Exam I Flashcards
1
Q
What types of receptor proteins are there?
A
- Regulatory proteins
- Enzymatic proteins
- Transport proteins
- Structural proteins
2
Q
What are orphan receptors?
A
Identified receptors with an unidentified endogenous ligand (approximately 500 unidentified).
3
Q
What are the seven receptor targets for drugs?
A
- Seven-transmembrane (7TM) receptors (GPCRs)
- Ligand-gated channels
- Ion channels
- Catalytic receptors
- Nuclear receptors
- Transporters
- Enzymes
4
Q
In Cell Signaling, what protein actually modifies cellular metabolism, function, movement, etc. ?
A
The Effector protein
5
Q
Name the cell signaling components in order starting with the signaling molecule (i.e. drug, endogenous ligand, etc.)
A
1st - Signaling molecule, endogenous ligand
2nd - Receptor where ligand attaches
3rd - Signal transduction proteins and second messengers send signal.
4th - Effector protein receives signal and effects change.
6
Q
Some drugs affect gene expression and in doing so have a lag period, why is this? how long is this typically?
A
- The lag period results from the process of transcription to translation to protein creation occurring.
- Responses seen 30 minutes to several hours.
7
Q
Dose response to the coupling of a drug to a receptor can be _____ or _____. Explain the difference between the two.
A
- Linear or exponential.
1. In linear the number of receptors capture is directly related to effect, 25% receptors bound vs 50%.
2. In exponential, 1 receptor could send a signal cascade where 100’s or 1000’s of effector proteins are engaged for the one drug attached to the receptor.
8
Q
What are kinase’s and what is their role in the cell signaling phosphorylation cascade?
A
Kinases are a phosphate group that binds to a signaling or secondary messenger protein and induces a cascade of messages reaching the effector proteins.
9
Q
What are phosphatase’s and what is their role in the cell signaling phosphorylation cascade?
A
Phosphatases block phosphorylation cascade from continuing to occur by deleting a protein (or a phosphate group?) and blocking downstream effects.
10
Q
What are the mechanisms for transmembrane signalling?
A
- Intracellular receptors (need to be lipid soluble)
- Cell Surface receptors (3)
- Ion channels - Catalytic - GPCRs
11
Q
What are GPCRs? How many drugs are GPCRs?
A
- Guanine Triphosphide Protein Coupled Receptors (or just G-protein coupled receptors).
- 2/3rds of all non-antibiotics
- 500 identified, 500 orphan
12
Q
What characterizes a “fast” GPCR response?
A
- metabotropic ion channels causing a flood of ions (ex. B1)
13
Q
What characterizes a slow GPCR response?
A
Transcription factor activation
14
Q
What are the secondary messengers in the GPCR response? Which two of these messengers come from the cell membrane?
A
- cAMP (cyclated ATP)
- cGMP
- Calcium
- DAG
- IP3
DAG and IP3 come from phospholipids in the cell membrane.
15
Q
What are the primary ligands of Tyrosine Kinase Receptors (RTKs)?
A
- Growth factors
- Adhesions
16
Q
The process for RTKs (Receptor Tyrosine Kinase) binding is essentially three steps, what are these steps?
A
- 2 ligands bind and produce dimer.
- Dimer now has activated tyrosine regions that get phosphorylated by ATP (6 phosphates).
- The phosphorylated tyrosine regions are “docked” by relay proteins (causing a conformational change in the proteins) and multiple downstream responses are activated.
17
Q
Where are voltage gated channels found? What are their characteristics?
A
- Found in excitable cells
- Neurons, muscle, endocrine
- Closed at resting membrane potential
- Types based on what ion’s get through (Na+ vs K+ vs Ca2+)
18
Q
What are the two types of Ligand-Gated Ion channels? What is the difference between these two?
A
- Ionotropic - Ligand binds on protein and the protein opens a channel on itself to let an ion through. (ACh receptors)
- Metabotropic - Ligand activates a GPCR that initiates a sequence to open an ion channel.
19
Q
What types of ligands are able to reach intracellular receptors?
A
- Gasses (like NO, or CO2)
- Lipid soluble agents capable of passing through phospholipid bilayer.
20
Q
Why do steroids take a while to effect a change?
A
Steroids must:
- Cross phospholipid bilayer.
- Attach to steroid receptor in cytoplasm.
- Bind to receptor site on chromatin
- Chromatin then activates mRNA transcription to create proteins.
21
Q
Name 4 transmembrane signaling methods by which drug-receptor interactions exert their effects.
A
- Intracellular receptor (gasses. lipophillic molecules)
- ion channel
- Catalytic receptor
- GCPR
22
Q
What does Drug Biotransformation refer to? Is drug biotransformation going to inactivate all drugs?
A
- Termination of drug activity w/ mechanisms aside from renal.
- .Metabolic conversion (as with prodrugs)
- Some metabolites become active after biotransformation.
- .Metabolic conversion (as with prodrugs)
23
Q
Where does drug biotransformation primarily occur?
A
Liver
24
Q
Describe the process of the liver biotransforming a PO ingested drug. Include anatomy and physiology of the process.
A
- GI tract
- Local GI venous system
- Hepatic portal vein
- Sinusoids
- Hepatic vein
- Vena Cava
- Systemic circulation.
25
Describe the process path by which the liver would biotransform an IV injected drug?
1. Systemic circulation
2. hepatic artery
3. **Sinusoids**
4. Hepatic vein
5. Vena Cava
6. Systemic circulation
26
What characterizes Phase I reactions? What is the end purpose?
* Takes place in the liver.
* **CYP Enzymes** add or unmask a functional group (-OH, -NH, etc) thus making metabolite more active/polar.
* Uses oxidation, reduction, hydrolysis
* Inactivates drugs
* Makes drugs more readily excreted.
27
What characterizes a Phase II reaction?
* **Conjugation** to an endogenous substrate
* Adding a large group to the drug (protein, -SO4, or glucose, etc)
* Results in a higher molecular weight compound.
28
What is the most important method by which Phase I reactions occur? What is the process?
By far, the most important Phase I reaction is oxidation-reduction utilizing Cytochrome P450.
1. Drug enters liver lipophillic
2. Drug binds to P450
3. Oxidation-Reduction reactions occur
4. Drug is released in a hydrophillic form.
29
What are some characteristics (specificity, number known, location of origin, variants, etc) of Human Liver P450 enzymes?
* Low substrate specificity
* Over 50 human P450's
* Primarily found found in Granular ER (produced there?)
* Polymorphic variants
* CYPA1 (common wild type)
* CYPA2 ( mutation) can be good or bad.
30
What should be known about Cytochrome P450 inducers?
* CYP induction drugs enhance **native metabolism** resulting in:
* decreased drug effect **if** metabolism normally inactivates the drug.
* increased drug effect **if** metabolism normally activates the drug.
31
What should be known about a Cytochrome P450 Inhibitors?
* The drug will decrease or irreversibly inhibit Cytochrome P450 resulting in **decreased native metabolism** resulting in:
* Increased drug since no native drug metabolism is occurring.
* decreased drug if native metabolism yields an active drug from a prodrug.
32
What groups of CYP compose 78% of all known CYPs?
* 2B6
* 2D6
* 3A4
33
What should be known about brussel sprouts and CYPs?
* Cruciferous vegetable = Inducer of CYP1A2
* Warfarin inactivates CYP1A2 to reduce clotting
* So brussel sprouts will decrease warfarin levels and increase clotting.
34
What does a P450 Inducer drug do?
Potentiates the effects of the P450 enzyme. This can lead to 2 outcomes:
1. p450 is induced to **metabolize more drug resulting in drug inactivation.**
2. p450 is induced to **metabolize more prodrug resulting in drug activation.**
35
What does CYP1A2 metabolize?
Acetaminophen
36
What does CYP2E1 metabolize?
Ethanol (**21** to drink **E**thanol)
37
What does CYP2C9 metabolize?
Warfarin (Warfarin works on factors **2**, **9**, and protein **C**)
38
What does CYP2D6 metabolize?
Cardiovascular drugs (**2D** Echo)
39
What does CYP3A4 metabolize?
60% of all drugs
just guess this one if it doesn't fall into the other categories.
40
How can competitive inhibition of CYP450 enzymes occur?
By giving two drugs metabolized by that same particular enzyme. This results in inhibition of one drug or partial inhibition of both.
41
Do charged or uncharged drugs cross barriers more easy? What characteristic makes said drug cross barriers easier?
Uncharged. Lipophillic drugs cross the phospholipid bilayer much easier.
42
What are aqueous channels of cells called?
Aquaporins
43
What are the 4 ways that drugs permeate (pharmacokinetics) into a cell?
1. Aqueous Diffusion
2. Lipid Diffusion
3. Special Carriers
4. Endocytosis and Exocytosis
44
What prevents a drug from permeating through aqueous diffusion?
* If the drug is highly charged or bound to large protein carriers.
45
Which of the 4 drug permeation methods is often the limiting factor for successful permeation? Why?
Lipid Diffusion (I think that this means lack of lipid solubility)
There are often many lipid barriers to cross.
46
What characterizes permeation through special carriers? Which two methods of transport are used with this method?
* Drug is bound to protein and moves with the protein across a barrier.
* Active Transport and facilitated diffusion.
47
What is the mechanism of action of cocaine?
* Cocaine blocks the reuptake of several important endogenous ligands. Notably dopamine and norepinephrine.
* Specifically, NET (Norepinephrine Transporter protein) is blocked from “picking up” the NE, so it continues to circulate.)
48
Give examples of endocytosis and exocytosis in regards to drug permeation?
* Endocytosis - clathrin pit mechanism for endocytosis.
* Exocytosis - GI cells pull in drugs, and “spit” back out to nervous system.
49
What is the blood volume to weight ratio for a 70kg person?
0.08L/Kg = 5.6L/70kg person
50
What is the blood plasma volume to weight equation for a 70kg person?
0.04L/Kg = 2.8L/70kg person
51
What is meant by a high Vd?
A high Vd means that a drug will be dispersed out of the blood and into the tissue.
52
What does a low Vd mean and what numbers actually denote a low value?
A low Volume of Distribution (Vd) means that the drug will primarily stay in the blood.
5-10 would characterize a low Vd
53
Describe the difference between clearance and rate of elimination.
* Clearance is the volume of blood that is cleared of drug in a given time. (Usually ml/min)
* Rate of elimination is the clearance multiplied by the concentration of drug in the blood.
54
How is rate of elimination calculated?
Rate of Elimination = CL (clearance) x drug concentration in blood.
55
For the scenario of first order elimination, out of clearance and rate of elimination, which of these two is constant? which varies?
* Clearance is a constant number (in L/min) while rate of elimination varies because the drug concentration in the body will vary.
56
In regards to zero order elimination, which of clearance and rate of elimination is constant? which varies?
* In Zero Order Elimination, the rate of elimination is constant because the body's ability to get rid of the drug is maxed out.
* The clearance percentage varies because the actual amount of drug cleared in constant.
57
What is capacity-limited elimination? What order of elimination results from this situation?
* This is a situation where the clearance is non-linear because the drug concentration increases.
* The drug starts out as 1st order but as the body gets maxed out, it becomes a zero order elimination situation.
58
What is the Vmax ? When is this term exemplified?
Vmax is the maximal elimination capacity. This occurs in zero order elimination where the body is maxed out and only gets rid of so much drug per minute.
59
Which drugs are characterized by capacity-limited elimination?
* Zero order elimination drugs such as:
* aspirin
* phenytoin
* ethanol
60
What is flow-dependent elimination?
How the drug is metabolized/extracted by the liver i.e. First Pass Effect
61
What does an extraction ration \> 0.7 mean?
Highly extracted
62
What does and extraction ratio inbetween 0.3 - 0.7 mean?
The drug has an intermediate extraction ratio
63
What does an extraction ratio of \< 0.3 mean?
It means the drug has a low extraction ratio. (it's not filtered out quickly by your organs)
64
In regards to flow dependent elimination, what results from kidney or liver damage?
Kidney and/or liver damage results in decreased blood flow in those organs which results in decreased capacity to extract drugs (Blood flow = Q)
65
If your extraction ratio is high (0.7-1.0) and your blood flow (Q, L/hr) is high, then what is your Clearance going to be? How does this differ from all other situations?
* If extraction is ⇡ and blood flow is ⇡ then clearance will be high.
* In all other scenarios:
* ⇡ extraction, ⇣ Q = low clearance
* ⇣ extraction, ⇡ Q = low clearance
* etc.
66
How many half-life periods are required for a drug to get to a therapeutic dose _or_ for the drug to become effectively eliminated?
4 half-life periods
67
Describe the process of accumulation in regards to half-life. Draw a graph.
Not all of the drug is eliminated by the time of the next dosing. Because of this, the drug concentration (mg/ml) “stacks”.
68
What is the most important factor when maintenance dosing?
Clearance is the most important factor when considering a maintenance dose.
69
How is loading dose calculated and what should be said about the rate of administration for a loading dose?
* LD = Vd x TC (target concentration)
* Rate of administration is critical and should be low enough to allow for distribution into different body compartments.
70
What is the Emax ?
The Emax is the point at which further dosage increases will have no further effect.
71
What is sensitivity in regards to pharmacokinetic variables?
Sensitivity is how one can hypo-react or hyper-react to the drug.
72
What are the components of Therapeutic Drug Monitoring and what are the subcomponents of each?
-Dose
**-Clearance**
1. **Most important**
2. Kidney and Liver most relevant
-Blood Flow (Q)
1. Albumin Concentration (drug binding)
2. Protein binding
73
How do dosages need to be calculated for drugs with a low Vd ?
IBW (Ideal Body Weight) needs to be utilized since most of the drug will be staying in the blood (as opposed to different tissues such as fat).
74
What are the factors affecting bioavailability?
1. Drug Properties (of the drug, pka, hydrophillicity)
2. Route
3. GI Tract
4. Other drugs interaction
5. Individual's health & Circadian Rhythm
75
What is the study of Pharmacology?
Study of Chemical Interactions with living systems, exogenous
76
What is Toxicology?
Undesirable effects of chemicals on living systems
77
Who was the "first" writer of the Materia Medica and what is it?
- Dioscorides
- Collections of works through history
- Botany and Medicinal substances
- precursor to pharmacy
78
Who is Imhotep?
- Ancient Egypt
- 1st recorded physician
- 3000 BCE
79
Describe Prehistoric Medicine
- shamanism, animism, spiritualism, divination
- all involved eating things outside of the body, often psychoactive substances.
80
Most known practitioner of ancient greek medicine?
- Hippocrates
81
Who is Paracelsus?
- Father of Toxicology
- "The dose makes the poison"
82
How many drug groups are there?
70 groups
- Important to know prototypical drugs from each group (1-2)
83
Branches of Pharmacology
Pharmacodynamics, Pharmacokinetics, Pharmacogenomics, and Toxicology
84
Drugs are either _____ or \_\_\_\_\_\_.
Agonists or Antagonists
85
What should be known about drug size?
- Expressed in Molecular Weight (MW)
- Most Drugs 100 - 1000 MW
- \> 1000MW can't diffuse well
86
Receptor interactions require what characteristics between the ligand and the receptor to happen?
- Appropriate size
- Electrical charge
- Shape
- Atomic Composition
87
Types of Bonds
- Covalent (strongest but least specific)
- Electrostatic (medium strength and specificity)
- ---- Charged molecules, H-bonds, Van der Waals
- Hydrophobic - Lipid-soluble drugs (weakest bond strength but most specific)
88
Orthosteric drugs bind at the \_\_\_\_\_.
native ligand active site
89
Where do allosteric drugs bind on the targeted protein? What does this binding do to the protein?
Away from the active (orthosteric) site on the protein surface and allosterically change the conformation of the protein binding site.
90
Describe the main characteristics of receptor agonists.
- Drug bind to receptor and activates response
- effect may be greater or lesser than native ligand
91
Describe receptor antagonists. What response is elicited by the binding of a receptor antagonist?
- Bind to receptor site to prevent binding of native ligand
- No response due to the blocking of native ligand.
92
What is the definition of Kd50?
Drug concentration where 50% of receptors are captured.
93
Explain what EC50 means in its entirety.
- Drug concentration needed to achieve 50% of whatever the maximum response is.
- Response can be individual ( individual feeling sleepy at 50% vs unconscious at 100%)
- Response can be in a group where 50% of population receiving drug sees its effects.
94
Allosteric Activators do what to the receptor agonist?
Potentiate its effects and cause a much greater response. Essentially, the allosteric activator makes the orthosteric site MORE hospitable to the receptor agonist.
95
Allosteric Inhibitors do what to the receptor agonist?
Reduce capability of receptor agonist to bind to protein by changing protein structure completely
96
Can competitive inhibitors (antagonists) be overcome? If yes, how?
Yes by introducing more agonist until an effect is reached and all receptors are engaged.
97
Insurmountable receptor antagonist interactions are characterized by what?
- irreversible changing of the protein receptor
- Usually a Covalent bonding occurs
- Prolonged effect of whatever drug it is due to inability to compete with the agonist.
98
Partial agonists differ from full receptor agonists how?
- Produce a lower response even at the same level as the full receptor agonist.
- Block against full receptor binding by the full agonist.
99
What mechanisms of antagonism exist aside from competitive inhibitors, partial agonist inhibitors and allosteric inhibitors?
- Opposite charge inhibition
ex. Protamine (+) bind to and inhibits heparin (-) due to opposite charges attracting each other in the blood stream.
- physiologic antagonism
- - Drugs act at different receptor sites to counteract effects of other drugs.
100
What is an endogenous ligand?
This is an agonist native to the body that binds to a native receptor site on a protein.
101
What is the Bmax and what other variable is it associate with?
- Bmax is the point at total receptor saturation.
- Bmax is assosicated with Kd which is 50% receptor saturation
102
What is Emax and what other variable is it related to?
Emax is the point at which we have 100% drug efficacy. E50 is associated with this and is the point of 50% efficacy.
103
Can non-competitive inhibition be overcome?
No, the effect is decreased until the proteins are recycled.
104
Describe the difference between a competitive inhibitor and a partial agonist.
- Competitive inhibitors bind to the orthosteric site and block the full agonist from binding. No effect occurs
- Partial agonists bind to the orthosteric site and block the full agonist from binding. Some effect occurs usually akin to the full agonist but less in nature.
105
What is the range of energy needed to break a covalent bond?
50-150 kcal/mol
106
What is the range of energy needed to break a charged electrostatic bond?
5-10 kcal/mol
107
What is the range of energy needed to break an H-bond?
2-5 kcal/mol
108
What is the range of energy needed to break hydrophobic bonds?
0.5 - 1 kcal/mol
109
Adequately explain the difference between Kd and EC50. Give an example illustrating the difference.
Kd denotes the point where we have 50% of receptors "captured" or effectively bound to. This is completely different from drug response, which is what EC50 refers to; where EC50 means the drug concentration where we have achieved the 50% effect that we were looking for.
Ex. A drug is given that has a low Kd where very little drug is required to adequately capture most receptor sites. This means that the drug is potent. Another drug could require a lot of drug to reach the EC50 mark where we could quite possible have poisoned the patient by giving so much just to get a 50% effect.
110
What are the two receptor configurations? Which one is the favored state? Does this change with an agonist present?
- Active state (Ra)
- Inactive state (Ri)
- Inactive is the favored state with no agonist present. IF an agonist is bound to the orthosteric site then the active form is favored.
111
In the absence of a full agonist, a partial agonist will act as \_\_\_\_\_.
A regular agonist, just with a lesser effect than the original, full agonist.
112
In the presence of a full agonist, a partial agonist will act as a \_\_\_\_\_\_. Give an example.
Antagonist, Beta Blockers like propanolol that inhibit constituent activity. Not like carvedilol which is an inverse agonist
113
What is an inverse agonist? What form does it have a greater affinity for? What type of activity does it exhibit? Give an example.
Inverse agonists bind to the orthosteric site and produce the opposite effect of the full agonist (epi vs beta blockers). They have a greater affinity for the inactive receptor form and exhibit "antagonistic" activity.
Ex. Carvedilol binding to orthosteric site and causing bradycardia.
114
Explain the difference between an antagonist and an inverse agonist. Give an example.
An antagonist will block the receptor site and keep constituent activity. (propanolol keeping HR at ≈ 70bpm)
An inverse agonist will bind to the receptor site and produce the opposite effect of the agonist past the normal activity. (Carvedilol lowering HR to 50bpm)
115
Explain the difference between a full agonist and an indirect (mimic) agonist.
A full agonist binds to the orthosteric receptor site and produces an effect but a mimic will bind somewhere different and produce the same effect.
(Epinephrine bind to B1, cocaine does not but produces the same effect.)
116
What are the 3 duration of drug actions? (i.e. how long the drug will last)
1. Just as long as the drug binds to the receptor
2. Until downstream effectors wear off. (Or until the receptor is degraded if it is covalently bonded.)
3. Until the receptor is desensitized.
117
What are good receptor properties?
- Selectivity
- Alteration (ability to conformationally change protein)
118
What are bad receptor properties?
- When a molecule binds to a drug and causes no change. (Inert binding site)
119
What are bad receptors "good" at?
Bad receptors are good drug carriers because they won't bind to the wrong tissue whilst moving about the body.
120
What is the most common drug carrier? What causes decreased levels of this carrier?
Albumin is the most common and is decreased if one has liver damage or malnutrition.
121
Give an example of a situation of albumin carrying a drug. What factors should one consider in this situation? Can a carried drug be displaced?
- Albumin carries phenytoin with only 10% of phenytoin being free and the rest being bound to albumin (slowly released over time).
- Disease states such as liver damage could increase the levels of circulating phenytoin due to lack of albumin
- Yes, carbamazepine can "boot" phenytoin off albumin and cause much higher levels of phenytoin systemically.
122
How many binding sites does albumin have? Are the drugs that bind to albumin mostly acidic or basic?
- 2 binding sites
- drugs that bind to albumin are mostly acidic
123
What carrier molecule binds to neutral pH drugs?
Lipoproteins (such as cholesterol)
124
What carrier molecule binds mostly to basic drugs?
alpha1-acid glycoproteins
125
Differentiate EC50 and ED50.
EC50 refers to the concentration of drug in the bloodstream to produce a 50% effect.
ED50 refers to the amount of drug given to produce a 50% effect.
126
What is the Maximal Efficacy? What are some considerations? Does the clinical effectiveness of a drug depend on maximal efficacy or potency?
- The greatest possible response a drug can deliver, regardless of dose
- Dependent on interaction with receptors.
- Toxicity has to be taken into account.
- Highly individual.
Clinical effectiveness is derived from maximal efficacy.
127
Which of these dose response curves indicates the most potent drug?
B is the most potent drug having the lowest log drug dose to produce a response.
128
Which of these drugs is the most efficacious?
A is the most efficacious but C and D could be considered efficient as well.
129
A narrow gap between the drug dose response curves between ED50 and LD50 (lethal dose) is indicative of what?
A very narrow Therapeutic index.
130
Is LD50 used in human studies? If not, what is used instead?
No, TD50 (median toxic dose) is used instead.
131
How is Therapeutic Index measured in human studies? Give an example and determine if the example has a narrow or wide therapeutic index.
TI = TD50 / ED50
- Digoxin is an example where 2mg induces cardiac contractility but 4mg produces arrythmias. TI = 4mg / 2mg = 2. This is a very narrow TI drug.
132
What are some examples of drugs with wide TI's?
* Ibuprofen
* Acetaminophen
* Antibiotics (most)
* Antihistamines
* Multivitamins
133
What are some examples of drugs with narrow TI's?
* Digoxin
* Warfarin
* Lithium
134
What is drug tolerance? Are toxic effects tolerated as well?
* Drug tolerance is where the body's response changes over the course of therapy.
* Not necessarily, opioids lose their ability to provide pain relief but the side effects such as constipation remain.
135
What is tachyphylaxis?
- A rapidly developing tolerance to a drug. Nitric Oxide is an example.
136
What is the first cause of variation in drug response? What are these factors collectively called?
Alteration in concentration of drug that reaches receptor
* Rate of absorption, distribution and clearance
* Age
* Weight
* Sex
* Disease state
Pharmacokinetics
137
What are the _four factors of variation_ in drug responsiveness?
1. Alteration in concentration of drug that reaches the receptor.
2. Variation in amount of endogenous receptor ligand.
3. Alteration in number or function of receptors.
4. Changes in downstream response.
138
What is the largest and most important cause of variation?
* Changes in downstream response of receptor.
* Post receptor process.
* Body has natural ability to compensate.
139
In order to cross barriers, drugs need to be \_\_\_\_\_\_.
Uncharged and/or lipophillic
140
Acids _____ H+ into solutions.
release
141
Bases _____ H+ in solutions.
Accept
142
In practice, pKa is pH where ionized and un-ionized concentrations are \_\_\_\_.
equal
143
If pH \< pKa then \_\_\_\_\_\_\_\_\_.
Protonated is favored.
144
Where are most drugs filtered at in the kidney? Can drugs be trapped in urine? What is this urine trapping dependent on?
* Glomerulus. (concentration in renal tubule is pH dependent)
* Yes, drugs can be trapped in urine
* weak acids excrete in alkaline urine.
* weak bases excrete in acidic urine.
145
After the firstline treatment of naloxone for morphine overdose, what drug can be given to help trapping and excretion of the morphine?
Ascorbic acid, morpine is a weak base and will bind with the slightly more acidic urine and be excreted easier.
146
Acidic drugs bind primarily to what molecule?
Albumin
147
Basic drugs bind primarily to what molecule?
a-1acid glycoproteins
148
What do neutral drugs bind to?
lipoproteins
149
How many binding sites does Albumin have?
2
