutic implications of ACE
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
ACE side effects
```
hypotension
cough
hyperkalemia
renal failure
fetal injury
angioedema
```
91
any drug ending in 'pril
is an ace inhibitor
92
Epinephrine stimulates
Alpha 1
Alpha 2
Beta 1
Beta 2
93
Norepinephrine stimulates
Alpha 1
Alpha 2
Beta 1
94
Norepinephrine is
Recycled in the nerve terminal
Or broken down by monoaminoxydase
95
Epi
Disassociates and floats away and is metabolized by the liver
96
Atropine
The antidote to muscarinic overdose
97
Acetylcholine is broken down by
Acetylcholinesterase
98
Atropine is anticholinergic
Used for pre-anesthesia
99
Tubocurarine and atracurium
Block nic m receptors
Does not effect cns
Antidote is physostigmine
100
Physostigmine
Antidote give atropine
101
RAAS
Angiotensinogen stimulates release of renin -> AT1 -> AT2 -> stimulates release of aldosterone -> AT3
102
Hemoglobin A1C- _______% or greater is diagnostic
6.5%
103
Glycosylated Hemoglobin (HBA1)
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
What are the consequences of COX 1 and 2 inhibition
COX 1 – gastric erosion, ulceration, bleeding, renal impairment, MI/CVA protection
COX2- suppression of inflammation, pain relief, decreased fever, renal impairment.
105
What are the two forms of COX
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
Latent Auto immune Diabetes of Adulthood (Diabetes 1 and ½- LADA)
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
List symptoms of hyperthyroidism
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
List symptoms of hypothyroidism
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
What is the MOA of acetaminophen
Moa unlike other NSAIDS, limited to CNS- good for pain and fever.---not for inflammation
110
ADE of acetaminophen
liver injury in over dosage,
does not cause GI issues, renal impapirment does not promote bleeding, no link to reyes syndrome
111
LIVER DAMAGE pertaining to acetaminophen
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
What is Glutathione-
our bodys own antidote for acetaminophen poisoning
113
acetylcysteine (mucomyst) helps reduce tylenol overdose by
Acetylcysteine may protect against acetaminophen overdose-induced hepatotoxicity by maintaining or restoring hepatic concentrations of glutathione.
114
What drug is used for hypothyroidism?
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
Pre-Diabetes-
IGT (OGTT with 2 hr. PP at 140-199 mg/dl) and/or IFG (FPG b/w 100 and 125).
116
Diabetes control and complications trial (DCCT)-
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
UKPDS
type 2 population- loosely controlled( A1C 7.9%) and tightly controlled A1C 7%. Cannot reduce the risks of macrovascular (heart attacks and strokes)
118
Random plasma glucose more >______ mg/dl (with symptoms)- thirsty, polyuria is used to diagnose diabetes.
200
119
Another diagnostic tool is a FPG level > or = _______mg/dl (repeat on separate day)
126
120
2 hour OGTT> __________ mg/dl (repeat on separate day) Pregnant women have to do this
200
121
Extravasation of adrenergic agonists. What happens? How to reverse
If extravasation of adrenergic agonist, tissue necrosis and gangrene will occur unless you administer a ADRENERGIC ANTAGONIST such as PHENTOLAMINE.
122
BPH and Treatment
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
Therapeutic uses for exogenous Epinephrine
Used in Anaphalectic Shock
Epi-Pen
124
Why are Beta Blockers Contraindicated for Diabetics
Takes away hypoglycemia Indicators such as increased Heart Rate.
Patient wont realize their sugars are low.
125
Autonomic Control
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
Erection is caused by the
parasympathetic
127
Ejaculation and prostate contraction is caused by the
sympathetic
128
Which nervous system solely innervates the vascular system.
sympathetic
129
Rebound HTN
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
First Dose Phenomenon
Bad orthostasis on the first dose, not after
Seen with Alpha Blockers
```
Example:
Prazosin
Terazosin
Doxazosin
Tamulosin
Phentolamine
```
131
Pre-Term Labor. How to abate? By What Mechanism? What Drugs.
Beta 2 stimulation ,
causes bronchodilation, Relaxation of Smooth Muscle, skeletal muscle contraction, increase blood glucose
Drugs:
Terbutaline
Isoproterenol
Epinepherine
132
IV Dopamine and Concentration Dependent receptor activity
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
Hypothalamus produces TRH (thyrotropin releasing hormone)-> which stimulates the__________
Pituitary->
134
The Pituitary produces
THS (thyroid stimulating hormone)----->
135
THS (thyroid stimulating hormone) stimulates the ________
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
Hypothalamus sends Corticotropin Releasing Hormone (CRH) to
Anterior Pituitary which stimulates ACTH which goes to the adrenal cortex and causes release of cortisol
so CRH->ACTH->Cortisol
137
Basal
24 hours a day constantly produced
138
Bolus
Insulin that is released when high glucose parameter is sensed. such as after you eat.
139
Mix insulin Clear before Cloudy
These Insulins cannot be mixed:
Insulin Detmir
Insulin Glargine
Pramlinitide (Symlin)
140
What are the three types of cholinergic receptors
Nicotinic N- nerves- pns and sns
Nicotinic M- muscles. Somatic
Muscarinic. On target organs. The locks. Key is acetylcholine.
141
Agenergic receptors
Sympathetic
```
Alpha 1
Alpha 2
Beta 1
Beta 2
Dopamine
```
142
Alpha 1 Stimulation
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
Whoa receptor
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
Beta 1 Stimulation
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
Beta 2 Stimulation
Arteries. Dilation
Sympathetic
Lungs- cause bronchi dilation- albuterol
Liver- glycogen breakdown
Skeletal muscle- enhances contraction
146
Epinephrine stimulates
Alpha 1
Alpha 2
Beta 1
Beta 2
147
Norepinephrine stimulates
Alpha 1
Alpha 2
Beta 1
148
Dopamine stimulates
Alpha 1
Beta 1
Dopamine
149
Cholinergic receptors are stimulated by
Acetylcholine
Primarily pns
150
Dopamine Stimulation
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
Alpha Blockade (Alpha Antagonist)
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
Beta Blockade (Beta antagonist)
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
Metoprolol is a better beta blocker for people that have
asthma because it is more selective (Beta 1) than Propranolol (beta 1-2)
154
Arterial Blood Pressure
(Afterload)
| = Peripheral Vascular Resistance x Cardiac Output
155
Sulfa Allergic
cant take
celebrex
Loop Diuretics:
Furosemide
Bumetamide
Torsemide
sulfonylureas:
Glipizide
Glyburide
Glimepiride
156
Creatinine Clearance
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.
