Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/213

Click to flip

213 Cards in this Set

  • Front
  • Back
PHARM - Pharmacology and Therapeutics - Section 1 Exam
Principles of Pharmacology
Define a drug (in the broadest sense).
Any chemical agent that affects living protoplasm
Define a drug (= medication).
Any chemical agent used for treatment, prevention, or (rarely) diagnosis of disease.
Define a medicine.
A preparation that contains at least one active drug.
What subdivision of pharm deals with the absorption, distribution, biotransformation, and excretion of drugs?
Pharmacokinetics
What subdivision of pharm deals with the biochemical/physiologic effects of drugs, mechanisms of action and drug-receptor interactions?
Pharmacodynamics
What biological item may be used as a model for drug-receptor interactions?
Enzymes
T/F: Drugs can give new function to cells/tissues.
False, they can only modify what is already existing!
Drugs have two very basic effects on tissues: 1 ___________ and 2 __________.
Stimulate and depress
What molecules in the living organism do drugs bind to?
Receptors
Most drug receptors are ___________. What are the three types of receptors (as listed in the textbook)?
Macromolecules. 1. Enzymes 2. Nucleic acids 3 Membrane parts
Name the one irreversible and strongest bond. Name the three weakest, reversible bonds from increasing to decreasing strength.
Covalent. Ionic bonds>Hydrogen bonds>Van der Waal's forces
Why is it better to plot dose-intensity relationships on logarithmic scales instead of arithmetic (From the book)?
Arithmetic scales are hard to compare to each other, and often the intensity rises so fast it is impossible to determine the exact ED50
Define an agonist.
A drug that has an affinity for (attaches to and activates) receptors and produces an effect
What equilibrium equation is used for drugs and their receptors? What is this equiilibrium called (from the book)? What are five required criteria for this equilibrium to hold true (from the book)?
{D}+{R}<-> {DR} -->E . Occupation theory. 1 One drug must bind to one receptor 2 There can be no interactions between DR complexes 3 Receptors must have equal access 4 Only a portion of the total drug can bind 5 Proportional biologic response must exist
Define an antagonist.
Drugs that interact with the receptor to inhibit the action of an agonist without producing any effect themselves.
Competitive, non-competitive antagonist, or partial agonist? Inhibition can be overcome by increasing the concentration of the agonist (which ultimately achieves the desired effects).
Competitive antagonist
Competitive, non-competitive antagonist, or partial agonist? The log dose-response curve is shifted to the right.
Competitive antagonist
Competitive, non-competitive antagonist, or partial agonist? Usually combines irreversibly with the receptor,
Non-competitive antagonist
Competitive, non-competitive antagonist, or partial agonist? The log dose-response curve shows reduced efficacy but the same potency.
Non-competitive antagonist
Competitive, non-competitive antagonist, or partial agonist? Acts on the same receptor as does the full agonist, but produces less than maximal effect
Partial agonist
Potency or efficacy: When a drug has greater biologic activity per unit mass.
Potency
Potency or efficacy: Relates to DOSE
Potency
Potency or efficacy: Maximum/'ceiling' effect that it produces is greater than that of another drug.
Efficacy
Drug Safety and Effectiveness
Define a probit.
One standard deviation
When plotting quantal drug-response curves, what is plotted on the x axis? What is plotted on the y-axis?
X axis = Dose in micrograms/gram. Y axis = Percent of subjects that respond (yes, or no, not intensity of effects)
Define margin of safety.
The amount of a drug that can be safely given.
What is ED50? What is LD50?
ED50 is the dose of a drug at which 50% of the subjects respond (to a specified extent, like sleep). LD50 is the dose of a drug at which 50% of the subjects responsd (to a specified extent, like death).
What is TI? How do you calculate TI? According to the FDA, what is the desired TI (at least)?
TI is Therapeutic Index, or Margin of Safety. TI = LD50/ED50. FDA wants TI at least 20, but the farther apart the curves for ED and LD are, the safer the drug will be.
What is the ratio of LD to ED that makes up the Clinical Margin of Safety?
LD1/ED99, but this measurement is not as accurate as TI.
When comparing two drugs on a graph, if the two drugs have parallel lines, they have (the same/different) mechanisms. If two drug curves are not parallel, they have (the same/different) mechanisms.
The same (probably). Different, for sure, definitely.
Name the two special types of hyporeactivity, and what causes them.
1. Tolerance - previous exposure over time makes a subject less responsive to the same amount of drug 2. Tachyphylaxis - tolerance develops rapidly after a few doses
Name 7 factors of drug effectiveness that are primarily related to patient characteristics.
1 Weight/body surface area 2 Age 3 Pregnancy 4 Genetic factors 5 Disease 6 Adherence 7 Allergy
What is one thing a prescriber can do to increase patient adherence to drug regimens?
WRITE the instructions
Differentiate side effect from toxic effect.
Side effect is any effect other than the intended effect, while toxic effect is a side effect that is undesirable.
T/F: Drugs can have no side effects.
False, there is no known drug that has no side effects.
Is this performed in animals or man? Determine ED50
Animals
Is this performed in animals or man? Evaluate toxicity using acute, subacute, or chronic doses
Animals
Is this performed in animals or man? Determine the best route of administration
Animals
Is this performed in animals or man? Develop analytical methods and study the kinetics of the drug
Animals
Is this performed in animals or man? Small doses to determine safety
Man
Is this performed in animals or man? Trials to evaluate safety and efficacy
Man
Is the nonproprietary name considered the generic or trade name?
Generic, which we should know!!
Drug Administration and Pharmacokinetics
Name the 4 basic routes of drug administration.
1 Enteral 2 Parenteral 3 Pulmonary 4 Dermal
What is the most common route of drug administration? Why?
Oral, because it is 1 Convenient 2 Economic 3 Safe (from book)
In the GI tract, where are most drugs absorbed?
Duodenum
What is first-pass biotransformation?
Biotransformation of a drug due to enterocytes/hepatocytes (mainly hepatocytes)
Name the three specific types of enteral drug administration that avoid first-pass biotransformation.
1 Sublingual 2 Buccal 3 Rectal
What is the fastest route of drug administration, and therefore, the most dangerous?
Intravenous
What type of drug administration is usually used for solid tumors?
Intra-arterial
What type of drug administration is usually used for CSF?
Intrathecal
What type of drug administration is usually used for rabies and hemodialysis?
Intraperitoneal
What three forms of drugs can be taken up by the pulmonary system?
1 Gas 2 Vapor 3 Aerosol
What mechanism is used by the epidermis to take up dermally-administered drugs?
Simple diffusion
Are water soluble or lipid soluble drugs more efficiently taken up by dermal administration?
Lipid-soluble (think of lotion!)
Define absorption.
Transfer of a drug from the site of administration to the blood stream
What is the most common mechanism for drug absorption?
Passive diffusion
Regarding passive diffusion, molecules that are (water/lipid) soluble and (non/ionized) will diffuse more readily.
Lipid, Non-ionized molecules
What is the partition coefficient?
Measure of relative solubility in fat compared to water
T/F: Rates of transfer across barriers are directly related to the partition coefficient.
TRUE
Does the stomach more readily absorb weak acids, weak bases, or both?
Weak acids
Does the small intestine more readily absorb weak acids, weak bases, or both?
Both
Explain how you do calculations if a question asks, "Drug A has a pKa of X. At equilibrium between gastric juice of pH 1, and plasma of pH 7, the higher concentration of drug will be in… plasma, gastric juice, or equal concentrations?"
Plug and chug into Henderson-Hasselbalch, and compare the two answers
Define distribution.
Movement of drugs through the body
Name 5 things that determine how drugs are distributed (from book).
1 Physicochemical properties of the drug 2 Cardiac output and regional blood flow 3 Membranes 4 pH 5 Binding of the drug
What is the largest molecular size that can diffuse across capillary membranes (in Angstroms and in Kilodaltons)?
30 Angstroms, 60 Kilodaltons
What type of drugs are better for crossing the Blood-Brain Barrier, Water or Lipid Soluble?
Lipid-soluble
What is the major plasma protein used for binding drugs? What plasma protein do basic drugs readily bind to (from book)?
Albumin. Alpha1 Acid Glycoprotein, AKA Orosomucoid
Does drug binding to tissue (increase/decrease) the rate of elimination? What organ system is a large reservoir for tissue-bound drugs?
Decreases. Muscle.
What is the equation used for calcuating the volume of an unknown container?
Vd = Dose of drug/Concentration of free drug in plasma
What organ is the major site for drug biotransformation? What enzyme is mainly involved?
Liver. Cytochrome P450
Define enzyme induction.
This is the stimulation of microsomal enzymes, which lends to increased tolerance to drugs
Esterase/amidase hydrolysis: Is this reaction Phase I or Phase II? Is it Non or Microsomal? Is it Hydrolysis, Reduction, or Oxidation?
Phase I, Non-microsomal, Hydrolysis
Reduction of alcohols: Is this reaction Phase I or Phase II? Is it Non or Microsomal? Is it Hydrolysis, Reduction, or Oxidation?
Phase I, Non-microsomal, Hydrolysis
Alcohol Dehydrogenase: Is this reaction Phase I or Phase II? Is it Non or Microsomal? Is it Hydrolysis, Reduction, or Oxidation?
Phase I, Non-microsomal, Oxidation
Aliphatic hydroxylation: Is this reaction Phase I or Phase II? Is it Non or Microsomal? Is it Hydrolysis, Reduction, or Oxidation?
Phase I, Non-microsomal, Oxidation
Aromatic hydroxylation: Is this reaction Phase I or Phase II? Is it Non or Microsomal? Is it Hydrolysis, Reduction, or Oxidation?
Phase I, Non-microsomal, Oxidation
Deamination: Is this reaction Phase I or Phase II? Is it Non or Microsomal? Is it Hydrolysis, Reduction, or Oxidation?
Phase I, Non-microsomal, Oxidation
MAOIs: Is this reaction Phase I or Phase II? Is it Non or Microsomal? Is it Hydrolysis, Reduction, or Oxidation?
Phase I, Non-microsomal, Oxidation
Does microsomal biotransformation make drugs (more/less) polar, (more/less) hydrophilic, and (more/less) likely to penetrate?
More polar, more hydrophilic, less likely to penetrate
Hydrocarbon chain oxygen addition: Is this reaction Phase I or Phase II? Is it Non or Microsomal? Is it Hydrolysis, Reduction, or Oxidation?
Phase I, Microsomal, Oxidation
Ring hydroxylation: Is this reaction Phase I or Phase II? Is it Non or Microsomal? Is it Hydrolysis, Reduction, or Oxidation?
Phase I, Microsomal, Oxidation
N, O, or S-dealkylation: Is this reaction Phase I or Phase II? Is it Non or Microsomal? Is it Hydrolysis, Reduction, or Oxidation?
Phase I, Microsomal, Oxidation
Oxidative Deamination: Is this reaction Phase I or Phase II? Is it Non or Microsomal? Is it Hydrolysis, Reduction, or Oxidation?
Phase I, Microsomal, Oxidation
N-oxydation or N-hydroxylation: Is this reaction Phase I or Phase II? Is it Non or Microsomal? Is it Hydrolysis, Reduction, or Oxidation?
Phase I, Microsomal, Oxidation
Nitro group reduction: Is this reaction Phase I or Phase II? Is it Non or Microsomal? Is it Hydrolysis, Reduction, or Oxidation?
Phase I, Microsomal, Reduction
Azoreduction: Is this reaction Phase I or Phase II? Is it Non or Microsomal? Is it Hydrolysis, Reduction, or Oxidation?
Phase I, Microsomal, Reduction
Reductive dehalogenation: Is this reaction Phase I or Phase II? Is it Non or Microsomal? Is it Hydrolysis, Reduction, or Oxidation?
Phase I, Microsomal, Reduction
Epoxidation: Is this reaction Phase I or Phase II? Is it Non or Microsomal? Is it Hydrolysis, Reduction, or Oxidation?
Phase I, Non-Microsomal AND Microsomal
Name the four Phase II Reactions.
1 Glucuronide formation 2 Acetylation 3 Sulfate conjugation 4 S,O,and N methylation
What is the major excretion route for drugs?
Kidneys
How do you calculate Renal Clearance? What is the normal Glomerular Filtration Rate?
Renal Clearance = (Urine Concentration X Urine Volume) / Plasma Concentration. Normal GFR = 125-130 mL/min
Most drugs follow (zero/first) order kinetics.
???
What equation is used to calculate half-life? What equation is used to estimate amount of a drug in the body at some point after it is given?
Half life = kt=0.693. Concentration at time t = Amount of drug at time zero/2^number of half lives that have gone by since time zero
On dose vs. elimination scales, what happens to graphs when the dose concentration is changed?
The graphs differ like crazy, since rate of absorption and of elimination are changed.
On dose vs. elimination scales, what happens to graphs when the absorption amount is changed?
Peaks slightly differ, but the curves are very similar
On dose vs. elimination scales, what happens to graphs when the excretion amount is changed?
The graphs show a buildup near the peak and different curves at the tail ends
Why do we give "loading doses"?
To establish the plateau amount more quickly (get the rate of elimination to match the rate of administration)
How are loading doses calculated?
Loading dose = Concentration at steady state X Volume distributed
The time required to attain the plateau is ONLY dependent on what?
Half-time for elimination!
Normally, how many half-lives of a drug must pass to reach the plateau?
4-5 half-lives
What is APA? How do you calculate it?
APA is Average Plateau Amount. APA = 1.5 X Amount of drug given in one half-life
How do you calculate Dosing Interval? How do you calculate the average concentration at the Steady State?
Dosing Interval = (1.44 X Dose in mg X half-life)/APA… Concentration at steady state = APA/Volume distributed
Generally, dosage must be (reduced/increased) in patients with renal impairment. How do you calculate the appropriate dose for a patient with renal impairment?
Reduced. Dose for the renally-impaired patient = (Dose for a normal patient X Half life in a normal patient)/ Half life in a renally-impaired patient
Autonomic Drugs
hey
Ach. AcH. Norepinephrine
Generally, ganglia for parasympathetics are (close to/far) from the spinal cord. Generally, ganglia for sympathetics are (close to/far) from the spinal cord.
Far from the spinal cord, IN the organ innervated!... Close to the spinal cord, still in the CNS
What enzyme catalyzes the production of Ach from Choline and Acetyl CoA? What enzyme hydrolyzes AcH release from their receptors?
Choline acetyltransferase. Acetylcholinesterase
What two neurotransmitters stimulate muscarinic receptors? What two neurotransmitters stimulate nicotinic receptors?
Muscarinic = Muscarine and AcH. Nicotinic = Nicotine and AcH
Name the four places that Nicotinic receptors are found.
1 Autonomic ganglia 2 Adrenal medulla 3 CNS 4 Skeletal muscle
In general, what do Cholinergic Stimulants do to the body?
increase GI/saliva, decrease heart rate, cause repeated erections…
Name the 5 Muscarinic, Direct Stimulants.
1 Acetylcholine 2 Pilocarpine 3 Cevimeline 4 Carbachol 5 Bethenachol
Acetylcholine: Class of drug, use.
Muscarinic, Direct Stimulants- topical miotic *for constricted, (seedy) beady eyes
Pilocarpine, Cevimeline: Class of drug, use.
Muscarinic, Direct Stimulants - to treat xerostomia *to pile on the drool
Bethenachol, Carbachol: Class of drug, use.
Muscarinic, Direct Stimulants - to treat urinary retention and GI paresis *Beth’s in the car and she just peed/poo-ed herself
Why are Bethenachol and Carbachol unique?
They are Acetylcholinesterase-resistant, so they last for a long time
Name the 3 Muscarinic, Indirect Stimulants.
1 Neostigmine 2 Physostigmine 3 Echothiophate
Neostigmine: Class of drug, use.
Muscarinic, Indirect Stimulants - to treat myasthenia gravis and neuromuscular blockade
Physostigmine: Class of drug, use.
Muscarinic, Indirect Stimulants - to treat atropine poisoning
Echothiophate: Class of drug, use.
Muscarinic, Indirect Stimulants - to treat glaucoma
Why is Echothiophate unique?
It is an irreversible cholinergic stimulant
Name the 1 Nicotinic stimulant, and its use.
Nicotine - to overcome nicotine addiction
Why is nicotine an oddball cholinergic stimulator?
It causes HYPERtension and convulsions instead of hypotension and calmness
In general, what do Cholinergic Blockers do to the body?
Prevent drowning in saliva, inhibits “voiding” of bladder and GI tract
Name the 2 Muscarinic blockers.
1 Atropine 2 Scopalamine
Atropine: Class of drug, use.
Muscarinic Blocker - to decrease secretions, stop diarrhea *also causes adverse effects: Blind as a bat, red as a beet, dry as a bone, wild as a hare *CSI! Give physostigmine if overdosed
Scopalamine: Class of drug, use.
Muscarinic Blocker - to prevent motion sickness and insomnia *puts you to sleep so you don’t puke on the Scope boat
Name the 1 Nicotinic blocker, and its use.
Mecamylamine - last resort for decreasing blood pressure, only used when aorta is about to burst! *give it to my camel with high HIGH HIGH blood pressure
Describe how norepinephrine is made. Where is epinephrine made?
Tyrosine > DOPA > Dopamine > Norepinephrine. Epinephrine is made in the adrenal medulla
Describe the two mechanisms that get rid of Norepinephrine from a postganglionic fiber.
1 Reuptake into the preganglionic neuron 2 Breakdown by MAO or COMT
What is the normal function of Alpha-1 Receptors?
Vasoconstriction
What are the two normal functions of Alpha-2 Receptors?
1. Vasoconstriction (peripherally) 2 Block norepinephrine release from the postganglionic neurons (in CNS)
What are the two normal functions of Beta-1 receptors?
1 Increase heart rate 2 Increase contractile force
What is the normal function of Beta-2 receptors?
Relax bronchial smooth muscles
In general, what do Alpha-1 Adrenergic Stimulants do to the body?
Increase heart rate, vasoconstrict, and dilate pupils
Name the 1 Alpha-1 Adrenergic Stimulant, and its use.
Phenylephrine - increases heart rate, vasoconstrict, and dilate pupils * replaced pseudoephedrine as Sudafed’s main ingredient, mmm
In general, what do Alpha-2 Adrenergic Stimulants do to the body?
Decrease heart rate, vasodilate, and constrict pupils (Gets you 2 relax)
Name the 4 Alpha-2 Adrenergic Stimulants.
1 Clonidine 2 Methyldopa 3 Guanabenz 4 Guanfacine
Clonidine: Class of drug, use
Alpha-2 Adrenergic Stimulant - treats hypertension
Methyldopa: Class of drug, use
Alpha-2 Adrenergic Stimulant - treats hypertension
Why is methyldopa an oddball Alpha-2 Adrenergic Stimulant?
Adrenergic receptors see it as NE, but they DON'T activate
Guanabenz/Guanfacine: Class of drug.
Alpha-2 Adrenergic Stimulant (centrally acting?)
In general, what do "all alpha" adrenergic stimulants do to the body?
Increase heart rate and contractile force, Vasoconstrict
Name the 1 "all alpha" adrenergic stimulant, and its use in dentistry.
Norepinephrine. Used in local anesthetics to prevent washout
In general, what do Beta-1 Adrenergic Stimulants do to the body?
Increase contractile force and cardiac output
Name the 3 Beta-1 Adrenergic Stimulants.
1 Dobutamine 2 Dopamine 3 Norepinephrine
Dobutamine/Dopamine: Class of drug, use
Beta-1 Adrenergic Stimulants - treat heart failure *DOH, my heart is failing, give me some Dobutamine or Dopamine
Why is Dopamine an oddball Beta-1 Adrenergic Stimulant?
Releases NE into the heart
Norepinephrine: Class of drug, use
"All alpha" AND Beta-1 Adrenergic Stimulants
Why is Norepinephrine an oddball adrenergic drug?
It stimulates all alpha receptors and Beta-1 receptors
In general, what do Beta 2 Adrenergic Stimulants do to the body?
Relaxes bronchial smooth muscle *Bet you want 2 breathe now, smokaaaa*
Name the 3 Beta 2 Adrenergic Stimulants.
1 Albuterol 2 Terbutaline 3 Metaproterenol
Albuterol/Terbutaline/Metaproterenol: Class of drug, use
Beta 2 Adrenergic Stimulants - treats bronchoconstriction due to asthma/emphysema
In general, what do "all beta" adrenergic stimulants do to the body?
Increases contractile force and cardiac output, Relaxes bronchial smooth muscle
Name the 1 "all beta" adrenergic stimulant, and its use.
Isoproterenol - to relieve bronchoconstriction *I’m So Pro at getting oxygen now
Name the 1 "all adrenergics" stimulant.
Epinephrine *duh
Name the 5 indirect adrenergic stimulants.
1 Amphetamine 2 Ephedrine 3 Cocaine 4 Tricyclic Antidepressants 5 MAOI*spews more NE
Amphetamine: (helps release more NE/keeps NE readily available in the synapse)
Spews more NE
Ephedrine: (helps release more NE/keeps NE readily available in the synapse)
Spews more NE
Cocaine: (helps release more NE/keeps NE readily available in the synapse)
Keeps NE in the synapse
Tricyclic Antidepressants (helps release more NE/keeps NE readily available in the synapse)
Keeps NE in the synapse
MAOI: (helps release more NE/keeps NE readily available in the synapse)
Keeps NE in the synapse
In general, what do Alpha-1 Adrenergic Blockers do to the body?
Decrease heart rate, vasodilate, constricts pupils
Name the 2 Alpha-1 Adrenergic Blockers.
1 Prazosin 2 Terazocin
Prazosin/Terazocin: Class of drug, use
Alpha-1 Adrenergic Blockers - treat hypertension *To block someone from eating A1 Steak Sauce is a Sin
Why is Prazosin a unique Alpha-1 Adrenergic blocker?
It has a First-Dose phenomenon, where you get lightheaded at first dose
In general, what do “All Alpha” Adrenergic Receptor Blockers do to the body?
Decrease heart rate, vasodilate, constricts pupils, bind to norepinephrine receptors
Name the 2 “All Alpha” Adrenergic Receptor Blockers.
1 Phenoxybenzamine 2 Phentolamine
Phenoxybenzamine/Phentolamine: Class of drug.
“All Alpha” Adrenergic Receptor Blockers
In general, what do Beta-1 Adrenergic Blockers do to the body?
Prevent bronchoconstriction
Metoprolol/Acebutolol/Atenolol/Esmolol: Class of drug, use
Beta-1 Adrenergic Blockers - treat hypertension or angina pectoris
In general, what do “All Beta” Adrenergic Receptor Blockers do to the body?
Decrease heart rate and contractile force, too much will cause bronchoconstriction and death *OLOLs
Propranolol : Class of drug, use
“All Beta” Adrenergic Receptor Blockers - treat hypertension
Why is propranolol an oddball “All Beta” Adrenergic Receptor Blocker?
It increases insulin release and can cause hypoglycemia
Timolol: Class of drug, use
“All Beta” Adrenergic Receptor Blockers - treat hypertension or angina pectoris
Why is Timolol an oddball “All Beta” Adrenergic Receptor Blocker?
It decreases IOP and treats glaucoma (but I'd rather have medicinal marijuana!)
Carteolol/Pindolol/Penbutolol: Class of drug, use
“All Beta” Adrenergic Receptor Blockers - treat hypertension
Why should you use Carteolol/Pindolol/Penbutolol instead of other “All Beta” Adrenergic Receptor Blockers?
They're both beta blockers AND stimulators, so there's less bradycardia
In general, what do “ALL Adrenergic” Receptor Blockers do to the body?
Decrease heart rate, Vasodilates
Name the 1 “ALL Adrenergic” Receptor Blocker.
Labetalol
In general, what do indirect adrenergic receptor blockers do to the body?
These throw out all the Norepinephrine from storage vesicles
Name the 2 indirect adrenergic receptor blockers.
1 Reserpine 2 Bretylium
Reserpine: Class of drug, use, mechanism
indirect adrenergic receptor blockers - treats hypertension - *can’t store NE in vesicles, causes depression (no EPI, how sad)
Bretylium: Class of drug, use, mechanism
indirect adrenergic receptor blockers - treats hypertension and arrhythmias *NE stored in vesicles is depleted (who stole all my EPI?!)
Autacoids
Name the three locations that have H1 receptors.
1 Bronchi/Bronchioles 2 Arterioles 3 Ileum (all have smooth muscle)
In general, what does an H1 blocker do?
Prevent normal histamine rxn
Name the three locations that have H2 receptors.
SAM 1 Stomach 2 Arterioles 3 Mast Cells
If histamine reaches the endothelial cells of the stomach, what will the stomach do?
Release acid
Diphenhydramine/Dimenhydrinate
H1 Blocker (1st generation) *Prevent normal histamine reaction
Promethazine /Chlorpheniramine /Cyproheptadine/Meclizine: Class of Drug, use
H1 Blocker (1st generation) haha, tricked you, didn't put Allegra/Benadryl on this list! *Prevent normal histamine reaction
Fexofenadine/Loratadine
H1 Blocker (2nd generation) *Prevent normal histamine reaction
Epinephrine/Aminophylline/Corticosteroids: Class of Drug. use
H1 Blocker *Severe allergic reactions
Name three things that CANNOT be "cured" with H1 blockers.
1 Asthma 2 Bronchoconstriction 3 Edema due to dental procedures
In general, what does an H2 blocker do?
Decrease gastric acid secretion, constrict arterioles, prevents degranulation of mast cells
Cimetidine, Ranitidine, Famotidine, Nizatidine: Class of Drug, use
H2 blocker, decrease secretion of gastric acid *SAM can't drive his H2 into the TIde and DINE
In general, what do Serotonin enhancers do?
Elevate the mood, increase GI motility, vasoconstrict/dilate, increase sensitivity of pain receptors *I'm so happy I just poo-ed myself, but I'm crying because you poked me and I'm sensitive :(
Tryptophane/SSRIs/MAOIs: Class of drug, use.
Serotonin enhancers, treat depression
Reserpine/Cyproheptadine: Class of drug, use.
Serotonin blockers, treat HBP *I got a little too happy and by heart is racing
What kind of molecule is Angiotensin II?
Peptide
Describe the mechanism that converts angiotensinogen to Angiotensin II.
Angiotensin in the liver combines with Renin from the kidney --> Angiotensin I, which is converted in the lung by ACE --> Angiotensin II
In general, what do ACE inhibitors do?
Lower BP, Increase secretion of aldosterone
Captopril, Enalapril, Lisinopril, Ramipril, Benazepril: Class of Drug, use
ACE Inhibitors - Lower BP, increase secretion of aldosterone *ACE the class in aPRIL
In general, what do AT1 blockers do?
Lower BP, Increase secretion of aldosterone
Losartan, Valsartan, Irbesartan: Class of Drug, use
AT 1 blockers - Lower BP, Increase secretion of aldosterone *we had dR. TAN's class AT 1 PM
In general, what do Prostaglandin enhancers do?
Increase muscular constriction, mediate inflammation
Alprostadil: Class of Drug, use.
Prostaglandin enhancer - Treat male impotence
Misoprostol: Class of Drug, use.
Prostaglandin enhancer - Decrease gastric damage due to NSAIDs
Latanoprost: Class of Drug, use.
Prostaglandin enhancer - Treat glaucoma
PGE2 and PGF Alpha: Class of Drug, use.
Prostaglandin enhancer - Induce labor