Term
| Why was medicinal therapy heavily influenced by religion? |
|
Definition
Because medicine men were both priests and physicians; used plants which contained intoxicating substances
These substances allowed for an alteration of state of consciousness and facilitated communication w/ the gods. |
|
|
Term
| 2 examples of hallucinogenic natural compounds? |
|
Definition
Psilocybe mushroom in Mexico
Peyote cactus in N. America; contains MESCALINE |
|
|
Term
| What is the active hallucinogen in the Psilocybe mushroom? |
|
Definition
|
|
Term
| 3 examples of the influence of posions on medicine? What medicines did they derive? |
|
Definition
Calabar bean - derived physostigmine (glaucoma treatment)
Curare - derived modern anaesthetics by blocking ACh transmission and neuromuscular junctions
Ergot - ergotamine (migraine treatment), ergonovine (force uterine contractions) |
|
|
Term
| Where is the drug physostigmine (used for glaucoma treatment) derived from? |
|
Definition
| The Calabar bean used in ordeal trials in Africa |
|
|
Term
| What are the effects of the poison "curare"? |
|
Definition
| Blocks ACh transmission at neuromuscular junctions by blocking the ACh receptor (receptor antagonist) |
|
|
Term
| 4 symptoms of ergot poisoning? |
|
Definition
1) Burning in limbs (Holy Fire)
2) Vasoconstriction (could lead to necrosis in peripheral tissues)
3) Hallucinations & convulsions
4) Abortion (forced uterine contractions) |
|
|
Term
| Effects of ergonovine and ergotamine? |
|
Definition
Ergotamine - used to treat migraines (cerebral vasoconstrictor)
Ergonovine - induces uterine contractions |
|
|
Term
| What type of drug was Ma Huang classified as in China? What was it used for? What drug(s) has it now spawned? |
|
Definition
Classified as a medium drug; used to treat coughs, influenza & fevers
Influenced development of EPHEDRINE |
|
|
Term
| What medical lexicon was discovered in ancient Egypt and what was its use? What was the main class of drug it focused on? |
|
Definition
Ebers Papyrus - used as a textbook for medical students
Focused on PURGATIVES (used to cause bowel movements) - included, castor oil, figs & senna |
|
|
Term
| What purgative was used in both the Egyptian and Shakespearian times? |
|
Definition
|
|
Term
| What did Theophrastus write a book on in 380 BC? |
|
Definition
| Book on Therapeutics, focusing on OPIUM |
|
|
Term
| Who isolated crystals of morphine from opium? How much morphine is contained in opium? |
|
Definition
Seturner, pharmacist in Germanhy in 1803
Opium contains 10% morphine |
|
|
Term
| Most effective analgesic available? |
|
Definition
| MORPHINE ("gold standard" of analgesics) |
|
|
Term
| What is heroin available in Canada to treat for? |
|
Definition
| Only used to treat terminal cancer pain in special treatment units |
|
|
Term
| What type of receptors does morphine act on in the CNS (i.e. what normally acts on these receptors)? |
|
Definition
| Morphine acts on receptors for endogenous analgesic compounds, such as enkephalins & endorphins |
|
|
Term
| How much codeine is contained within opium? What over the counter drug contains codeine? |
|
Definition
Opium contains 0.5% codeine
Tylenol I contains codeine and is an OTC drug |
|
|
Term
| Where was the original treatment for gout introduced, and what was used? |
|
Definition
| In Spain/Persia/Mesopotamina, used COLCHICUM for gout (now use colchicine, extract of colchicum) |
|
|
Term
| Who introduced digitalis purpurea into medicine, and when did this occur? What is the function of digitalis extract? |
|
Definition
Withering introduced D. purpurea into medicine in 1785.
The extract increases the pumping ability of the heart muscle. |
|
|
Term
| What modern drug is a derivative of the D. purpurea extract used by Withering? |
|
Definition
| Use Digoxin nowadays to treat patients - used to treat ARRHYTHMIAS |
|
|
Term
| 2 different uses of nitroglycerine (both don't have to be medicinal)? |
|
Definition
Medicinal - used to treat angina pectoris
Non-medicinal - powerful explosive material |
|
|
Term
| 1st used agent to treat angina? Who recommended it? What succeeded it and why? |
|
Definition
1st = amyl nitrate; introduced by Brunton
Surpassed by nitroglycerin because it was longer acting |
|
|
Term
| Who introduced nitroglycerin into medicine as a treatment of angina? |
|
Definition
| Murrell introduced NG in 1879 |
|
|
Term
| What is the physiological mechanism of NG? |
|
Definition
| NG causes vasodilation in coronary BVs (and elsehwere) to increase O2 supply to heart and decrease O2 requireents of heart |
|
|
Term
| Where was quinine isolated from? What is it used to treat? |
|
Definition
| Quinine was isolated from the bark of the Cinchona tree; used to treat arrhythmias (quinine and quinidine are the extracts) |
|
|
Term
| What plant are chlorpromazine and reserpine isolated from? |
|
Definition
|
|
Term
| What two drugs are isolated from the Rauwolfia plant? |
|
Definition
| Reserpine & chlorpromazine |
|
|
Term
| Who isolated reserpine and from what plant? |
|
Definition
| A Swiss pharmaceutical company isolated reserpine from the Rauwolfia plant and showed a tranquilizing effect in aggressive animals |
|
|
Term
| Why is chlorpromazine preferred to reserpine? What is reserpine still effective in treating though? |
|
Definition
| Hard to find correct dose of reserpine for patient. Still use reserpine to treat HTN. |
|
|
Term
| Who isolated LSD and where is it from? |
|
Definition
| Albert Hofmann isolated LSD, based on components of ergot |
|
|
Term
| What discovery did LSD show about mental illnesses? |
|
Definition
| The illnesses may be due to production of potent substances in the brain producing psychic disturbances |
|
|
Term
|
Definition
Father of chemotherapy
Designed organoarsenicals
Created a cure for syphilis |
|
|
Term
|
Definition
| Introduced sulfa drugs in Germany in the 1930s; they were the first successful synthetic drugs in treating bacterial disease |
|
|
Term
| Who introduced the first SYNTHETIC drugs successful for treating bacterial disease? |
|
Definition
| Gerhard Domagk (sulfa drugs) |
|
|
Term
| Who's discovery led to the cure of syphilis? |
|
Definition
|
|
Term
|
Definition
Discovered the 1st antibiotic = penicillin (naturally occurring)
Used to treat GRAM-POSITIVE bacteria |
|
|
Term
|
Definition
Discovered streptomycin
Turning point in treatment of Tb and GRAM-NEGATIVE bacterial disease |
|
|
Term
| Who made discoveries which helped treat gram-positive vs. gram-negative bacterial related diseases? |
|
Definition
Positive = Fleming w/ penicillin
Negative = Waksman w/ streptomycin |
|
|
Term
| What is the main value of ergonovine? |
|
Definition
| To ARREST BLEEDING post-birth (due to strong uterine contractions) |
|
|
Term
| Who discovered one of the 1st anesthetics used in surgery and what was it? However, when were the 1st public demonstrations of its effects shown? |
|
Definition
Humphrey Davy introduced NITROUS OXIDE in 1800
Not shown until Colton gave demonstrations in the 1840s |
|
|
Term
| Who was the first dentist to use nitrous oxide in his procedures? |
|
Definition
|
|
Term
| Who showed that ether had similar chemical properties to NO? |
|
Definition
|
|
Term
| Where was the first operation carried out under anesthesia performed? What was used? |
|
Definition
| Ether was used by Morton at Mass. General Hospital, while he was still a medical student at Harvard |
|
|
Term
| What is the major use of quinine (non-CV use)? |
|
Definition
|
|
Term
| What are some drug advertising techniques used? |
|
Definition
Catch audience attention to draw their focus
Use celebrities to endorse
Fear
Offer easy solution to problems
Before-After technique
Discredit other drugs, while praising your own |
|
|
Term
| What happened in 1938 that led to changes for regulations for introducing drugs into therapeutic use? |
|
Definition
| Sulfonamide antibacterial dissolved in solvent was introduced in therapeutics, and 100 deaths resulted |
|
|
Term
| What happened when thalidomide was introduced to therapeutics? |
|
Definition
Introduced as a sleeping tablet, later shown it caused fetal malformations if taken during pregnancy
Showed that you needed to show both safety AND efficacy of a drug before introducing it into therapeutics |
|
|
Term
| What steps are required before a manufacturer can introduce a new drug into therapeutics? |
|
Definition
1. Submit proof of safety AND efficacy in several animal species
2. Detail methodology of clinical trial w/ humans
3. Manufacturer's submission is evaluated by regulatory sceinists |
|
|
Term
| What are the phases of a clinical trial? |
|
Definition
Phase 1 - study conducted in limited # of HEALTHY volunteers
Phase 2 - determine efficacy of drug; test in limited number of people w/ condition
Phase 3 - test efficacy in a larger # of people (usually 1000)
If proven safe after phase 3; released for marketing in general use |
|
|
Term
|
Definition
An inert substance which masquerades as a drug
Derived from the Latin "I shall please" |
|
|
Term
|
Definition
| Effects which occur due to drug administration and have NOTHING TO DO with the pharmacological effects of the drug |
|
|
Term
| Who conducted one of the most comprehensive studies of placebo effects? What was concluded? |
|
Definition
Beecher in 1955
Found the likelihood of placebo effects is greater in sick, anxious patients under stress
Note: approximately 35% of patients respond to placebo |
|
|
Term
| When is it not ethical to compare a new drug to a placebo and why? |
|
Definition
| Not ethical when there is an older drug of proven value to compare with the newer drug; this is because individuals cannot be deprived of effective therapy, if available |
|
|
Term
| In what population is the likelihood of placebo effects greater? |
|
Definition
| Greater in those who are sick, anxious and have high stress levels |
|
|
Term
| When is a cross-over design for a phase III trial appropriate? What is flawed in this design? |
|
Definition
In cross-over, divide people into two groups - at one time one receives drug, other receives placebo; at later time, switch drugs w/ groups
Because groups are NOT compared at the same time, not really valid (could be differences in second occasion)
Only useful with chronic and stable long-term diseases |
|
|
Term
| What type of design are most phase III trials? |
|
Definition
| Parallel design - divide into 2 groups randomly and one group gets drug, one does not (either placebo/old drug) |
|
|
Term
| What is the best way to randomize an experiment? |
|
Definition
| Use table w/ random #s and random sequence generation by a computer |
|
|
Term
| Design elements of a phase III trial? |
|
Definition
Population of the study
Comparator
Rnadom assignment
Outcome
Blinding
Control |
|
|
Term
|
Definition
The amount of drug that must be given to obtain a particular response
E.g. If drug A is more potent, you need less of it to get the same effect |
|
|
Term
|
Definition
Refers to the MAXIMUM effect that is obtainable
E.g. Morphine has a greater efficacy compared to aspirin in terms of pain relief (can relieve a greater degree of pain at max dosage) |
|
|
Term
| If the maximum effect of drug B is greater than that of drug A, what can be said? |
|
Definition
| Drug B has a higher EFFICACY compared to drug A (comparison of max. effects) |
|
|
Term
| If drug A exerts a similar effect to drug B at a lower dose, what can be said? |
|
Definition
| Drug A is more potent than drug B |
|
|
Term
| Why is 10% sulphuric acid toxic to weeds but not cereal grass? What is this an example of? |
|
Definition
It is an example of selective toxicity by accumulation
The weeds' exterior has no wax and causes accumulation of the acid in the weeds. The exterior of the grass is smooth and waxy and the acid is not absorbed. Therefore the acid only affects the weeds. |
|
|
Term
| What are two examples of multidrug resistance proteins found in cancer cells? |
|
Definition
1st found = P-glycoprotein
2nd found = MRP (multidrug resistance protein) |
|
|
Term
| Who coined the term "chemotherapy"? |
|
Definition
| Paul Ehrlich, as he is considered to be the "father" of chemotherapy |
|
|
Term
| Who discovered that diseases were caused by microbes? |
|
Definition
| Pasteur and Koch in the 19th century |
|
|
Term
| How did Ehrlich reason out his selectively toxic organoarsenical binding method? What analogy did Ehrlich use to describe their method? |
|
Definition
Realized some dyes stained certain body tissues and others did not - wanted to design chemicals which would preferentially bind microbes, with toxic groups attached that could kill the microbes.
Ehrlich likened these selectively toxic compounds to a poison arrow |
|
|
Term
| In Ehrlich's time, what was the consensus view on how drugs acted? What did he believe? |
|
Definition
Most people thought that drugs acted by stimulating the body's defenses
Ehrlich believed "bodies do not act unless fixed" - needed drug to be attached to parasite to work |
|
|
Term
| What was the compounds that was used to treat syphilis? Who discovered it? |
|
Definition
| It was discovered by Ehrlich and he named it Salvarsan (to save health) |
|
|
Term
| According to Ehrlich, what 4 requirements are needed for research success? |
|
Definition
Geld - MONEY
Geduld - PATIENCE
Geschick - CLEVERNESS
Gluck - LUCK |
|
|
Term
|
Definition
Drug discovered by Domagk while working at Bayer factory
Selectively toxic drug to streptococcus bacteria
Split in the liver to give the active principle - sulfanilamide |
|
|
Term
| What is the active principle of Prontosil? Where is it activated? |
|
Definition
| Activated in the liver; active principle = sulfanilamide |
|
|
Term
|
Definition
Compound developed by Ehrlich to treat syphillis
Means "to save health" |
|
|
Term
| What is the selectively toxic mode of action of sulfanilamide? |
|
Definition
It is the active form of prontosil & used to treat strep.
Because bacteria require folic acid to be transported into the cell for growth, they take up a compound called PABA, which is used to synthesize folate within the cell.
Sulfanilamide is similar in structure to PABA, so it is taken into the cell instead, leading to no folic acid production and a halting of bacterial growth.
Since human cells used pre-formed folic acid, it does not require PABA and is unaffected |
|
|
Term
| Antimetabolite + example of 1 |
|
Definition
Antimetabolites are substances which act against certain substances required for an organism's metabolism
E.g. Sulfanilamide is a PABA antagonist (stops bacterial cell growth) |
|
|
Term
| Important differences between cancerous and normal cells? |
|
Definition
Some cancer cells cannot synthesize ASPARAGINE and need it from the blood
Cancer cells divide at a much faster rate than normal cells |
|
|
Term
| Two treatments of cancer that are specific to cancer cells? |
|
Definition
Asparaginase - certain cancer cells cannot synthesize asparagine, so they need it from blood; used to treat childhood acute leukemia
DNA replication inhibitors - used due to the highly dividing rates of cancer cells; however, cells of bone marrow & GI tract also divide rapidly and are affected |
|
|
Term
| Most cases of accidental poisoning with drugs occur... |
|
Definition
| In children under 5 years of age |
|
|
Term
| One of the most common drugs implicated in accidental overdose is... |
|
Definition
| Aspirin (predominantly in children under 5 years of age) |
|
|
Term
| Major drug group implicated in suicide attempts? |
|
Definition
| Barbiturates - CNS depressants |
|
|
Term
| What are 4 adverse effects to drugs? |
|
Definition
Extension of therapeutic effect
Effects unrelated to main drug action
Idiosyncrasy
Drug allergy |
|
|
Term
| Example of idiosyncrasy as an adverse drug effect... |
|
Definition
Succinylcholine - used to produce muscle relaxation; normally inactivated by enzyme present in the blood
About 1 in 3000 patients lack this enzyme and cannot inactivate the drug, leaving it longer-acting than normal |
|
|
Term
| What is succinylcholine used for? |
|
Definition
|
|
Term
|
Definition
| May have had abnormal colour vision due to consumption of digitalis (adverse effect unrelated to main drug action) |
|
|
Term
| What are the 3 stages of introduction that most new drugs pass through (3 P's)? |
|
Definition
Panacea - new marketing of drug makes people think it is a large advancement
Poison - due to adverse effects, sales drop
Pedestrian - w/ further passage of time, realize it is somewhere between panacea & poison |
|
|
Term
| 4 reasons why drugs may only be realized as being toxic much later in their usage? |
|
Definition
Toxic event is rare
Toxic event may only occur after prolonged use
Toxic event may not be detectable in animals (only seen in humans)
Toxic event may be unique to specific period (e.g. fetal malformations) |
|
|
Term
|
Definition
| LD50 - this is the dosage that is lethal to 50% of the population of animals tested |
|
|
Term
|
Definition
| ED50 - dose that is effective in 50% of the population tested |
|
|
Term
| What is the therapeutic index of the drug? What does it measure? Do you want it to be high or low? |
|
Definition
LD50/ED50 of the drug
The larger the figure, the more safe the drug is (want lethal dose to be >>> compared to effective dose) |
|
|
Term
| What is phenytoin used for? |
|
Definition
| Used to prevent epileptic attacks |
|
|
Term
| Paraenteral vs. Enteral Route of Administration (what is the difference?) |
|
Definition
Enteral - drug enters directly into GI tract
Paraenteral - drug bypasses GI tract |
|
|
Term
| What are 3 examples of enteral routes of administration of a drug? |
|
Definition
1. Taken in mouth
2. Rectal administration
3. Sublingual (under tongue) administration |
|
|
Term
| What are 5 examples of paraenteral routes of administration? |
|
Definition
1. Intramuscular
2. Subcutaneous
3. Intravenous
4. By inhalation
5. Via spinal canal (epidural) |
|
|
Term
| Who invented the hypodermic syringe? |
|
Definition
|
|
Term
| Who discovered/popularized amyl nitrate vs. nitroglycerin? |
|
Definition
Amyl Nitrate = Brunton
Nitroglycerin = Murrell |
|
|
Term
| Who initially suggested that NO had anaesthetic properties? |
|
Definition
|
|
Term
| Advantages vs. Disadvantages of IV Drug Administration |
|
Definition
Adv. - directly into circulation, keep administration rate constant, may be less painful
Dis. - cannot be retrieved, if given rapidly, can be deadly, infection risk |
|
|
Term
| What is the fastest route of drug administration? |
|
Definition
| IV - goes directly into the circulation |
|
|
Term
| How long does it take drugs given by the intramuscular route before they begin to exert their actions? One example of a drug commonly injected intramuscularly? |
|
Definition
10 to 30 minutes
Some penicillin preparations are injected this way so they are absorbed slowly into the blood
Also give hormones & antipsychotics in this manner |
|
|
Term
| Which is faster acting, drug administered by intramuscular or subcutaneous route? |
|
Definition
| Intramuscular is slightly faster because of better blood flow to the skeletal muscle |
|
|
Term
| What insecticides frequently poison humans by absorption through the skin? What is their mechanism of action? |
|
Definition
Insecticides - parathion and malathion
Inhibit acetylcholinesterase, so get ACh build-up at the neuromuscular junctions |
|
|
Term
| Antidotes for malathion and parathion poisoning? |
|
Definition
Problem is too much ACh at nerve terminals
Atropine - ACh receptor blocker
Pralidoxime - regenerates the bound AChase (bound by the insecticides) |
|
|
Term
| Relationship between the dose of a drug administered and concentration in blood? |
|
Definition
VERY POOR relationship - due to genetic differences, env't factors, other drugs, etc.
Do have a good relationship between concentration in blood and therapeutic effect however |
|
|
Term
| 3 methods of drug absorption? |
|
Definition
Inhalation
Rectal administration
Oral administration |
|
|
Term
| How are most general anesthetics absorbed? |
|
Definition
| Most are absorbed through INHALATION via the lungs |
|
|
Term
| When is the absorption of drug taken by oral adminstration into the blood stream most favourable? |
|
Definition
| When the stomach is empty, allows more ready access of drug to the stomach wall |
|
|
Term
| What is the major site of drug absorption if the drug is taken orally? |
|
Definition
| Small intestine - large surface area |
|
|
Term
|
Definition
%age of drug contained in drug product that ENTERS systemic circulation in an unchanged form after administration
Includes the rate at which entry occurs into circulation |
|
|
Term
| Generic Name vs. Brand Name |
|
Definition
| Every drug has ONE generic name (non-proprietary), and as many different brand names (proprietary) as there are companies that sell it |
|
|
Term
| Is diazepam a brand name or a generic name? |
|
Definition
|
|
Term
| 5 brand names of "diazepam"? |
|
Definition
| Valium, Vivo, Novo-Dipam, Apo-Diazepam, Diazepam |
|
|
Term
| What is the generic name of "Valium"? |
|
Definition
| Diazepam (benzodiazepine drug) |
|
|
Term
| If the same "generic drug" produced by different brands produces vastly different blood levels what can be said about the different brand versions of it? |
|
Definition
| They have vastly different BIOAVAILABILITIES (% of drug that goes unchanged from the tablet to the general circulation |
|
|
Term
| What are 3 problems associated with and that contribute to the "therapeutic jungle"? |
|
Definition
1. Drugs have multiple brand names, making them confusing
2. When a new drug is introduced, many other similar drugs will come out with minor changes (overwhelming # of drugs introduced)
3. Large amount of advertising and marketing (hard to determine drug quality) |
|
|
Term
| What are the 3 mechanisms for termination of drug action? |
|
Definition
Redistribution
Excretion
Biotransformation |
|
|
Term
| Example of redistribution to terminate action? |
|
Definition
Thiopental (short acting barbiturate)
Injected intravenously, reaches high concentration in brain rapidly due to rapid perfusion (high blood concentration = high brain concentration)
Over time, concentration gradient causes thiopental to migrate towards fat (low concentration); increases concentration in fat, decreases in blood (leaves brain)
When blood leaves brain, patient awakens (15 to 30 minutes) |
|
|
Term
| Where are most drugs excreted via? |
|
Definition
| The kidney (NEED to be water soluble to do so) |
|
|
Term
| Where does most drug biotransformation occur? |
|
Definition
|
|
Term
| How does biotransformation usually occur in the liver? |
|
Definition
Usually by a series of enzymes - cytochromes P450
Either inactivate the drugs or convert them to be water soluble (then excreted by kidney) |
|
|
Term
| 5 types of drug interactions? |
|
Definition
Absorption
Displacement
Change Liver Handling (Alter Biotransformation)
Change Excretion
Interact with Food |
|
|
Term
| Example of absorption interactions (drug interactions): |
|
Definition
Tetracycline antibiotics & antacids w/ metals (Ca, Mg, Al)
Form a complex which cannot be absorbed into the blood |
|
|
Term
| What two forms is the drug typically present in in the blood? |
|
Definition
Free form
Bound to a protein
Need to be in free form to move out of blood into tissues to act |
|
|
Term
| Drug interaction between cimetidine (antiulcer) & theophylline (antiasthmatic)? |
|
Definition
| Climetidine prevents inactivation of theophylline by the liver (changes liver handling), and leads to toxic levels |
|
|
Term
| Drug interaction between phenobarbital & warfarin? |
|
Definition
| Phenobarbital increases liver inactivation of warfarin, results in FEWER warfarin levels in the blood |
|
|
Term
|
Definition
| Anti-coagulant (blood thinner) |
|
|
Term
| Function of PHENOBARBITAL |
|
Definition
|
|
Term
| MAO inhibitor & tyramine interactions? |
|
Definition
Drug/food interactions - MAO is an enzyme normally used to break down tyramine in the body
Use MAO inhibitors in treating depression, w/o MAO tyramine levels in the body rise, leading to a sharp increase in BP |
|
|
Term
| What is the ultra-short duration of action of thiopental due to? |
|
Definition
| Redistribution from the brain to muscle/fat tissues |
|
|
Term
|
Definition
| Forebrain, midbrain, hindbrain |
|
|
Term
| What hallucinogenic compound contains mescaline? |
|
Definition
|
|
Term
| Who stated that "all substances are poisons, and the right dose differentiates poisons from remedies"? |
|
Definition
|
|
Term
|
Definition
ACh receptor antagonist -> blocks ACh receptors at neuromuscular junctions
Therefore, when applied get a state of flaccid paralysis |
|
|
Term
| What can morphine be chemically converted into? |
|
Definition
|
|
Term
| What two conditions is digoxin used to treat? |
|
Definition
|
|
Term
|
Definition
Quinine = drug of choice for the treatment of malaria
Quinidine = used to treat cardiac arrhythmias |
|
|
Term
| What is Phase IV of a clinical trial? |
|
Definition
| It is known as "postmarketing surveillance" - continue to follow drug after its release to the public |
|
|
Term
| Approximately what proportion of patients respond to placebos? |
|
Definition
|
|
Term
| Who developed prontosil & what does it treat? |
|
Definition
| Domagk developed prontosil & it treats streptococcus in mice |
|
|
Term
| Components of the forebrain vs. midbrain vs. hindbrain |
|
Definition
Forebrain - cortex, diencephalon & pituitary
Midbrain - mesencephalon (connects forebrain & hindbrain)
Hindbrain - medulla + cerebellum |
|
|
Term
| What stimuli does the midbrain relay? |
|
Definition
|
|
Term
| What do drugs that affect the cerebellum cause? |
|
Definition
|
|
Term
| What are the somae of neurons packed with? |
|
Definition
| Rough ER, smooth ER & secretory vesicles |
|
|
Term
| Where do axons usually synapse? |
|
Definition
| Onto the dendrites or cell body of other neurons |
|
|
Term
| What are the two mechanisms by which the chemical transmitter is removed from the synapse? |
|
Definition
1) Degraded by enzymes
2) Re-uptake into presynaptic cell |
|
|
Term
| Where are receptors for neurons synthesized? |
|
Definition
| In the rough ER of the soma |
|
|
Term
| Where can cholinergic synapses be found? |
|
Definition
| Both in the peripheral NS and CNS |
|
|
Term
| Two subclasses of ACh receptors and their agonists? |
|
Definition
Nicotinic - stimulated by nicotine
Muscarinic - stimulated by muscarine |
|
|
Term
| What are ACh receptors in the brain involved with? |
|
Definition
Learning, memory & cognition
Loss of cholinergic neurons may lead to Alzheimer's |
|
|
Term
| What does hyperactivity vs. hypoactivity of the serotinergic synapses in the brain typically cause? |
|
Definition
Hyperactivity = anxiety
Hypoactivity = depression |
|
|
Term
| 3 main areas of DA pathways? |
|
Definition
Basal Ganglia
Brain Stem
Midbrain |
|
|
Term
| 3 central functions of dopamine in the brain? |
|
Definition
Hormonal pathways
Motor initiation (basal ganglia)
Reward pathways |
|
|
Term
| What types of DA receptors are there? What are their respective activities? |
|
Definition
D1 = excitatory
D2 = inhibitory |
|
|
Term
| Where do norepinephrine pathways ALWAYS begin in the brain? |
|
Definition
|
|
Term
| What type of receptors/synapses are alpha & beta adrenergic typically? |
|
Definition
Typically EXCITATORY
(The subclasses of the NE receptors are usually inhibitory) |
|
|
Term
| What is the primary excitatory neurotransmitter in the brain? What is the function of these neurons? |
|
Definition
| Glutamate; involved in LEARNING |
|
|
Term
| Two populations of neurons that are involved in learning? |
|
Definition
Cholinergic (Muscarinic variety)
Glutamatergic |
|
|
Term
| 3 main classes of opioid peptides? |
|
Definition
| Enkephalins, Endorphins, Dynorphins |
|
|
Term
| What appears to be the most widely distributed opioid receptor in the CNS? |
|
Definition
| The MU receptor (cortex, brain stem, hypothal., SC) |
|
|
Term
| Different central locations of each of the opioid receptor classes? |
|
Definition
MU - cortex, brain stem, hypothalamus, SC
DELTA - olfactory system & limbic system
KAPPA - caudate & putamen, hypothalamus |
|
|
Term
| Different functions of each of the opioid receptor types? |
|
Definition
MU = pain regulation
DELTA = olfaction, cognition, reward, coordination
KAPPA = food intake, H2O balance, pain perception, endocrine control |
|
|
Term
| In the somatic NS (efferent), what NT is released and what is the receptor on the postsynaptic cell? |
|
Definition
| ACh is released into the neuromuscular junction, and it acts on nicotinic (cholinergic) receptors on the muscle cell membrane |
|
|
Term
| Function of the autonomic NS? What are the general functions of the ANS otherwise known as? |
|
Definition
Maintain a relatively stable internal environment
Unconscious functions of ANS are also called "visceral" or "vegetative" functions |
|
|
Term
| How do the sympathetic and parasympathetic systems typically act? |
|
Definition
| Act in a BALANCED and OPPOSITE function |
|
|
Term
| What is the predominant type of autonomic activity at rest? |
|
Definition
| Mainly parasympathetic (sympathetic system is largely inhibited at rest) |
|
|
Term
| What is it that usually excites the sympathetic NS? |
|
Definition
|
|
Term
| NT & receptor of preganglionic neurons for sympathetic vs. parasympathetic? |
|
Definition
| BOTH release ACh onto nicotinic receptors at the autonomic ganglia |
|
|
Term
| Locations of the different types of adrenergic receptors? |
|
Definition
Alpha - smooth muscle (GI tract, uterus, BVs)
Beta-1 - in the heart
Beta-2 - in BVs, GI tract, lungs |
|
|
Term
| Functions of the different types of adrenergic receptors? |
|
Definition
Alpha - cause smooth muscle CONTRACTION
Beta-1 - increase force and rate of contraction of heart
Beta-2 - cause smooth muscle RELAXATION |
|
|
Term
| Which 2 adrenergic receptors are somewhat antagonistic in their functions? |
|
Definition
| Alpha (causes muscle contraction) and Beta-2 (causes muscle relaxation) |
|
|
Term
| NT & receptor of postganglionic parasympathetic neurons? |
|
Definition
| ACh is released onto MUSCARINIC receptors |
|
|
Term
| What are 2 structures that have ONLY sympathetic innervation? |
|
Definition
1. Peripheral BVs in skeletal muscle
2. Adrenal gland |
|
|
Term
Effects of parasympathetic vs. sympathetic innervation to BVs in:
a) skin
b) heart |
|
Definition
a) Parasympathetic causes dilation, sympathetic causes constriction
b) Parasympathetic causes constriction, sympathetic causes dilation |
|
|
Term
Effects of parasympathetic vs. sympathetic innervation to BVs in:
a) skin
b) heart |
|
Definition
a) Parasympathetic causes dilation, sympathetic causes constriction
b) Parasympathetic causes constriction, sympathetic causes dilation |
|
|
Term
| What BVs have NO parasympathetic innervation? |
|
Definition
| Those located in SKELETAL MUSCLE |
|
|
Term
| 2 drugs that block sympathetic activity & functions, and 1 drug that blocks parasympathetic activity & function |
|
Definition
Propranolol - B-blocker; blocks B receptors in heart
Prazosin - blocks a-receptors in blood vessels
Atropine - blocks muscarinic ACh receptors |
|
|
Term
| Function of central stimulants vs. depressants? |
|
Definition
Stimulants = can INCREASE activity of autonomic output
Depressants = can DECREASE activity of autonomic output |
|
|
Term
| How is synaptic transmission typically terminated? |
|
Definition
| Either by enzymatic degradation OR re-uptake into the pre-synaptic cell |
|
|
Term
| Definition of "drug addiction" |
|
Definition
| Intense pattern of use detrimental to individual and society |
|
|
Term
| Definition of "drug habituation" |
|
Definition
| Less intense (compared to addiction) form of drug use that produces detrimental effects ONLY on the individual |
|
|
Term
| Difference between drug addiction and habituation? Which is more severe? |
|
Definition
Drug ADDICTION is the more severe one
Addiction involves detriment to individual AND society
Habituation involves detriment only to individual |
|
|
Term
| Difference between drug "dependence" and "addiction"? |
|
Definition
Dependence = physiological/physical dependence
Addiction = psychological dependence |
|
|
Term
| Definition of "drug dependence" & 3 characteristics of it? |
|
Definition
Dependence = state of periodic or chronic intoxication due to repeated consumption of a drug; includes:
1) Overpowering compulsion to take drug and obtain by ANY means
2) Tendency to increase dose
3) Psychic addiction & physical dependence |
|
|
Term
| What are the 3 main characteristics of drug dependence from a PHARMACOLOGICAL standpoint? |
|
Definition
1) Drug Tolerance
2) Physical Dependence (Dependence)
3) Psychological Dependence (Addiction) |
|
|
Term
| Definition of "drug tolerance": |
|
Definition
| When repeated administration gives progressively smaller pharmacological effects OR, when an increase in dose size is necessary to obtain the same original effects |
|
|
Term
| How can you tell if someone is physically dependent on a drug? |
|
Definition
| Physical dependence is characterized by a specific group of symptoms (withdrawal syndrome) when the drug is stopped being taken, or is taken in smaller doses |
|
|
Term
| How is one's physical dependence on a drug gauged? |
|
Definition
| It is gauged by the severity of the withdrawal syndrome |
|
|
Term
| What is a state of "psychological dependence" characterized as? |
|
Definition
Characterized as a state in which non-physical symptoms are produced when drug use is stopped/lessened
See strong "craving" for drug, as user is both emotionally and psychologically preoccupied with obtaining the drug |
|
|
Term
| What is compulsive use of a drug? |
|
Definition
The person increases dose size and uses for a longer period than intended
May express desire to stop using, but cannot
Daily activities revolve around obtaining the drug; withdrawal from family & society to use the drug |
|
|
Term
| What is harmful use of a drug? |
|
Definition
Pattern of substance abuse damaging to health - either physical health OR mental health
Need actual mental and/or physical health damage to be considered harmful |
|
|
Term
| What features does the APA define drug abuse as having? |
|
Definition
Maladaptive pattern of use with significant adverse consequences related to the misuse, often occurring in the person's social life
Symptoms have NOT met criteria for dependence |
|
|
Term
| What are two key "absences" required for a person's use of a drug to be considered "drug abuse"? |
|
Definition
NO harm to mental or physical health of person
NO sign of substance dependence |
|
|
Term
| Social vs. medical perspective of DRUG ABUSE: |
|
Definition
Social - when an individual self-administers a drug in a manner which deviates from the approved medical & social practices governing its use in the culture
Medical - maladaptive pattern of use leading to significant adverse consequence's in the person's social realm, without any physical/mental harm or signs of dependence |
|
|
Term
| What 3 factors does the "abuse potential" of a given drug consider? |
|
Definition
Intrinsic dependence liability
Availability of drug
Inherent harmfulness to cause physical/psychic harm |
|
|
Term
| What 3 factors determine dependence liability? |
|
Definition
1) Nature of the drug (how strong of a reinforcer it is)
2) Route of administration (faster absorption = higher liability)
3) Amount used/frequency of use |
|
|
Term
| What is the only class of drugs that do not have the ability to produce tolerance, physical dependence & psychic dependence? What is excluded? |
|
Definition
| Hallucinogens (LSD, mescaline, etc.) cannot produce PHYSICAL DEPENDENCE |
|
|
Term
| What is the CNS depression of sedative-hypnotics dependent on? |
|
Definition
| The CNS depression is "dose dependent"; they can produce anywhere from anxiolytic, to sedation, to general anesthesia depending on the dose size |
|
|
Term
| What can sedatives also be used as hypnotics? |
|
Definition
| Because their CNS depression is DOSE DEPENDENT (just need to increase dose size to change their effects) |
|
|
Term
| 1st agents introduced as sedative/hypnotics? |
|
Definition
| Bromides in the 19th century |
|
|
Term
| What is "bromism"? What replaced the substances that caused this disorder? |
|
Definition
Syndrome due to the accumulation of bromides in the body - see mental aberrations, skin rash and GI disturbances
Later introduced chloral hydrate & paraldehyde which were safer |
|
|
Term
| What drug ushered in the age of the barbiturates? |
|
Definition
| PHENOBARBITAL (intro'd in 1912) |
|
|
Term
| What drug ushered in the era of the benzodiazepines? |
|
Definition
| CHLORDIAZEPOXIDE (in 1961) |
|
|
Term
| What are the drugs of choice for antianxiety relief (what are anxiolytics of choice)? |
|
Definition
|
|
Term
| Therapeutic uses of the sedative/hypnotic classes of drugs? |
|
Definition
General CNS depression
Anticonvulsants for epilepsy
Treating EtOH withdrawal syndrome
Treating muscle spasms |
|
|
Term
| Why are benzodiazepines useful in treating EtOH withdrawal? |
|
Definition
| See cross-dependence between diazepam and EtOH |
|
|
Term
| What is the mechanism of CNS action of the benzodiazepines? |
|
Definition
Bind to receptors in the cortex, cerebellum & limbic system to:
1) Increase synaptic inhibition to dampen activity
2) Receptor binding enhances GABA transmission to further inhibit cortex, cerebellum & limbic system |
|
|
Term
| What is the therapeutic index of benzodiazepines (relative)? |
|
Definition
| HIGH therapeutic index (safe) |
|
|
Term
| Pharmacological effects of benzodiazepines... |
|
Definition
Anxiolytic, sedation, hypnosis
Decrease aggression
Minimal suppression of REM sleeo
Skeletal muscle relaxation
Anti-convulsant |
|
|
Term
| What property do the benzodiazepines have considerable differences of? |
|
Definition
| Different PHARMACOKINETICS; have different durations of action (diffn't metabolism by liver) |
|
|
Term
What two things is diazepam typically used for?
What is flurazepam typically used for? |
|
Definition
Diazepam = anticonvulsant & anxiolytic
Flurazepam = hypnotic |
|
|
Term
| Effects of short term use of BENZODIAZEPINES - low/moderate dose vs. high dose |
|
Definition
Low/moderate dose - anxiolytic, calmness, nausea, respiratory depression, motor incoordination
High dose - appear to be drunk/intoxicated; impaired thought & slow reflexes; sedation may progress to hypnosis or coma |
|
|
Term
| Lethality of benzodiazepines? |
|
Definition
| Commonly involved in drug overdose, but due to the high therapeutic index of the drug fatal overdoses are quite rare |
|
|
Term
| Tolerance is seen to which of the effects of benzodiazepines? |
|
Definition
See tolerance develop to SEDATIVE and MOTOR IMPAIRMENT effects
Tolerance to the ANXIOLYTIC effect is uncommon |
|
|
Term
| With what other drugs do benzodiazepines develop a strong cross tolerance? |
|
Definition
| Develop strong cross tolerance with EtOH and barbiturates (other CNS depressants) |
|
|
Term
| Likelihood of physical dependence/withdrawal with cessation of benzodiazepine use? |
|
Definition
| Low risk if use is acute (only a few months); may see withdrawal in chronic users if drug is stopped suddenly |
|
|
Term
| What are among the most widely prescribed drugs in the world? |
|
Definition
|
|
Term
| Potential for abuse for benzodiazepines? |
|
Definition
LOW dependence liability
LOW inherent harmfulness
Therefore, LOW potential for abuse |
|
|
Term
| What does death from barbiturate overdose typically result from? |
|
Definition
| Extreme respiratory depression leading to respiratory failure |
|
|
Term
| What is the main use of barbiturates nowadays? |
|
Definition
| As anticonvulsants in epileptic patients (e.g. Phenobarbital) |
|
|
Term
| Relative selectivity of barbiturates vs. benzodiazepines in their mechanism of action? |
|
Definition
| Barbiturates are LESS SELECTIVE than benzodiazepines in the actions on the CNS |
|
|
Term
| Relative therapeutic index of benzodiazepines vs. barbiturates? |
|
Definition
Benzodiazepines = HIGH therapeutic index
Barbiturates = LOW therapeutic index |
|
|
Term
| Mechanism of CNS action of the barbiturates? |
|
Definition
Less selective than the benzodiazepines, and do not bind to the benzodiazepine receptor
Potentiate the inhibitory effects of GABA at its receptor by modulating Cl channels |
|
|
Term
| Properties of barbiturates? |
|
Definition
Dose dependent respiratory depression
Full spectrum of CNS depression
Anticonvulsants (phenobarbital)
Supress REM sleep
Short acting anesthetics (thiopental)
Depress cardiovascular system at high doses |
|
|
Term
| How are barbiturates classified (example of each)? |
|
Definition
Ultrashort Acting - thiopental
Short-Acting - secobarbital
Long-Acting - phenobarbital |
|
|
Term
| Route of administration of thiopental vs. phenobarbital? |
|
Definition
Phenobarbital is ORAL
Thiopental is IV |
|
|
Term
| Effects of long-term barbiturate use? |
|
Definition
| Chronic Inebriation - mood swings, depression, thinking & memory impairments |
|
|
Term
| Lethality of barbiturates? |
|
Definition
| Frequent in barbiturate overdose and is also seen during barbiturate withdrawal syndrome |
|
|
Term
| Rates of tolerance development to barbiturates? |
|
Definition
Tolerance to mood alteration and sleep induction develop rapidly
Tolerance to motor impairment develops more slowly
Tolerance to anticonvulsant effects develops the most slowly (non-relevant clinically) |
|
|
Term
| Barbiturate withdrawal syndrome after low doses vs. after chronic use? |
|
Definition
Low dose = sleep disturbances
Chronic use = anxiety, tremors, insomnia, hypotension, seizures, fever, delirium (symptoms peak between 24 and 72 hours) |
|
|
Term
| Abuse liability of barbiturates? |
|
Definition
Equal to or greater than that of EtOH
Significant reinforcement (higher dependence liability)
HIGH inherent harmfulness |
|
|
Term
| What can be used to treat for benzodiazepine poisoning? How is this accomplished? |
|
Definition
| Use FLUMAZENIL - GABA(a) receptor antagonist (blocks benzodiazepine effects) |
|
|
Term
|
Definition
| Zolpidem is a new GABA receptor agonist that may be better than benzodiazepines because it disrupts REM sleep less |
|
|
Term
| What is busiprone? Why is it useful? |
|
Definition
Busiprone acts on the 5-HT receptor as an anxiolytic
Better than other sedative hypnotics because there are no ADDITIVE effects |
|
|
Term
| What does the term "opioid" refer to? |
|
Definition
| Any natural or synthetic substance which exerts actions similar to morphine AND is blocked by naloxone |
|
|
Term
| What chemicals does the term "opioid" include? |
|
Definition
Opiate narcotics - natural opiates from the poppy
Structurally related substances to morphine
Synthetic drugs with different structures from morphine
Endogenous opioids (enkephalins & endorphins) |
|
|
Term
| 3 known families of endorphins? |
|
Definition
| B-endorphins, enkephalins, dynorphins |
|
|
Term
| What two effects do the mu-opioid receptors in the brain mediate? |
|
Definition
Mediate analgesia of opioid compounds
Mediate respiratory depression due to morphine |
|
|
Term
| What variety of opioid receptor has enkephalins as its endogenous ligand? |
|
Definition
| THe delta-opioid receptors |
|
|
Term
| What receptors do the mixed agonist/antagonist opioids act on? |
|
Definition
|
|
Term
| In terms of opioid use, what do each of the receptor subclasses mediate? |
|
Definition
Mu = analgesia & respiratory depression
Delta = analgesia & emotional response
Kappa = analgesia, dysphoria & miosis (pin-point pupils) |
|
|
Term
| Other than the CNS, where else are opioid receptors located? What does this cause? |
|
Definition
| Also located in the GI tract, causes constipation |
|
|
Term
| What is the prototype opioid antagonist? |
|
Definition
|
|
Term
| Classification of opioids/opiates (3 groups) |
|
Definition
Agonists (morphine, heroin, methadone)
Mixed Agonist/Antagonist (pentazocine)
Antagonist (naloxone) |
|
|
Term
| What kind of opioid is "pentazocine"? |
|
Definition
It is a mixed agonist/antagonist
When given on its own, it is an agonist, but if given together with morphine it can block part of the response (antagonist) |
|
|
Term
| What is naltrexone used to treat? |
|
Definition
| It is an opioid antagonist used to treat EtOH dependence |
|
|
Term
| 4 different uses for opioid antagonists? |
|
Definition
Treat opioid dependence
Reverse opioid overdose
Diagnose opioid dependence
Naltrexone - opioid antagonist to treat EtOH withdrawal |
|
|
Term
| Two different therapeutic uses of opioids? |
|
Definition
Treat severe pain
Treat diarrhea |
|
|
Term
| What is the basis of toxicity of opioids? |
|
Definition
| The respiratory depression they cause (mediated by mu opioid receptors) |
|
|
Term
| What type of drug is Lomotil? What is it used to treat? |
|
Definition
| It is a non-analgesic opioid to treat diarrhea; sold as an OTC drug |
|
|
Term
| What is the limiting factor in using morphine to treat pain? |
|
Definition
| The respiratory depression caused |
|
|
Term
| Pharmacological effects of opioids? |
|
Definition
Pain relief
Sedation & hypnosis
Respiratory depression
Constipation
Constricted pupils (miosis)
Euphoria/dysphoria
Cough suppression
Nausea/vomiting |
|
|
Term
| What opioid drug does NOT activate the opioid receptor? |
|
Definition
Naloxone
It blocks the receptors but DOES NOT activate them |
|
|
Term
| To what effects of opioids does tolerance not develop? |
|
Definition
| Pupil constriction (miosis) and constipation |
|
|
Term
| Difference in lethality between withdrawal syndrome of barbiturates vs. opioids? |
|
Definition
| Barbiturate withdrawal has the possibility of being fatal, where as opioid withdrawal is not life threatening |
|
|
Term
| What is the basis for the psychological dependence seen with opioids? |
|
Definition
| The strong reinforcing effect of the euphoria they produce (high reward) |
|
|
Term
| Treatment of opioid overdose? |
|
Definition
The cause of death will be respiratory failure
Treat with naloxone and assist ventilation of patient |
|
|
Term
| What are 4 factors that determine opioid abuse? |
|
Definition
Nature of drug - how much euphoria does it produce
Route of administration - IV is worse
Size of dose
Use of other drugs conjunctively |
|
|
Term
| What are 2 treatments of opioid dependence and how do they differ? |
|
Definition
Cessation of use - replace drug of abuse with methadone and slowly taper the dose over time; add counselling and rehab
Methadone maintenance - replace drug of abuse with methadone, BUT dose is kept constant and not reduced; risk-reduction method |
|
|
Term
| If an opioid addict was looking for a drug to use to help taper off his drug abuse, he would be given... |
|
Definition
|
|
Term
| Routes of administration of morphine? |
|
Definition
| Orally, smoked, sniffed, injected |
|
|
Term
| Effects of long-term morphine use? |
|
Definition
No marked physiological or psychological impairment
See some mood stability, pupillary constriction (poor night vision), constipation, respiratory impairment |
|
|
Term
| What is the only drug with a higher dependence liability than morphine? |
|
Definition
|
|
Term
| Potential for abuse for morphine? |
|
Definition
Only drug w/ higher dependence liability is heroin
Low to moderate inherent harmfulness at low doses |
|
|
Term
| What drug has the highest inherent dependence liability? |
|
Definition
|
|
Term
|
Definition
Diacetylmorphine
It is semi-synthetic (produced by altering structure of morphine) |
|
|
Term
| Difference in efficacy and potency between morphine & heroin? |
|
Definition
Heroin is MORE POTENT than morphine
Morphine is MORE EFFICACIOUS than heroin |
|
|
Term
| What is a bombita vs. a speed ball? |
|
Definition
Bombita = heroin + amphetamines
Speed ball = heroin + cocaine |
|
|
Term
| Difference between mainlining vs. skin popping in heroin administration |
|
Definition
Skin popping = subcutaneous administration
Mainlining = IV administration |
|
|
Term
| As the dosage of the opioid increases, what two things happen to the symptoms? |
|
Definition
| The magnitude of the symptoms increases AND the duration of the symptoms increases |
|
|
Term
|
Definition
| Heroin users have high neonatal mortality rate; if born, infant is often pre-mature w/ low birth weight |
|
|
Term
| Why does heroin have the highest dependence liability of all opioids? |
|
Definition
| Due to the euphoria it produces and its solubility |
|
|
Term
| What are psychoactive drugs? |
|
Definition
| Drugs that can act on CNS and alter perception, mood, behavior or consciousness |
|
|
Term
| What is the most practical way of classifying psychoactive drugs? |
|
Definition
| By their major behavioral effect (or major clinical use) |
|
|
Term
| True or False - Psychoactive drugs can create new behavioral or psychological responses |
|
Definition
| FALSE - they DO NOT create new responses, just modify existing ones |
|
|
Term
| What is the effect of 1) cocaine, 2) amphetamine, 3) caffeine, and 4) nicotine on NT's in the CNS and PNS? |
|
Definition
1) Cocaine blocks DA reuptake
2) Amphetamines cause DA release from presynaptic terminal
3) Caffeine is a competitive antagonist for adenosine receptors
4) Nicotine stimulates nicotinic cholingergic receptors |
|
|
Term
| What kind of drug are inhalants of abuse classified as? |
|
Definition
|
|
Term
| Half life of the Romeo & Juliet drug? |
|
Definition
| 8.4 hours (=42 hours divided by 5) |
|
|
Term
| 4 principles of CNS depressant use? |
|
Definition
1) Effects of CNS depressants are ADDITIVE
2) Use of a stimulant in a patient taking a CNS depressant may cause temporary arousal
3) Chronic use of CNS depressants causes physiological dependence (see rebound excitability when drug is stopped)
4) Cross tolerance can develop between depressants |
|
|
Term
| What often occurs during withdrawal from a CNS depressant? |
|
Definition
| Get rebound excitability from the drug being stopped |
|
|
Term
| What are phenothiazines used to treat? |
|
Definition
| Treat psychosis (are anti-psychotics) |
|
|
Term
| What kind of drug is lithium considered to be? |
|
Definition
|
|
Term
| Difference between ORGANIC and FUNCTIONAL psychoses? |
|
Definition
In psychoses there is a marked impairment in behavior
ORGANIC - understood and definable causes; loss of orientation, memory, behavioral organization
FUNCTIONAL - of unknown cause; retain orientation and memory, but with disordered thought/reasoning |
|
|
Term
| What is retained in functional psychoses that is lost in organic psychoses? Which is schizophrenia considered to be? |
|
Definition
In functional psychoses, retain orientation and memory
Schizophrenia is a functional psychosis |
|
|
Term
| What are affective disorders characterized by primarily? |
|
Definition
| Primarily characterized by a change in mood/emotion |
|
|
Term
| Difference between neuroses and psychoses? |
|
Definition
| In neuroses, the sufferer retains the ability to comprehend reality |
|
|
Term
| Positive vs. Negative Symptoms of Schizophrenia |
|
Definition
Positive - hallucinations & delusions, incoherence
Negative - apathy, anhedonia, social withdrawal |
|
|
Term
| What is the DA theory of schizophrenia? |
|
Definition
| The DA theory states that excess DA activity in the brain leads to the symptoms of schizophrenia |
|
|
Term
| Circumstantial evidence for DA theory of schizophrenia: |
|
Definition
1) Most antipsychotics block DA receptors
2) Drugs that increase DA activity can induce or aggravate schizophrenia
3) In schizophrenic individuals not treated with antipsychotics, see increased DA receptor density
4) PET scans have shown DA receptor density to be higher in those with schizophrenia |
|
|
Term
| What were the first antipsychotics introduced into therapy? What effects do these have on DA? |
|
Definition
| The PHENOTHIAZINES in the 1950s; they are DA receptor antagonists |
|
|
Term
| What DA systems are antagonized when antipsychotics are used? |
|
Definition
| Antagonize DA activity in the mesolimbic and mesofrontal systems of the brain |
|
|
Term
What happens when there is DA antagonism in:
a) Mesolimbic/mesofrontal systems
b) Nigrostriatal system
c) Hypothalamus |
|
Definition
a) Get antipsychotic effects
b) Get extrapyramidal movement disorders (Parkinson's)
c) Get hyperprolactinemia |
|
|
Term
| What other receptors are blocked by phenothiazine antipsychotics? |
|
Definition
Muscarinic cholinergic receptors
5-HT receptors
Histamine receptors
Alpha-adrenergic receptors |
|
|
Term
| 2 examples of typical vs. atypical antipsychotics? |
|
Definition
Typical = chlorpromazine, haloperidol
Atypical = risperidone, clozapine |
|
|
Term
| Difference in symptom treatment between typical and atypical antipsychotics? |
|
Definition
Typical - only relieves +'ve symptoms
Atypical - claim to relieve +'ve and -'ve symptoms; also claim to cause fewer extrapyramidal symptoms |
|
|
Term
| To therapeutic uses of lithium? |
|
Definition
Treat manic depression (bipolar)
Treat mania |
|
|
Term
| 3 possibilities of mechanism of action of lithium? Which appears to be the most likely? |
|
Definition
1. Effect on ion transport
2. Effect on NTs and their release
3. Effect on 2nd messengers which mediate NTs (MOST LIKELY) |
|
|
Term
| What type of receptors are IP3 and DAG crucial for? |
|
Definition
| Alpha-adrenergic & muscarinic |
|
|
Term
| Effects of lithium on 2nd messengers... (what happens) |
|
Definition
Li interferes with regeneration of PIP2 from IP2, IP, and I (blocks conversion to IP2 to IP and IP to I); because of this get depletion of PIP2
Then leads to depletion of IP3 and DAG (from PIP2), so it decreases activity of a-adrenergic + muscarinic receptors |
|
|
Term
| What drugs are often required in conjunction with Li during the manic and depressive episodes of bipolar disorder? |
|
Definition
During manic episodes = often also need antipsychotic or benzodiazepine
During depressive episodes =often need antidepressant |
|
|
Term
|
Definition
Nausea, vomiting
Hypothyroidism
Edema & weight gain
Polydipsia
Acne & skin conditions |
|
|
Term
| Alternatives to Li in treatment? |
|
Definition
| Valproic acid, carbamazepine, clonazepam |
|
|
Term
| Different types of depression? |
|
Definition
Reactive (Secondary) - most common; due to real stimuli
Major Depression (Endogenous) - generally biochemical disturbance
Associated with Manic-Depressive Disorder - least common |
|
|
Term
| Most common form of depression? |
|
Definition
| Reactive (secondary) depression (60%) in response to real stimuli such as grief or illness |
|
|
Term
| What is the amine hypothesis? |
|
Definition
| Belief that depletion in amine stores in individuals leads to depression (mainly concerning 5-HT, NE, and DA) |
|
|
Term
| Evidence for Amine Hypothesis of Depression |
|
Definition
Common side-effect of reserpine was induction of depression; noted that it inhibited re-uptake of 5-HT and NE in animals, leading to depleted amine stores
Also, all antidepressants deal with storage, metabolism, or re-uptake of NE, 5-HT, or DA |
|
|
Term
| What does the neurotrophic hypothesis of depression suggest? |
|
Definition
| Suggests depression is associated with reduced neurotrophic support (less growth and interconnectivity of neurons); antidepressants function by stimulating neurogenesis and synaptic connectivity |
|
|
Term
| Neurotrophic vs. Amine Hypotheses? |
|
Definition
Neurotrophic - depression is due to lack of neurotrophic connections in the brain; antidepressants stimulate neurogenesis and synaptic connectivity
Amine - depression is due to depletion in amine stores (5-HT, NE, DA); antidepressants function by increasing the amount of amines available |
|
|
Term
| What kind of antidepressant is imipramine? |
|
Definition
|
|
Term
| 2 examples of atypical/2nd generation antidepressants? |
|
Definition
|
|
Term
| What type of antidepressant is fluoxetine (Prozac)? |
|
Definition
| It is an SSRI (selective serotonin reuptake inhibitor) |
|
|
Term
| Why are SSRIs less toxic than tricyclic antidepressants? |
|
Definition
Tricyclics are also anticholinergic, antiadrenergic and have antihistamine actions as well
SSRIs have less of an effect on the autonomic NS |
|
|
Term
| What are 3 other effects that are unrelated to the therapeutic properties of tricyclic antidepressants, but contribute to their toxicity? |
|
Definition
| They have antihistamine, anticholinergic (muscarinic), and antiadrenergic effects (see adverse effects in autonomic NS) |
|
|
Term
| What is the therapeutic effect of venlafaxine? |
|
Definition
Blocks transporters for serotonin and NE (block 5-HT and NE reuptake)
Safer than tricyclics because of better safety profile |
|
|
Term
| Different types of MAO enzyme, and their significance in relation to depression and its treatment? |
|
Definition
Have MAO-A and MAO-B; A is responsible for NE, 5-HT, and tyramine metabolism; B is responsible for DA metabolism
Therefore, most MAO inhibitors target MAO-A inhibition |
|
|
Term
| Why are phenelzine & tranylcypromine useful in treating depression? |
|
Definition
They are NON-SELECTIVE MAO inhibitors (inhibit both MAO-A and MAO-B); combine irreversibly and have a LONG duration of action
Inhibition with phenelzine lasts 2-3 weeks
Inhibition with tranylcypromine lasts 7 days |
|
|
Term
| What are the durations of action of phenelzine and tranylcypromine? What class of drug are they? |
|
Definition
They are NON-SELECTIVE MAO inhibitors
Phenelzine effects last 2-3 weeks after last dose
Tranylcypromine effects last 7 days after last dose |
|
|
Term
| Example of a SELECTIVE MAO-A inhibitor? |
|
Definition
| Moclobemide (short-acting reversible MAO-A inhibitor) |
|
|
Term
| Name 5 classes of antidepressants and one example for each? |
|
Definition
Tricylic - imipramine
Atypical - bupropion
SSRIs - fluoxetine (Prozac)
MAO inhibitors (non-selective) - phenelzine
MAO-A inhibitors (selective) - moclobemide |
|
|
Term
| Mode of action of tricyclics vs. MAO inhibitors vs. SSRIs? |
|
Definition
Tricyclics - block presynaptic transporters for 5-HT and NE equally
MAO inhibitors - block amine metabolism by inhibiting MAO activity
SSRIs - selective blockage of 5-HT transporters, and NE transporters to a much lesser extent |
|
|
Term
| Adverse effects of tricylic antidepressants? |
|
Definition
Urinary retention, constipation, blurred vision (anticholinergic effects)
Orthostatic hypotension
Sexual dysfunction
Sedation & weight gain
Development of cardiac arrhythmias |
|
|
Term
| What endogenous compounds are amphetamines structurally similar to? |
|
Definition
|
|
Term
| 3 common amphetamine compounds? |
|
Definition
| Methamphetamine, amphetamine, dextroamphetamine |
|
|
Term
| What is the primary method of action, centrally, of amphetamine compounds? |
|
Definition
| Cause release of NE and DA from nerve terminals |
|
|
Term
| What are the CVS effects of amphetamines? What receptors do they act on and what effects are caused? |
|
Definition
See increased sympathetic activity due to release of NE from postganglionic sympathetic terminals, acting on alpha and beta-1 receptors
Leads to - increased HR, increased BP, flight/fight response |
|
|
Term
| What are the CNS effects of amphetamines due to? |
|
Definition
| See increased release (by displacement) and inhibition of active reuptake of DA and NE in the CNS |
|
|
Term
| What are some of the CNS effects of amphetamines? |
|
Definition
Anorexia
Increased respiratory rate
Psychomotor stimulation/alertness; convulsions
Hyperthermia
Increased transmission in SC |
|
|
Term
| What 4 areas of the brain do amphetamines work on? |
|
Definition
Reticular activating system
Medial forebrain bundle
Hypothalamus
Limbic system |
|
|
Term
| Relative potency of the different types of amphetamines? |
|
Definition
| Methamphetamine > dextroamphetamine > amphetamine |
|
|
Term
| What part of the brain activated by amphetamines is responsible for the reward aspect? |
|
Definition
| The medial forebrain bundle (MFB) |
|
|
Term
| Therapeutic uses of "amphetamine-like" drugs? |
|
Definition
Narcolepsy
ADHD
Parkinson's |
|
|
Term
| What is the drug of choice for treating narcolepsy? |
|
Definition
| Methylphenidate (amphetamine-like drug) |
|
|
Term
| What two conditions is methylphenidate used to treat for preferentially? |
|
Definition
|
|
Term
| Why are amphetamines widely abused? |
|
Definition
| Produce a strong euphoria and are CNS stimulants |
|
|
Term
| What is more deteriorating physiologically, long-term use of amphetamines or heroin? |
|
Definition
| Long-term use of amphetamines is more harmful physiologically |
|
|
Term
| To which effects of the amphetamines does tolerance develop? |
|
Definition
Euphoric effects, anorectic effects, lethal effect
Does NOT develop to drug-induced psychosis |
|
|
Term
| What is cocaine classified as pharmacologically? |
|
Definition
| A local anesthetic and a CNS stimulant |
|
|
Term
| Relative duration of CNS effects of cocaine vs. amphetamines? |
|
Definition
| Duration of effects for cocaine is much shorter than those of amphetamines (cocaine effects usually wear off within the hour) |
|
|
Term
| Mode of action of cocaine in the CNS? |
|
Definition
| Inhibits DA and NE reuptake into presynaptic terminal |
|
|
Term
| Aside from general CNS stimulation, what other effect does cocaine have? What produces this effect? |
|
Definition
| Is also a LOCAL ANESTHETIC; this effect is due to its blockade of nerve impulses in sensory fibers |
|
|
Term
| Main differences between the effects of cocaine and amphetamines? |
|
Definition
Cocaine has a shorter duration of action
Lower incidence of complications (cocaine is usually sniffed or smoked)
Tolerance does not develop as readily to behavioral effects of cocaine |
|
|
Term
|
Definition
| Metabolized to inactive form of benzoylecgonine and is excreted in the urine |
|
|
Term
| What is one side-effect of both amphetamines and cocaine that a tolerance does NOT develop to? |
|
Definition
| Tolerance does not develop to the drug induced psychosis of either |
|
|
Term
| What is the most widely and regularly used drug in the world? |
|
Definition
|
|
Term
| What two systems does caffeine affect? |
|
Definition
|
|
Term
| CNS effects of caffeine? CVS effects? |
|
Definition
CNS - increase mental performance & motor activity; increase respiration and HR
CVS - increased HR and BP; at high doses can see arrhythmias develop |
|
|
Term
| What is the mode of action of caffeine? |
|
Definition
| Competitively blocks adenosine receptors in the brain; normally adenosine is inhibitory, so when its effects are decreased, get CNS stimulation |
|
|
Term
| What kind of dependence develops in response to long-term caffeine use? |
|
Definition
| Both physiological and psychological dependence |
|
|
Term
| 3 most used non-medical drugs in canada? |
|
Definition
| Caffeine, Alcohol, Tobacco/Nicotine |
|
|
Term
| 1st sedative-hypnotic used by ancient physicians? |
|
Definition
|
|
Term
| Traditionally, what are the 3 major uses of EtOH? |
|
Definition
Medicinally as a sedative-hypnotic
Religiously as a part of certain occasions
Recreational use |
|
|
Term
| Equalities in terms of drink size for various types of alcohol? |
|
Definition
1 drink is the same as...
341 mL beer (12 oz)
170 mL wine (6 oz)
43 mL liquor (if 40%; 1.5 oz)
17 mL pure ethanol |
|
|
Term
| How much alcohol can the liver metabolize each hour? |
|
Definition
| It can metabolize 10-13 mL of absolute alcohol each hour (just less than 1 drink per hour) |
|
|
Term
| What is the overall absorption rate for a given dose of ethanol affected by? |
|
Definition
Stomach emptying time; how long it takes for alcohol to reach the small intestine (its mjr site of absorption)
Ethanol concentration in the GI tract |
|
|
Term
| How is ethanol excreted and metabolized in the body? |
|
Definition
95% is biotransformed and eliminated via the liver
5% is excreted in breath, urine, sweat |
|
|
Term
| What is the metabolic breakdown pathway of EtOH metabolism? |
|
Definition
| EtOH is converted by ADH to acetaldehyde, which is then converted into acetic acid by ALDH (acetic acid can be metabolized by tissues) |
|
|
Term
| What two drugs treat alcohol dependence and how do they function? |
|
Definition
| Disulfram & calcium carbimide function to inhibit ALDH so there is an accumulation of acetaldehyde in the body (makes individual feel ill) |
|
|
Term
| Why is the metabolism of alcohol somewhat uncommon? |
|
Definition
| Because it occurs at a constant rate, IRRESPECTIVE of the blood-alcohol concentration (constant amount metabolized each hour) |
|
|
Term
| Changes in behavioral effects at different BACs of alcohol intoxication? (in mg/100 mL) |
|
Definition
50 - euphoria, slight incoordination & motor disturbance
60 - increased motor disturbance & nystagmus
80 - driving inability, changes in EEG patterns
100-150 - gross motor incoordination
200-300 - amnesia for drinking experience |
|
|
Term
| What are the changes in sleep pattern associated with EtOH? |
|
Definition
| Get INCREASE in slow-wave sleep, and DECREASE in REM sleep (feeling of sleeping poorly) |
|
|
Term
| When is the maximum BAC usually reached after the last drink? |
|
Definition
|
|
Term
| What adverse effects are seen with chronic EtOH use and what are the associated symptoms? |
|
Definition
See axonal destruction of central neurons, leading to dementia
See increased vitamin B1 (thiamine) metabolism - leads to thiamine deficiency causing Wernicke's encephalopathy and Korsakoff's psychosis
See peripheral neuropathy leading to loss of feeling in the extremeties |
|
|
Term
| What is seen with chronic use of ethanol? |
|
Definition
| See decreased intensity of action, or a shortened duration of action; need a larger dose to produce the same effect (definition of tolerance) |
|
|
Term
| What is the mechanism for ethanol tolerance? |
|
Definition
Metabolic - get increased metabolic rate of EtOH, so it is excreted more rapidly
CNS - CNS adapts to its effects |
|
|
Term
| What plays the largest role in development of a tolerance to EtOH? |
|
Definition
|
|
Term
| What kind of tolerance, if any, develops to the lethal dose of alcohol? |
|
Definition
| There is MINIMAL tolerance that develop's the EtOH's lethal dose |
|
|
Term
| What kind of cross-tolerance develops alongside EtOH abuse? |
|
Definition
| See cross-tolerance develop to other sedative-hypnotics and general anaesthetics |
|
|
Term
| What does the basis of physical dependence on alcohol involve? What happens during withdrawal? |
|
Definition
| The basis for the dependence is the CNS - removal of the CNS depressant (alcohol), leads to CNS stimulation and hyperexcitability (tremors, hyperthermia, increased HR) |
|
|
Term
| Treatment of the withdrawal syndrome of EtOH dependence? |
|
Definition
| Treat with diazepam (benzodiazepine sedative); based on the principle of cross-dependence (diazepam is similar enough to alcohol to make the withdrawal syndrome more manageable) |
|
|
Term
| What drug is used to treat the psychological addiction to alcohol? |
|
Definition
| Naltrexone (opioid antagonist similar to naloxone) |
|
|
Term
| Effects of alcohol use on the CVS (acute vs. chronic) |
|
Definition
Acute - vasodilation of BVs in skin; arrhythmia at high doses
Chronic - cardiomyopathy, increased risk of CAD, HTN, and CVA |
|
|
Term
| Effects of alcohol use on the GI tract? |
|
Definition
Low dose, acute - can increase GI secretions to stimulate appetite
High doses - irritate lining of the stomach leading to gastritis |
|
|
Term
| Stages of Alcoholic Liver Disease: |
|
Definition
I - fatty liver; accumulation of fat causes liver to grow in size; asymptomatic
II - alcoholic hepatitis; inflammation of tissues; usually still reversible
III - cirrhosis; permanent liver damage with replacement of necrotic cells with scar tissue |
|
|
Term
| What is a teratogen? Example? |
|
Definition
An agent which causes malformation of an embryo
E.g. Alcohol; when consumed by mother during pregnancy leads to FAS |
|
|
Term
| Features of fetal alcohol syndrome? |
|
Definition
CNS dysfunction, growth deficiency, facial abnormalities
Malformations in other organ systems |
|
|
Term
| Difference between FAS and FAE? What is the difference in prevalence of the two? |
|
Definition
FAE - fetal alcohol effects; some but not all of the effects of FAS
FAE is 5x more common than FAS |
|
|
Term
| Difference in alcohol's effects on liver metabolism of OTHER drugs in acute vs. chronic conditions? |
|
Definition
Acute - because alcohol is still present in the body, it inhibits the metabolism of other sedative-hypnotics & phenytoin
Chronic - because it caused an increase in smooth ER of the liver (although EtOH is no longer present), get increased drug metabolism of other sedative-hypnotics & phenytoin |
|
|
Term
| What effect does alcohol have on vitamin B metabolism? |
|
Definition
Increases metabolism of B1 (thiamine), leading to thiamine deficiency
This can lead to Wernicke's encephalopathy & Korsakoff's psychosis |
|
|
Term
| What are the two different varieties of Cannabis sativa? |
|
Definition
| Resin-producing (for psychoactive drugs) and fiber producing (for hemp) |
|
|
Term
| What are compounds found only in C. sativa called? How many are there? |
|
Definition
| There are approximately 60 compounds that are unique to C. sativa, and they are known as CANNABINOIDS |
|
|
Term
| How many chemical compounds are there in C. sativa? |
|
Definition
|
|
Term
| Legal vs. pharmacological classification of marijuana? |
|
Definition
Legal - is a narcotic
Pharmacological - CNS depressant, euphoriant & hallucinogen (at high doses) |
|
|
Term
| Different receptors for THC and their locations? |
|
Definition
CB1 receptors - located centrally in brain; responsible for psychoactive effects
CB2 receptors - located in periphery; appear to mediate only effects on the immune system |
|
|
Term
| What is believed to be the endogenous ligand for the THC receptors? |
|
Definition
| Anandamide (involved in memory & learning processes) |
|
|
Term
| THC's effects on the immune system? |
|
Definition
| Binds to CB2 receptors on lymphocytes to cause its IMMUNOSUPPRESSIVE effects |
|
|
Term
| What delay is seen with oral ingestion of marijuana (delay = time between ingestion and effects)? What can be said about absorption of THC from the GI tract? |
|
Definition
Takes 30-60 minute delay for the effects of THC to kick in if taken orally
Absorption of THC from the GI tract is SLOW and INCOMPLETE |
|
|
Term
| What were cannabis extracts once widely used as? |
|
Definition
| Widely used to be prescribed as sedative-hypnotics |
|
|
Term
| Synthetic THC derivatives used to treat nausea from cancer chemotherapy? |
|
Definition
|
|
Term
| Difference between marijuana vs. hashish vs. hashish oil? |
|
Definition
Marijuana = dried leaves
Hashish = dried resin from flowers
Hashish Oil = cannabinoids extracted from hashish |
|
|
Term
| Long term psychological effects of chronic cannabis use? |
|
Definition
Amotivational syndrome (usually disappears when drug is stopped)
Loss of short-term memory, abstract thinking, and concentration |
|
|
Term
| What contains more carcinogens cannabis smoke or tobacco smoke? |
|
Definition
|
|
Term
| What is responsible for the long-term effects of smoking? |
|
Definition
| NOT NICOTINE, but other compounds found in tobacco and tobacco smoke |
|
|
Term
| What does nicotine's actions on central nicotinic receptors cause? |
|
Definition
| Causes release of DA and 5-HT within the brain |
|
|
Term
| What ganglia are stimulated by nicotine peripherally? |
|
Definition
| Sympathetic ganglia are stimulated to increase HR and BP |
|
|
Term
| What is responsible for the dependence in tobacco products? |
|
Definition
| NICOTINE - due to its strong reinforcing properties |
|
|
Term
| Through "normal smoking", how much nicotine is absorbed? |
|
Definition
| Approx. 20% of the nicotine |
|
|
Term
| Where else can nicotine be absorbed from/through? |
|
Definition
| GI tract, oral mucosa, and across the skin (transdermal) |
|
|
Term
| Half life of nicotine vs. cannabis (THC)? |
|
Definition
Nicotine 1/2life = 2 hours
THC 1/2life = 30 hours |
|
|
Term
| What offsets a portion of the cost that smoking has on the health care system? |
|
Definition
Tobacco taxes
Reduced pension payments
Reduced costs to the elderly |
|
|
Term
| What components of smoke are responsible for cardiovascular disease? |
|
Definition
| Nicotine & carbon monoxide |
|
|
Term
| What reduce's RBC's ability to carry O2? |
|
Definition
| Carbon Monoxide (of cigarette smoke) |
|
|
Term
| Smoking increases the cancer risk in what areas? |
|
Definition
| Throat, bladder, lung, oral cavity & uterus |
|
|
Term
| How many people die from cancer induced by passive smoke? What can this increase the risk of in children? |
|
Definition
300 people will die this year from lung cancer due to passive smoke
In children, have increased risk of bronchitis, asthma, pneumonia, and sudden infant death syndrome |
|
|
Term
| What kind of dependence occurs with nicotine? |
|
Definition
| BOTH psychological and physical |
|
|
Term
| What kind of tolerance develops to nicotine? |
|
Definition
| Appear to have NO real biological tolerance to nicotine; usually just try to keep nicotine level in blood constant throughout day to avoid withdrawal |
|
|
Term
| What is the abuse liability of nicotine? |
|
Definition
| HIGH - due to its strong reinforcing properties |
|
|
Term
| What are the 3 major classes of anti-anginal drugs? |
|
Definition
1) Organic nitrates (NG)
2) B-adrenergic antagonists (propranolol)
3) Ca-channel blockers |
|
|
Term
| Who was the first person to describe angina? |
|
Definition
|
|
Term
| Duration of action of amyl nitrate vs. nitroglycerin/glyceryl trinitrate (sublingual)? |
|
Definition
Amyl nitrate = onset to 30 to 60 seconds; duration was 5 mins
NG = duration was 20 to 30 mins |
|
|
Term
| What typically causes angina pectoris? |
|
Definition
| Usually due to lipid deposits (atherosclerotic plaques) present in the coronary circulation; choke off blood flow to the heart muscle |
|
|
Term
| What are the 4 E's that precipitate angina pectoris? |
|
Definition
| Eating, Exercise, Excitement, Exposure (to cold) |
|
|
Term
| What is the mode of action of organic nitrates (NG, isosorbide dinitrate)? |
|
Definition
They relieve pain by 2 mechanisms:
1) They relax large vein to cause vasodilation -> reduces CO, BP, and therefore decreases O2 demand of heart
2) They dilate large coronary arteries -> increase the supply of O2 to the heart muscle |
|
|
Term
| What is the mechanism by which NG causes dilation of blood vessels? |
|
Definition
NG enters BVs and is converted into nitric oxide, which is a potent vasodilator
Then, NO is converted to guanylyl cyclase, leading to vasodilation |
|
|
Term
| Where is endogenous nitric oxide synthesized and what is its precursor? |
|
Definition
Arginine is cleaved into NO and citrulline by nitric oxide synthase in the endothelial cells
NO is synthesized in endothelial cells |
|
|
Term
| Difference in site of synthesis of endogenous nitric oxide vs. that derived from NG? |
|
Definition
Endogenous NO is synthesized from arginine in endothelial cells
In contrast, NG enters smooth muscle cells of BV's and is then converted into NO there |
|
|
Term
| Alternate name for sublingual nitroglycerin? |
|
Definition
| Glyceryl trinitrate (GTN) |
|
|
Term
| When are the effects of GTN most intense? |
|
Definition
| When it is administered via the sublingual route |
|
|
Term
| When does the concentration of GTN in the plasma peak when it is administered sublingually? Via 2% ointment? |
|
Definition
Sublingual GTN = peaks 5 mins after administration
2% ointment = peaks 1 hour after administration |
|
|
Term
| Duration of action for sublingual GTN vs. 2% ointment of GTN? |
|
Definition
Sublingual = 20-30 minutes
Ointment = 3 hours or more |
|
|
Term
| What can be said about the tolerance that develops to GTN over time? |
|
Definition
See NO tolerance develop to SUBLINGUAL GTN
See tolerance develop in NG use in explosives and with the transdermal patch of GTN |
|
|
Term
Which form of GTN would be best for:
1) Treating an individual attack
2) Preventing an individual attack
3) As a chronic prophylaxis |
|
Definition
1) Sublingual (pain relief in 2 mins)
2) Sublingual (increases tolerable exertion of heart)
3) Long acting nitrate = ISOSORBIDE DINITRATE |
|
|
Term
| What is isosorbide dinitrate used for? |
|
Definition
| It is a LONG-ACTING organic nitrate used as a chronic prophylaxis of anginal attacks |
|
|
Term
| Why does an increase in SNS activity lead to angina? |
|
Definition
| Because increased SNS activity leads to an increased HR and BP, therefore it increases the workload of the heart and its O2 requirements |
|
|
Term
| What is the drug of choice for angina treatment? |
|
Definition
|
|
Term
| Why could GTN be considered superior to propranolol in treating angina? |
|
Definition
Because GTN decreases the O2 requirements of the heart AND increases the amount of blood going to the heart
In contrast, propranolol only decreases the O2 requirements of the heart (by lowering myocardial contractility) |
|
|
Term
| For patients with frequent anginal attacks what drug(s) are generally prescribed? |
|
Definition
Typically prescribe either propranolol OR isosorbide dinitrate
Also patient has bottle of GTN pills for acute attacks |
|
|
Term
| How does nifedipine help reduce contractility of the BVs? |
|
Definition
Blocks Ca channels in smooth muscle cell membrane to prevent Ca influx
Cannot form Ca-calmodulin complex, no myosin light chain phosphorylation, no interactions with actin to contract cell |
|
|
Term
| What vessels are particularly sensitive to nifedipine? |
|
Definition
|
|
Term
| What is the effect of Digitalis on the heart and how does it achieve this? |
|
Definition
It causes an INCREASE in the force of contraction of the heart by binding to the Na-K-ATPase on the myocardial membrane
It prevents the extrusion of Na to increase the intracellular concentration of Ca to increase the force of contraction |
|
|
Term
| Why is digitalis useful in treating cardiac arrhythmias as well? |
|
Definition
| It increases the # of impulses from the atria to the ventricles to improve electrical conduction (slows ventricular contractions) |
|
|
Term
| Products of D. lanata vs. D. purpurea (cardiac glycosides)? |
|
Definition
D. purpurea = digitoxin only
D. lanata = digitoxin & digoxin |
|
|
Term
| What is the main cardiac glycoside used in Canada? |
|
Definition
|
|
Term
| What drug name refers to all of the cardiac glycoside compounds? |
|
Definition
|
|
Term
| Where is ouabain derived from? What type of drug is it? |
|
Definition
| It is a cardiac glycoside derived from the seed of Strophanthus |
|
|
Term
| Adverse effects of Digitalis use? |
|
Definition
Nausea - activate vomit center in medulla
Arrhythmia
Visual disturbances - abnormal colour vision, blurred vision
Neurological effects - headache & fatigue |
|
|
Term
| What other drugs can be used in heart failure? How do these compare to the glycosides? |
|
Definition
Diuretics (reduce fluid load), ACE inhibitors, aldosterone blockers
Drugs aimed at NON-cardiac tissues (mentioned above) are MORE effective in prolonging life than glycosides |
|
|
Term
| True or False - Drugs aimed at non-cardiac tissues are more effective at prolonging life than cardiac glycosides? |
|
Definition
|
|
Term
| NG is converted into what potent vasodilator in smooth muscle cells lining BVs? |
|
Definition
|
|
Term
| What disease is the leading cause of death for men and women in western countries? |
|
Definition
| Atherosclerosis (leading to coronary artery disease) |
|
|
Term
| What are the 3 major types of lipids? |
|
Definition
| Cholesterol, cholesterol esters and triglycerides |
|
|
Term
| Approximately how much cholesterol is synthesized on a daily basis? Where does this synthesis occur? |
|
Definition
| Approximately 1000 mg of cholesterol is synthesized each day in the LIVER (also get synthesis in intestines) |
|
|
Term
| Two different sites of cholesterol synthesis in the body? |
|
Definition
|
|
Term
| What are fats packaged into and transported in? Why is this? |
|
Definition
| They are transported in LIPOPROTEINS due to their hydrophobic nature |
|
|
Term
| What lipoproteins are the largest? Where are they formed? |
|
Definition
| Chylomicrons are the largest lipoproteins and are formed in the intestines (transport triglycerides obtained from the diet) |
|
|
Term
| Source of secretion and function of VLDL? |
|
Definition
| Secreted from liver; transport triglycerides to the body's tissues |
|
|
Term
| Why is HDL considered the "good lipoprotein"? |
|
Definition
| Because it transports cholesterol away from the arteries to the liver where it can be transformed into bile salts |
|
|
Term
| Difference between primary and secondary hyperlipoproteinemias? |
|
Definition
Primary - from single gene defect; or interaction of subtle genetic & environmental factors
Secondary - from underlying metabolic disturbance (DM, hypothyroid, EtOH abuse) |
|
|
Term
| What are desirable cholesterol levels in the blood? What are borderline and high levels? |
|
Definition
Desirable levels are LESS than 200 mg/dL
Borderline levels are between 200-239 mg/dL
High levels are 240 mg/dL and greater |
|
|
Term
| An elevation in either of which two parameters corresponds with a major risk factor for atherosclerosis? |
|
Definition
Elevated TOTAL blood cholesterol
OR
Elevated LDL levels |
|
|
Term
| What was the goal of the lipid research clinic's primary prevention trial? What evidence did it accumulate? |
|
Definition
Goal was to establish a definitive link between hyperlipoproteinemia and coronary heart disease
Determined that there was strong evidence that showed a decrease in LDL levels corresponded with a decreased risk of CHD |
|
|
Term
| Non-pharmacological therapeutic measures in the treatment of hyperlipoproteinemia? |
|
Definition
Remove aggravating factors - stop smoking, treat HTN or DM, treat EtOH abuse, increase exercise
Change diet - eliminate simple sugars and fats; increase fibre intake and complex carbs |
|
|
Term
| What type of fats lower blood cholesterol and improve the HDL/LDL ratio? Where can these be found? |
|
Definition
| POLYUNSATURATED fats are useful in doing this and can be found in fish and vegetable oils |
|
|
Term
| Cholestyramine - structure and general function? |
|
Definition
Large, insoluble, positively charged resin
Binds to bile salts in the intestine to prevent their reabsorption and increase their excretion |
|
|
Term
| How does cholestyramine lead to decreases in blood LDL levels? |
|
Definition
Cholestyramine is a positive resin that binds to negative bile salts and prevents their reabsorption (increased excretion of them)
This leads to increased biotransformation of cholesterol into bile salts in the liver; therefore, to replenish this cholesterol, need to increase LDL uptake by liver
Increased LDL uptake by liver leads to lower LDL levels in the blood |
|
|
Term
| What hyperlipoproteinemias is cholestyramine most useful in treating? |
|
Definition
| Those in which LDL levels are elevated (because it functions to decrease LDL levels in the blood) |
|
|
Term
| What drug was used to decrease LDL levels in the lipid research clinic's primary prevention trial? |
|
Definition
|
|
Term
| What hyperlipoproteinemias are most effectively treated by cholestyramine? |
|
Definition
| Those in which LDL levels are elevated |
|
|
Term
| What type of hyperlipoproteinemia is GEMFIBROZIL (Fibrates) most effective in treating? |
|
Definition
|
|
Term
| In triglyceridemia, what lipoprotein level is elevated? What drug can be used to treat this condition? |
|
Definition
Have elevated VLDL levels (because VLDL transports triglycerides to body tisses; with more triglycerides, need more VLDL)
Therefore can use GEMFIBROZIL to treat |
|
|
Term
| What is the mode of action of gemfibrozil? |
|
Definition
Used to treat hypertriglyceridemias
Function is to decrease VLDL levels in the plasma, so there is more triglyceride breakdown, and less VLDL secretion by the liver |
|
|
Term
| What drug was used in the Helsinki Heart study? What were the findings of this study? |
|
Definition
Used GEMFIBROZIL
Found that total mortality was not changed by treatment; showed that gemfibrozil should NOT be prescribed to those with combined hyperlipidemia and have signs of atherosclerosis |
|
|
Term
| To what group of patients should gemfibrozil NOT be prescribed to? |
|
Definition
| Those with COMBINED hyperlipidemia (more than one elevated lipid) and those who show signs of atherosclerosis |
|
|
Term
| What is the most effective agent in increasing HDL levels? |
|
Definition
|
|
Term
| What is the mode of action of niacin (B3) in treating hyperlipoproteinemias? |
|
Definition
| Decreases secretion of VLDL from the liver, and lowers plasma levels of both VLDL and LDL in the body |
|
|
Term
| How do the "statins" function? |
|
Definition
| They inhibit the enzyme involved in the rate limiting step of cholesterol biosynthesis |
|
|
Term
| What is the enzyme involved in the RLS of cholesterol biosynthesis? What agents used to treat hyperlipoproteinemias are used to inhibit this? |
|
Definition
The enzyme used to catalyze the RLS of cholesterol biosynthesis is HMG CoA reductase
The "statins" (lovastatin, simvastatin, fluvastatin) are used to inhibit this enzyme |
|
|
Term
| What group of drugs are most effective in lowering LDL levels and total cholesterol? |
|
Definition
|
|
Term
| What drug was used in the Scandanavian hypercholesterolemia study? |
|
Definition
|
|
Term
|
Definition
| It inhibits intestinal absorption of cholesterol and plant sterols |
|
|
Term
| What drug can be used to inhibit intestinal absorption of cholesterol and plant sterols? |
|
Definition
|
|
Term
| What are the 3 classifications of HTN? |
|
Definition
Mild - basal diastolic P of 90-105 mmHg
Moderate - diastolic P of 106-130 mmHg
Severe - diastolic P > 130 mmHg |
|
|
Term
| How do anti-hypertensive drugs lower BP (3 methods)? |
|
Definition
1) Decrease blood volume (diuretics)
2) Relax blood vessels to increase diameter (ACE inhibitors)
3) Reduce the pumping force of the heart (B-blockers) |
|
|
Term
| How long does an individual need to take anti-hypertensives? |
|
Definition
| INDEFINITELY, because they DO NOT cure HTN, they simply help manage it |
|
|
Term
| Why is there often low compliance with anti-hypertensive therapy? |
|
Definition
High cost of drugs
Difficult to comply with lifestyle changes
Adverse effects from drugs
Long time period of therapy |
|
|
Term
| What 3 factors control blood pressure? |
|
Definition
BP is controlled by:
1) Blood volume
2) Resistance to blood flow in circulation
3) RAA System |
|
|
Term
| What is the main system that controls the resistance to flow in the circulatory system? |
|
Definition
Sympathetic NS activity
Increased activity = increased resistance
Decreased activity = decreased resistance |
|
|
Term
| What is the synthesis pathway for ANG II? |
|
Definition
Start with renin release from kidney; combines with alpha2-globulin in blood to form ANG I
ANG I is converted to ANG II via ACE |
|
|
Term
| What chemical does ANG II cause release of and where is this from? What are its effects? |
|
Definition
ANG II causes release of aldosterone from the adrenal cortex
Aldosterone increases reabsorption of Na and water, to cause an increase in BP |
|
|
Term
| How does hydrochlorothiazide exert its antihypertensive effects? |
|
Definition
| It causes increased excretion of salt and water to lower blood volume AND it lowers the resistance of blood vessels |
|
|
Term
| What is the mode of action of prazosin? |
|
Definition
| It is an alpha-adrenergic blocker; binds to alpha receptors on BVs to cause dilation (decrease resistance of circulation) |
|
|
Term
| 4 examples of SNS blocking agents used to treat HTN? |
|
Definition
Propranolol - B-blocker
Prazosin - a-blocker
Reserpine - destroys storage vesicles in adrenergic neurons
Clonidine - centrally acting |
|
|
Term
| What is the mode of action of reserpine? |
|
Definition
| It destroys storage vesicles in adrenergic neurons to decrease their NE stores, thereby decreasing SNS activity |
|
|
Term
| What is the mode of action of hydralazine, and what is it used to treat? |
|
Definition
| Hydralazine is used as an anti-hypertensive, and causes direct relaxation of arterioles by an unknown mechanism |
|
|
Term
| Example of an ACE inhibitor? |
|
Definition
|
|
Term
| In terms of treating HTN, what should you start therapy with? What should follow if this is ineffective? |
|
Definition
Start therapy with low-dose diuretic (thiazide) or B-blocker (propranolol)
If ineffective, combine diuretic and B-blocker OR use monotherapy with a-blocker, ACE inhibitor or Ca-channel blocker |
|
|
Term
| What are the KEY drugs in treating HTN? |
|
Definition
Thiazide diuretics
Effacious when used alone AND increase efficacy of other drugs used |
|
|
Term
| Which anti-hypertensives are most effacious in the elderly and African American populations? |
|
Definition
|
|
Term
| Effects of B-blockers on respiratory system? |
|
Definition
Blocks B-receptors in the bronchi, leading to bronchospasm
DO not use in those with asthma or other obstructive lung diseases |
|
|
Term
| One of the advantages of ACE inhibitors over other anti-hypertensives? |
|
Definition
| Do not cause sexual dysfunction |
|
|
Term
| To whom should ACE inhibitors not be prescribed? |
|
Definition
| Pregnant women (causes fetal injury in 2nd and 3rd trimester) |
|
|
Term
| Where did Fleming isolate penicillin from? |
|
Definition
| From the penicillium mold that appeared to be inhibited the growth of S. aureus |
|
|
Term
| Definition of an antibiotic? |
|
Definition
| Chemical substance produced by microbes that suppresses the growth of other microbes |
|
|
Term
| Difference between ANTIBIOTICS and ANTIMICROBIAL compounds? |
|
Definition
Antibiotics - suppress growth of microbes and are PRODUCED by microbes
Antimicrobials - synthetic chemicals which suppress microbial growth |
|
|
Term
| What are the 2 different ways antibiotics can be classified? |
|
Definition
Spectrum - narrow vs. broad
Actions - bactericidal vs. bacteriostatic |
|
|
Term
| Example of narrow spectrum vs. broad spectrum antibiotic? |
|
Definition
Narrow - pen G (only for gram positive)
Broad - tetracyclines and chloramphenicol (for positive and negative) |
|
|
Term
| Difference in what destroys the bacteria in bactericidal vs. bacteriostatic antibiotics? |
|
Definition
Bactericidal - antibiotic KILLS bacteria (pen G)
Bacteriostatic - growth of bacterium is stopped, and immune system kills bacterium (tetracyclines) |
|
|
Term
| Mechanism of action of PENICILLIN: |
|
Definition
| It inhibits cross-link formation in the cell walls (masquerades as D-alanyl-D-alanine) of bacterium, leading to instability; high turgor pressure causes cell lysis |
|
|
Term
| What chemical is closely related to the structure of penicillin that is normally included in bacterial cell walls? |
|
Definition
|
|
Term
| What are bacterial cells formed without cell walls known as? |
|
Definition
|
|
Term
| What was the first "natural" penicillin that was extracted from the penicillium mold? |
|
Definition
|
|
Term
| What are the two classifications of penicillin G as an antibiotic? |
|
Definition
| It is narrow spectrum (for gram +) and is bactericidal |
|
|
Term
| Why is pen V more stable than pen G when taken orally? |
|
Definition
| It is more acid stable, so it better survives the acidic secretions of the stomach |
|
|
Term
| When is pen V typically prescribed over pen G? |
|
Definition
| When it needs to be administered orally |
|
|
Term
| Examples of semi-synthetic penicillins? |
|
Definition
Penicillin V
Cloxacillin
Ampicillin, Amoxacillin
Carbenicillin |
|
|
Term
| What semi-synthetic penicillin is resistant to the "penicillinase" enzyme produced by some resistant-strains of bacteria? |
|
Definition
|
|
Term
| What differs between pen G and amoxcillin/ampicillin? |
|
Definition
Ampicillin and amoxacillin have a wider range of activity (broad spectrum)
Used to treat gram negative infections also, for example from E. coli |
|
|
Term
| What type of penicillin could be used to treat a UTI due to E. coli? |
|
Definition
| Amoxacillin or ampicillin (broad spectrum) |
|
|
Term
| Broadest spectrum of activity of penicillin derived compounds? |
|
Definition
|
|
Term
| Best penicillin that can be used to treat a P. aeurginosa infection? |
|
Definition
| Carbenicillin (broadest spectrum of activity) |
|
|
Term
| What combination of drugs does "Augmentin" contain? |
|
Definition
| Combination of a semisynthetic penicillin (amoxacllin) and a penicillinase inhibitor (clavulinic acid) |
|
|
Term
| What is the benefit of clavulinic acid? |
|
Definition
| It is a penicillinase inhibitor |
|
|
Term
| Most common adverse reaction to Penicillins? |
|
Definition
| Allergic reaction (seen in 1-10% of the population) |
|
|
Term
Difference between penicillin G vs...
Penicillin V
Cloxacillin
Ampicillin/Amoxacillin
Carbenicillin |
|
Definition
Pen V - more acid stable
Cloxacillin - penicillinase resistant
Ampicillin/Amoxacillin - broader spectrum of activity
Carbenicillin - bro |
|
|
Term
| Mode of action of cephalosporins? |
|
Definition
| Like penicillins, are selective inhibitors of cell wall synthesis |
|
|
Term
| Generations of cephalosporins? |
|
Definition
1st - cephalothin; good activity against +, moderate against -
2nd - cefmandole; increased activity against +, same vs. -
3rd - ceftriaxone; less active against +, more active against -
4th - cefepine; broader spectrum, increased stability to penicillinase |
|
|
Term
| Examples of each generation of cephalosporins? |
|
Definition
1st = cephalotin
2nd = cefamandole
3rd = ceftriaxone, cefotaxime
4th = cefepine |
|
|
Term
| What is the drug of choice for treatment of gonorrhea? What is it classified as? |
|
Definition
| Ceftriaxone (3rd generation cephralosporin) |
|
|
Term
| Mode of action of fluoroquinolones & example of one? |
|
Definition
Example = ciprofloxacin (BROAD spectrum)
They act by inhibiting DNA synthesis and are synthetic antimicrobials (NOT produced by bacteria) |
|
|
Term
| What kind of infections can erythromycin be used to treat? When is it useful? |
|
Definition
Gram positive infections
Useful if individual is allergic to penicillin |
|
|
Term
| What is the mode of action of erythromycin? |
|
Definition
| It selectively inhibits bacterial protein synthesis |
|
|
Term
| Where are arithromycin & clarithromycin derived from? |
|
Definition
| They are chemically modified forms of erythromycin |
|
|
Term
| General features of tetracyclines? |
|
Definition
Broad spectrum activity
BacterioSTATIC effects by inhibiting protein synthesis
Now have given rise to many resistant bacteria because of overuse |
|
|
Term
Mode of action of...
Penicillins
Cephalosporins
Fluoroquinolones
Erythromycin
Tetracyclines |
|
Definition
Penicillins - inhibit cell wall formation
Cephalosporins - inhibit cell wall formation
Fluoroquinolones - inhibit DNA synthesis
Erythromycin - inhibit protein synthesis
Tetracyclines - inhibit protein synthesis |
|
|
Term
| Why is chloramphenicol now rarely prescribed? |
|
Definition
| Due to it causing bone marrow failure in 1 in 30000 individuals (only used as last resort) |
|
|
Term
| What group of antibiotics to gentamycin & streptomycin belong to? |
|
Definition
|
|
Term
| What kind of bacterial infections are aminoglycosides typically used to treat? |
|
Definition
| Gram NEGATIVE infections (P. aeruginosa, tuberculosis, etc.) |
|
|
Term
| What is the 1st line treatment of Tb? 2nd line of treatment? |
|
Definition
1st line = isoniazid + rifampin daily for 6 months & pyrazinamide daily for the 1st two months
2nd line = streptomycin |
|
|
Term
| What drug combination is included in co-trimoxazole? What is it used to treat? |
|
Definition
Contains sulfamethoxazole and trimethoprim
Used to treat recurrent UTI and infections of respiratory and GI tracts |
|
|
Term
| What is tetrahydrofolic acid necessary for in bacteria? |
|
Definition
| Needed for one-carbon units (used to make DNA and proteins) |
|
|
Term
| Mechanism of action of co-trimoxazole in treating infection? |
|
Definition
The sulfmethoxazole inhibits conversion of PABA to dihydrofolic acid (DHFA)
The trimethoprim inhibits DHFA reductase to stop formation of THFA
Leads to folic acid deficiency in bacteria and a slowing of growth |
|
|
Term
| Why is trimethoprim selectively toxic in treatment? |
|
Definition
| It is more inhibitory to bacterial enzyme (DHFA reductase) than the human enzyme |
|
|
Term
| What is the mode of action of amphotericin B? |
|
Definition
Used to treat severe fungal infections
Binds to ergosterol (membrane sterol) of fungus and causes leakage through cell membrane |
|
|
Term
| What antifungals are effective when taken orally? |
|
Definition
The imidazoles
NOTE: Amphotericin B needs to be administered via IV for systemic fungal infection |
|
|
Term
| Mode of action of imidazoles (azoles)? |
|
Definition
Inhibit ergosterol synthesis, so improper cell membrane is formed
Specficially inhibits cytochrome P450 |
|
|
Term
| Drugs used to treat yeast infections? |
|
Definition
| Imidazoles (Azoles; antifungal class) |
|
|
Term
| What can be used to prevent influenza from the influenza A virus? |
|
Definition
|
|
Term
|
Definition
| It is a neuroaminidase inhibitor, and prevents spread of the flu virus from cell to cell |
|
|
Term
| DIfference in usage of amantidine vs. tamiflu? |
|
Definition
Amantidine is more of a prophylaxis; prevents infection from influenza A virus
Tamiflu prevents spread of virus from cell to cell as a neuroaminidase inhibitor |
|
|
Term
| What is the drug of choice for the herpes simplex virus? |
|
Definition
|
|
Term
| What two uses does acyclovir have? |
|
Definition
Treat HSV infection/as a prophylaxis for recurrences
Treat infections from varicella-zoster virus |
|
|
Term
| 1st drug introduced to treat HIV infection? |
|
Definition
| Zidovudine (AZT), which is a reverse transcriptase inhibitor |
|
|
Term
| Drugs approved by FDA for HIV infected individuals in 1996? |
|
Definition
Two nucleoside analogues - lamivudine & stavudine
3 protease inhibitors - saquinavir, ritonavir, indinavir |
|
|
Term
| Optimal therapy for HIV infection? |
|
Definition
| 2 nucleoside analogues (AZT, lamivudine, stavudine) plus a protease inhibitor (saquinavir, ritonavir, indinavir) |
|
|
Term
| New classes of HIV drugs? |
|
Definition
Entry inhibitors
Integrase inhibitors (e.g. raltegravir) |
|
|
Term
| What classification of drug is raltegravir, used in HIV treatment? |
|
Definition
| It is an INTEGRASE INHIBITOR |
|
|
Term
| Disadvantages of using antibiotic combinations? |
|
Definition
Unnecessary added cost
Increased likelihood of toxicity
Increased likelihood of bacterial resistance
Decrease normal bacteria in our bodies (give rise to superinfection) |
|
|
Term
| Why is combination drug therapy necessary to treat endocarditis? What drugs are used? |
|
Definition
Use combination of a penicillin and aminoglycoside
Penicillin damages cell wall to allow aminoglycoside to enter and inhibit protein synthesis |
|
|
Term
| When are antibiotic combinations useful (justified)? |
|
Definition
When the bacteria causing the infection is unknown
With a mixed infection, need to kill multiple species
For treating TB to reduce likelihood of resistant bacteria emerging
When two have an additive effect (treating endocarditis with a penicillin and aminoglycoside) |
|
|
Term
| Are viruses susceptible to antibiotics? |
|
Definition
|
|
Term
| Reasons for over prescription of antibiotics? |
|
Definition
High pressure from patient
Use broad spectrum instead of diagnosis
Pressure from pharmaceutical representatives
Lack of laboratory equipment |
|
|
Term
| Is prophylactic use of antibiotics successful? |
|
Definition
| In some situations it is highly effective; in others it can be valueless |
|
|
Term
| Successful use of antibiotic prophylactics in certain scenarios (list 3)... |
|
Definition
Prevent recurrent UTI infection with co-trimoxazole
Prevent wound infection after surgery
Prevent infections post-dental surgery with valvular heart defects |
|
|
Term
| What genus is the protozoa that causes malaria from? |
|
Definition
|
|
Term
| 4 species of malaria-causing protozoa? |
|
Definition
All are from Plasmodium
P. falciparum
P. vivax
P. ovale
P. malariae |
|
|
Term
| Lifecycle of malaria parasite... |
|
Definition
Infected Anopheles mosquito bites and injects parasite into individual (sporozite enters blood)
Sporozites carried to liver and enter liver cells, becoming schizonts
Schizonts emerge from liver, enter RBCs and cause lysis (now called merozoites) |
|
|
Term
| Difference between sporozite vs. schizont vs. merozoite in malaria parasite lifecycle? |
|
Definition
Sporozite - injected into blood stream by mosquito
Schizont - sporozite that has entered hepatocytes
Merozoite - enters RBCs and causes hemolysis |
|
|
Term
| What species of Plasmodium is chloroquinine ineffective in treating? |
|
Definition
| chloroquinine resistant P. falciparum |
|
|
Term
| What is the drug of choice in areas where plasmodia are resistant to chloroquinine? |
|
Definition
|
|
Term
| What groups of people should NOT take mefloquine for malaria? |
|
Definition
Pregnant women
Those with history of seizure disorder or psychosis
Those in which vertigo could be relevant |
|
|
Term
|
Definition
Adverse effects seen when taking QUININE for malaria treatment
Only used for multidrug-resistant strains of P. falciparum |
|
|
Term
| What is the use of Primaquine in malaria therapy? |
|
Definition
| Used to treat for relapse of infection due to persistent liver phase of the infection |
|
|
Term
| What Plasmodium species have a persistent liver phase during the infection? What can be used to treat for this? |
|
Definition
P. vivax & P. ovale
Use primaquine to treat for this phase to prevent recurrence |
|
|
Term
|
Definition
| Substance required for normal metabolic functioning that is NOT made by the body (needs to be acquired from an external source) |
|
|
Term
| How were most vitamins discovered? |
|
Definition
By studying many different deficiency diseases
Scurvy = vitamin C deficiency
Rickets = vitamin D deficiency |
|
|
Term
| Vitamin deficiency diseases for C, D, B12, and B3 |
|
Definition
C - scurvy
D - rickets
B12 - pernicious anemia
B3 - Pellagra |
|
|
Term
| Water soluble vs. Fat soluble vitamins? |
|
Definition
Water soluble = vitamin C and B vitamins
Fat soluble = A, D, E, K |
|
|
Term
|
Definition
Only when consumed in a chemically pure tablet form
If obtained in diet, are NOT drugs |
|
|
Term
| Vitamin Definitions: DRI, EAR, RDA, AI |
|
Definition
DRI - daily recommended intake
EAR - estimated average requirement; meets 50% of people for given group
RDA - recommended daily allowance; meets 97-98% of people's needs for given group
AI - adequate intake; RDI based on scientific data for specific groups |
|
|
Term
| What is the nutritional approach to vitamin therapy? |
|
Definition
| Try to meet the RDA for each vitamin though the diet or by a multivitamin supplement |
|
|
Term
| Alternate name for vitamin C? |
|
Definition
|
|
Term
|
Definition
60 mg for non-smokers; 100 mg for smokers
200 mg is the maximum body pool of vit C |
|
|
Term
| What is vitamin C required for within the body? |
|
Definition
| Formation of collagen and ground substance (hold framework of cells together) |
|
|
Term
| Who was the first to cure scurvy? |
|
Definition
| Jacques Cartier; gave his ship's crew spruce leaves |
|
|
Term
| What size doses of vitamin C did Pauling recommend in order to treat the common cold? |
|
Definition
| Daily doses in excess of 4000 mg (recall that RDA is 60 mg) |
|
|
Term
| Conclusions of Canadian study of vit C's effects on the common cold? |
|
Definition
| Did NOT prevent or shorten the length of the cold, but may have made the colds milder (less severe) |
|
|
Term
| Adverse effects of overdosing on vitamin C? |
|
Definition
Diarrhea
Kidney stones (increased oxalate excretion)
Rebound scurvy when dosage is stopped |
|
|
Term
| Alternate names for vitamin B1, 2, 3, 5, 6, 12 |
|
Definition
B1 = thiamine
B2 = riboflavin
B3 = niacin
B5 = patothenic acid
B6 = pyridoxine
B12 = cyanocobalamin |
|
|
Term
| What B vitamin has the largest RDA, and which the smallest? |
|
Definition
Largest = Niacin (B3) @ 19 mg/day
Smallest = Cyanocobalamin (B12) @ 2 micrograms/day |
|
|
Term
| What vitamin is important for pregnant women to reduce likelihood of neural tube defects? |
|
Definition
Folate (Vitamin B9)
For pregnant women RDA = 400 micrograms (normally is 200 micrograms) |
|
|
Term
| What B vitamin is associated with lower risk of heart disease when taken in high intake? |
|
Definition
|
|
Term
| What vitamin do most elderly americans have trouble absorbing? |
|
Definition
| Vitamin B12 (cyanocobalamin) |
|
|
Term
| RDA of retinol? What are the equivalents? |
|
Definition
RDA = 1000 ug retinol = 1000 equivalents
1 equivalent = 1 ug retinol = 6 ug B-carotene |
|
|
Term
| What is 1 equivalent of vitamin A equal to? |
|
Definition
|
|
Term
| Effects of vitamin A deficiency? |
|
Definition
Retarded growth & development
Poor night vision & dry eye
Increased risk of respiratory infection
Dry, thick skin |
|
|
Term
| Therapeutic uses of vitamin A |
|
Definition
Treatment of deficiency in impoverished countries
During periods of increased requirement - pregnancy, lactation, infancy
Treatment of acne & other skin conditions |
|
|
Term
|
Definition
| 400 IU = 10 ug of cholecalciferol |
|
|
Term
| Where do the various conversions of vitamin D into its (eventual) active form occur (2 conversions)? |
|
Definition
1st is converted into 25-hydroxyvitamin D in the liver
Then is converted into 1,25-dihydroxyvitamin D (active form in the kidney) |
|
|
Term
| What form is vitamin D present in in the skin? |
|
Definition
| In PROVITAMIN D (converted into vitamin D which is found in foods, etc.) |
|
|
Term
| What is the active form of vitamin D known as? |
|
Definition
| 1,25-dihydroxyvitamin D (calcitriol) |
|
|
Term
| What are some of the functions of vitamin D? |
|
Definition
Increase Ca and PO3 absorption from gut
Regulate blood calcium levels
Bone resorption to free calcium from old bone |
|
|
Term
| Results of vitamin D deficiency? What is this known as? |
|
Definition
Called "rickets"
Decreased calcium & phosphate absorption in intestines
Decreased blood calcium levels
Increased bone resorption to free calcium to raise plasma levels |
|
|
Term
| Effects of a megadose of vitamin D? |
|
Definition
Megadose > 50000 units
Hypercalcemia leading to calcium deposition in organs
EXCESS calcium removal from bones
Fatigue, nausea, impaired kidney function |
|
|
Term
|
Definition
May have protective effects against breast cancer
NO protective effects against prostate cancer |
|
|
Term
|
Definition
|
|
Term
| Effects of vitamin E on reproductive & muscular systems? |
|
Definition
Reproductive - appears vitamin E is necessary for normal reproduction and pregnancy in mammalian species
Muscular - deficiency leads to muscular dystrophy in NON-human mammals; no effect of deficiency in humans in relation to MD |
|
|
Term
| Summary of effects of vitamin E? |
|
Definition
Treat hemolytic anemia in babies
May be beneficial in reducing CVD if taken in high doses
In humans, ineffective in musc. dystrophy, abortion & sterility |
|
|
Term
| Conditions to be satisfied in the use of an OTC drug? |
|
Definition
Illness/symptoms are mild
If illness or symptoms become worse, need to consult physician
Self medication should NOT exceed two weeks without physician's consultation
If adverse events occur, stop taking OTC drug |
|
|
Term
|
Definition
| Any drug that can be purchased without a physician's prescription |
|
|
Term
| What is controlled by the government when it comes to OTC drugs? |
|
Definition
FDA controls safety, efficacy, advertising and sale of OTC products
All OTC drugs must undergo strict clinical trials before they can be sold |
|
|
Term
| What 3 effects does ASA have? |
|
Definition
| Analgesic, anti-inflammatory and antipyretic effects |
|
|
Term
| Mechanism for the effects of ASA? |
|
Definition
| Inhibition of prostaglandin synthesis (have roles in pain mediation, fever, and inflammation) |
|
|
Term
| What is the major toxicity of ASA? |
|
Definition
| The gastric irritation that occurs in roughly 2% of the population (breakdown of gastric mucosa leading to bleeding and ulcers) |
|
|
Term
| What OTC drug is associated with Reyes syndrome in children? |
|
Definition
ASA
In this case, given acetaminophen to children with fever |
|
|
Term
| Drug of choice when treating a child with a fever? |
|
Definition
Acetaminophen
NOT ASA, because it may cause Reyes syndrome |
|
|
Term
| If you are allergic to ASA, what are you also allergic to? |
|
Definition
| All salicylate containing food products (including yellow food colour) |
|
|
Term
| What is an effervescent analgesic? |
|
Definition
| Alka seltzer; contains ASA and a high concentration of sodium bicarbonate |
|
|
Term
| Effects of ASA vs. acetaminophen? |
|
Definition
ASA = analgesic, antipyretic, anti-inflammatory
Acetaminophen = analgesic & antipyretic only |
|
|
Term
| Mechanism of action of acetaminophen? |
|
Definition
| Inhibition of prostaglandin synthesis |
|
|
Term
| Effects of ibuprofen vs. acetaminophen vs. ASA |
|
Definition
Both ASA and ibuprofen are antipyretic, analgesic & anti-inflammatory
Acetaminophen is only antipyretic & analgesic |
|
|
Term
| What is likely the most efficacious OTC anti-inflammatory on the market? |
|
Definition
|
|
Term
| Method of action of ibuprofen? |
|
Definition
| Reversible inhibition of prostaglandin synthesis |
|
|
Term
| What do all internal analgesics have as their method of action? |
|
Definition
| Inhibition of prostaglandin synthesis |
|
|
Term
| What chemicals are contained in topical analgesics? |
|
Definition
| Camphor, menthol, methylsalicyate, capsicum, turpentine oils |
|
|
Term
| Recommendation of use of Aspergum (ASA in chewable gum form)? |
|
Definition
NO recommendation
Causes erosion of mucosa and ASA does not reach therapeutic levels in plasma |
|
|
Term
| Mode of action of topical analgesics? |
|
Definition
All are counter-irritants and cause vasodilation (feeling of warmth)
Camphor and menthol also block sensory pain receptors |
|
|
Term
| Drugs commonly used to treat the common cold (drug classes)? |
|
Definition
Antihistamines
Antitussives
Decongestants
Expectorants
Analgesics |
|
|
Term
| What are cold preparations often termed? |
|
Definition
| "Shotgun preparations" - combine variety of substances to best reduce symptoms |
|
|
Term
| In what group of people are cold preparations no longer used? |
|
Definition
| No longer used in children under 6 years of age, because some deaths resulted of possible overdose before |
|
|
Term
| What variety of receptors are blocked by curare? |
|
Definition
| Nicotinic (cholinergic) receptors |
|
|
Term
| What do antihistamines prevent histamine from doing? |
|
Definition
| Prevent histamine from binding to the H1 receptor to cause vasodilation & inflammation |
|
|
Term
| What properties do most antihistamines also possess? |
|
Definition
| Many have anti-cholinergic properties similar to atrophine (can decrease secretions) |
|
|
Term
| Efficacy of antihistamines in cold treatment? |
|
Definition
| Very limited role in alleviating symptoms |
|
|
Term
| What are all decongestants? |
|
Definition
| ALL are alpha-adrenergic receptor agonists (cause vasoconstriction to reduce congestion) |
|
|
Term
| What is the mode of action of decongestants? |
|
Definition
| They are a-adrenergic agonists, causing vasoconstriction to decrease congestion |
|
|
Term
| Efficacy of decongestants vs. antihistamines? |
|
Definition
Decongestants are considered effective because of their ability to relieve symptoms (congestion).
Antihistamines are less effective because of the very limited symptom relief that they provide |
|
|
Term
| How do centrally acting cough suppressants function? Peripherally acting suppressants? |
|
Definition
They block the cough center in the medulla to reduce frequency of cough (central)
The peripheral suppressants block nerve endings in throat and bronchioles |
|
|
Term
| Example of two CENTRALLY acting cough suppressants? |
|
Definition
| Codeine (ineffective b/c dose is too small for OTC), and dextromorphan HBr (effective dose = 30 mg) |
|
|
Term
| When is it rational to use cough suppressants? |
|
Definition
| If the cough is NON-productive (no mucus to clear) |
|
|
Term
| Function of expectorants? |
|
Definition
| They stimulate bronchial secretions in order to loosen phlegm in the upper respiratory tract |
|
|
Term
| What do medical experts recommend for cold therapy? |
|
Definition
Rest
Fluids
Analgesics/antipyretics - acetaminophen is preferred
Chicken soup? |
|
|
Term
| What are contained in mouth washes vs. lozenges? |
|
Definition
Mouth washes typically contain an antiseptic alone
Lozenges typically contain an antiseptic and a local anesthetic |
|
|
Term
| Major therapeutic benefit from lozenges? |
|
Definition
| Increase in salivary secretions produced (keeps throat moist) |
|
|
Term
| General thoughts on use of mouth washes and lozenges for treating sore throat/cold? |
|
Definition
Not considered too effective; contact time with bacteria is too short for antiseptic to be considered effective
Also, the major benefit of the lozenges is that they increase salivary secretions, something which could be accomplished by any normal hard candy |
|
|
Term
| Two main ingredients of a sleep preparation? |
|
Definition
| Antihistamine & analgesic (usually acetaminophen) |
|
|
Term
| What is hay fever (what kind of disease)? |
|
Definition
| It is an antibody-mediated inflammatory disease of the nasal mucosa (allergic reaction) |
|
|
Term
| Drugs of choice in treating hay fever? |
|
Definition
| Antihistamines (because histamine mediates many of the symptoms seen in hay fever) |
|
|
Term
| Differences between 1st and 2nd generation antihistamines? |
|
Definition
1st = all caused sedation & drowsiness; also anticholinergic (dry mouth)
2nd = no sedation; preferred agents |
|
|
Term
| E.g.'s of 2nd generation antihistamines? |
|
Definition
|
|
Term
| What can excessive use of decongestants lead to? |
|
Definition
|
|
Term
| What should be done if an individual comes into contact with poison ivy/oak/sumac? |
|
Definition
| Wash area with tide detergent & remove the resin |
|
|
Term
| Use of calamine lotion with posion ivy exposure? |
|
Definition
| Can be used to prevent itching, but not inflammation (used only if exposure is mild) |
|
|
Term
| Preferred OTC agent for topical treatment of posion ivy? |
|
Definition
| 0.5% hydrocortisone ointment - reduces inflammation associated with exposure |
|
|
Term
| Treatment of mild insect bites in non allergic individuals? |
|
Definition
| Same as poison ivy - calamine lotion for itching & 0.5% hydrocortisone for inflammation |
|
|
Term
| What kind of radiation is present in solar energy? |
|
Definition
| UVA, UVB and UVC radiation |
|
|
Term
| Relative wavelengths of solar radiation? |
|
Definition
UVC = 200-290 (high frequency)
UVB = 290-320
UVA = 320-400 (low frequency) |
|
|
Term
| What are each of the UV radiations contained in solar energy implicated with? |
|
Definition
UVC = screened out by ozone layer
UVB = tanning, sunburn, cancer
UVA = sunburn, drug photosensitivity |
|
|
Term
| What is the function of sunscreens and where are they absorbed? |
|
Definition
| Absorbed in the stratum corneum (outer layer) of the skin, and prevent UV radiation from reaching the dermis (inner layer) |
|
|
Term
| What is the formula for SPF? |
|
Definition
| = minimum erythema dose of protected skin divided by minimum erythema dose of unprotected skin |
|
|
Term
| What is the "minimum erythema" dose? |
|
Definition
| Time of exposure to UV radiation that will cause burn/reddening of skin |
|
|
Term
| Difference between systemic & non-systemic antacids? Examples? |
|
Definition
Systemic - absorbed by GI tract and can cause systemic alkalosis (e.g. sodium or calcium bicarbonate)
Non-Systemic - not absorbed by GI tract, cannot cause systemic alkalosis (e.g. aluminum or magnesium hydroxide) |
|
|
Term
| Cons of sodium bicarbonate use? |
|
Definition
May cause systemic alkalosis
Liberation of CO2 can perforate ulcer
Retention of Na may aggravate HTN |
|
|
Term
| How does aluminum hydroxide act as an antacid? |
|
Definition
| It acts as a DEMULCENT - it coats the mucous lining of the stomach to protect from the acid |
|
|
Term
| What is more effective, normal antacids or H2 antagonists? |
|
Definition
| H2 antagonists appear to be more effective in treating excess stomach acid |
|
|
Term
| Cathartics vs. Laxatives? |
|
Definition
Cathartics - imply fluid evacuation; ALWAYS due to increased GI motility
Laxatives - soft formed stool; either increased motility OR increased hydration of stool |
|
|
Term
| Examples of stimulant/contact cathartics? |
|
Definition
| Castor oil, senna, phenolphthalein, bisacodyl |
|
|
Term
| Which cathartics may enhance CCK secretion? |
|
Definition
| Saline cathartics (e.g. epson salt) |
|
|
Term
| What is methylcellulose an example of? |
|
Definition
|
|
Term
| Mode of action of bulk forming laxatives? |
|
Definition
| Get swelling of water to form viscous solution to maintain soft stool |
|
|
Term
| When are the effects of bulk forming laxatives observed? |
|
Definition
| Effect seen in 12-24 hours, but full effect occurs 2 to 3 days after therapy has commenced |
|
|
Term
| What type of OTC drugs can form soft stools WITHOUT causing peristalsis? |
|
Definition
|
|
Term
| Types of emollient laxatives and their methods of action? |
|
Definition
Surface active agents - decrease surface tension of stool to allow water to penetrate
Mineral oil - slows H2O absorption from GI tract to increase its levels in the stool |
|
|
Term
| Which emollient laxative is preferred? |
|
Definition
The surface acting agents are preferred (e.g. dioctyl sodium sulfosuccinate)
Mineral oil is not recommended because of decreased fat soluble vitamin absorption, pneumonia risk, and prevent complete bowel evacuation |
|
|
Term
| Adverse effects of mineral oil? |
|
Definition
Used as an emollient laxative
Decrease absorption of fat soluble vitamins
Cause "lipoid pneumonia"
Prevent complete evacuation of the bowel |
|
|
Term
| Major problem associated with diarrhea? |
|
Definition
|
|
Term
| Mode of action of classes of anti-diarrhea drugs? |
|
Definition
Adsorbents - kaolin & pectin; adds bulk to GI tract
Loperamide - synthetic opioid which inhibits peristalsis |
|
|
Term
| What is the anti-diarrheal OTC drug of choice? |
|
Definition
|
|
Term
| Difference between allopathic & homeopathic drugs? |
|
Definition
Allopathic - mainstream medicinals; have a DIN and have undergone proper testing
Homeopathic - plant products w/o DIN that often lack evaluation |
|
|
Term
| Difference between allopathic pharmaceuticals and phytopharmaceuticals? |
|
Definition
Allopathic - have a DINS; have full status as a drug
Phytopharmaceutical - drugs from plants used at therapeutic doses w/ scientific evidence and documented toxicity |
|
|
Term
| Why has the public wanted to switch to herbal remedies from allopathic medicine? |
|
Definition
Believe allopathic medicine has too many adverse effects
Believe herbal remedies to have fewer adverse effects
Allopathic medicine is too expensive
Lack of faith in allopathic medicine |
|
|
Term
| Problems associated with herbal remedies? |
|
Definition
Lack of efficacy and safety data
Lack of standardization between batches
Leaving off some ingredients listed
Adding non-herbal ingredients
Unknown toxicities
Drug interactions with concurrent allopathic medicine
Questionable source |
|
|
Term
| Main use of Valerian (herbal remedy)? |
|
Definition
|
|
Term
| What are the active ingredients in valerian? |
|
Definition
|
|
Term
|
Definition
|
|
Term
| What is the main use of devil's claw? |
|
Definition
| Treatment of inflammatory conditions (e.g. rheumatoid arthritis) |
|
|
Term
| What is echinacea used for? What is its mode of action? |
|
Definition
Echinacea is used to treat/prevent colds; also used in wound healing & anti-inflammatory
Mode of action = stimulation of immune system |
|
|
Term
| What cells is echinacea believed to stimulate? |
|
Definition
| It is believed to stimulate T-lymphocytes (believed to exert mode of action by boosting the immune response) |
|
|
Term
| What kind of remedy do herbalists consider ginseng to be? |
|
Definition
| An adaptogen - restores normal balance |
|
|
Term
| What herbal remedy has been shown to have true anti-depressant action? |
|
Definition
| St. John's Wort (still less effective than SSRIs and tricyclics though) |
|
|
Term
| What is a herbal remedy used to treat depression & heal wounds? |
|
Definition
|
|
Term
What are the main uses for the following herbal remedies:
Valerian
Feverfew
Devil's Claw
St. John's Wort |
|
Definition
Valerian = sedative hypnotic
Feverfew = treatment of migraines
Devil's Claw = anti-inflammatory disease treatment
St. John's Wort = depression & wound healing |
|
|
Term
| Definition of food additives? |
|
Definition
| Substances added to improve appearance, texture, storage, and nutritive value of food |
|
|
Term
| Two classes of food additives? |
|
Definition
Intentional - vitamins, flavours, colours, preservatives
Unintentional - fertilizers, pesticides, heavy metals |
|
|
Term
| What category of food additives is MSG under? |
|
Definition
|
|
Term
| What group of food additives may have the greatest potentials for toxicitiy? |
|
Definition
|
|
Term
| Most common allergic reaction to food colour? |
|
Definition
| Allergic to yellow dye (tartrazine; salicyate allergy; also means allergic to ASA) |
|
|
Term
| Where are food colourings derived from? |
|
Definition
|
|
Term
| Classes of food additives? |
|
Definition
Flavouring Agents
Food Dues
Texture Agents
Preservatives
Sweeteners |
|
|
Term
| What type of food additives are silicates & gums? |
|
Definition
| Texture agents (can be used to change viscosity) |
|
|
Term
| First preservative used historically? |
|
Definition
| Sodium chloride (table salt) |
|
|
Term
| What kind of activities does sodium benzoate have as a food additive? |
|
Definition
| Antibacterial and fungistatic properties |
|
|
Term
| What are the major antibacterial & antifungal additives of food? |
|
Definition
| Parabens (sodium benzoate derivatives) |
|
|
Term
| Use of antibiotics as food additives? |
|
Definition
| Would be considered the best antibacterial compounds, but NOT used in Canada to prevent emergence of resistant strains of bacteria |
|
|
Term
| Two examples of early preservatives used in food? |
|
Definition
|
|
Term
| Why is sodium nitrite added to meat? |
|
Definition
For colour (red colour)
Inhibit growth of Clostridium |
|
|
Term
| Adverse effects of sodium nitrite (food additive)? |
|
Definition
Decrease in BP
Blood cannot cary O2
Nitrosamine formation (carcinogenic) |
|
|
Term
| What is sulfur dioxide added to? |
|
Definition
| Added to wine as a preservative to prevent mould formation; should NOT be present in good wine |
|
|
Term
| Different types of antioxidant agents and examples? |
|
Definition
Water soluble - citric or ascorbic acid
Fat soluble - butylated hydroxyanisole & BHT |
|
|
Term
| Functions of water soluble vs. fat soluble anti-oxidants? |
|
Definition
Water soluble - prevent oxidation of carbohydrates (browning of fruit)
Lipid soluble - prevent fats from becoming rancid |
|
|
Term
|
Definition
Sweetener food additive shown to cause tumors in rats in large doses
Limited to pharmacy use in Canada |
|
|
Term
|
Definition
| Only in those with phenylketonuria because they cannot stand the phenylalanine in the aspartame |
|
|
Term
|
Definition
| Have the SAME caloric value, but aspartame is 200x sweeter and thus can be used in smaller amounts |
|
|
Term
What banned substances are used to....
Increase endurance
Increase strength
Decrease body weight
Decrease HR |
|
Definition
Endurance = amphetamines
Strength = anabolic steroids
Body weight = diuretics
HR = propranolol (B-blocker) |
|
|
Term
| In terms of performance enhancing drugs, what is "stacking"? |
|
Definition
| Use of multiple substances in the same class simultaneously (e.g. 3 anabolic steroids at once); allows for smaller doses to be used so it can be stopped closer to the competition |
|
|
Term
| Why are amphetamines used as performance enhancing drugs? |
|
Definition
| They increase both power and endurance through their psychomotor stimulation |
|
|
Term
| How do anabolic steroids compare with endogenous sex hormones? |
|
Definition
| There are fewer androgenic effects, but the anabolic effects are maintained (building muscle mass) |
|
|
Term
| Has it been conclusively show that anabolic steroids increase strength and physical appearance? |
|
Definition
Prior to the 1990s had no conclusive evidence that this was true.
Now know that size and strength can be increased, but NOT aerobic performance |
|
|
Term
| What do anabolic steroids NOT have an effect on? |
|
Definition
| Do NOT increase aerobic performance |
|
|
Term
| 3 possible mechanisms by which anabolic steroids exert their effects? |
|
Definition
1. Anti-catabolic response; prevent muscle breakdown to fuel training
2. Anabolic effects follow anti-catabolic effects; drugs produce new proteins
3. Motivational responses - aggressive behavior |
|
|
Term
| Summary of anabolic steroids? |
|
Definition
Low to moderate doses have modest effects on average ppl
Effect on inexperienced weight lifters is LESS than average workout program
In trained athlete, large doses yield significant increases in lean mass and strength
Aggressive behavior that accompanies them contributes to performance enhancing ability
Need high protein diet to exert full effects |
|
|
Term
| Toxicities associated with anabolic steroid use? |
|
Definition
Male infertility & decreased testosterone
Liver failure
CVD (increase LDL, decrease HDL)
Mood swings (roid rage) |
|
|
Term
| Cardiovascular effects of using anabolic steroids (toxic)? |
|
Definition
| Increase in LDL, decrease in HDL, so increased risk of CVD |
|
|
Term
| In what sporting events are B-blockers sometimes used? |
|
Definition
| Used in precision shooting to lower heart rate to aid in focus |
|
|
Term
| What kind of athletes use benzodiazepines prior to their sport? |
|
Definition
| Ski jumpers use it to calm nerves (used as an anxiolytic) |
|
|
Term
| Why is HGH not easily detected? |
|
Definition
| Because it clears the body quickly (rapidly excreted) |
|
|
Term
| 2 ways to increase O2 carrying capacity of body (illegal in sports)? |
|
Definition
Blood doping - inject own blood to increase [Hb]
EPO - used to stimulate RBC formation |
|
|
Term
| What is probenecid used by athletes for? |
|
Definition
| Used to block urinary excretion of other drugs |
|
|
Term
| Effects of FSH and LH on ovulation? |
|
Definition
FSH - causes the ovarian follicles to mature; eventually only one matures to its full extent
LH - when it peaks near day 14, ovulation occurs |
|
|
Term
| When does LH secretion typically peak during the ovarian cycle? |
|
Definition
| Near day 14 (around the same time estrogen levels peak) |
|
|
Term
| During the ovarian cycle, which hormone peaks first, estrogen or progesterone? |
|
Definition
| Estrogen peaks at day 14; progesterone secretion begins to increase AFTER estrogen secretion has peaked |
|
|
Term
| What structure secretes progesterone? |
|
Definition
|
|
Term
| Effects of progesterone vs. estrogen on the uterus? |
|
Definition
Estrogen - during first 14 days causes proliferation of endometrium
Progesterone - secretion causes endometrium to produce nutrients needed to support fertilized ovum |
|
|
Term
| When the endometrium is proliferating, what hormone maintains and supports it? |
|
Definition
| Progesterone (when progesterone levels drop, the endometrium is sloughed) |
|
|
Term
| What maintains the integrity of the endometrium immediately after implantation of the fertilized ovum? |
|
Definition
|
|
Term
| What does the term oral contraceptive refer to? |
|
Definition
| A product containing an estrogen and progestin (progesterone like compound); these are the most effective contraceptives developed to date |
|
|
Term
| What are estrogen and progesterone levels like at the beginning of the ovarian cycle? |
|
Definition
| They are LOW (allow for secretion of GRH, FSH, and LH) |
|
|
Term
| What is day 1 of the ovarian cycle considered to be? |
|
Definition
|
|
Term
| Difference in hormone levels of fixed combo and multiphasic contraceptives? |
|
Definition
Fixed combo = fixed amount of estrogen AND progestin
Multiphasic = fixed estrogen and variable progestin (progestin increases from week to week) |
|
|
Term
| Why are multiphasic contraceptives preferred to fixed combination? |
|
Definition
Keep the hormone dose smaller
Hormone pattern follows natural pattern for ovarian cycle
Fewer adverse effects compared to fixed combo |
|
|
Term
| How are transdermal contraceptives used? |
|
Definition
| Combination delivered at a constant rate for 7 days, use 3 patches for each cycle |
|
|
Term
|
Definition
Low dose progestin taken as long as drug is needed
Worse acceptability than combinations, and less effective |
|
|
Term
| What is Norplant (contraceptive)? |
|
Definition
Silicone tubes filled with L-norgestrel (progestin compound)
Implanted under the skin and good for 5 years
Cost is $700 |
|
|
Term
| What is depoprovera (contraceptive)? |
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Definition
| Injectable progestin that is injected every 3 months, provides about 3 months worth of contraception |
|
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Term
| Mode of action of estrogen-progestin combos? |
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Definition
Estrogen inhibits secretion of GRH, LH, FSH
Progestin keeps endocervical secretions thick to slow sperm migration
Endometrium is not optimal for implantation |
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Term
| 3 contraceptives that contain ONLY progestin? |
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Definition
Mini pill (low dose progestin)
Norplant (small silicone tubes)
DepoProvera (progestin injections) |
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Term
| Method of action of mini-pill, Norplant & DepoProvera? |
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Definition
Progestin inhibits GRH secretion
Endocervical secretions are thick to slow sperm
Endometrium is not optimal for implantation |
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Term
| What is the most popular form of oral contraceptive in the last decade? |
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Definition
| The phasic estrogen-progestin combinations |
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Term
| Adverse effects of depoprovera & mini-pill? |
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Definition
Increase LDL, decrease HDL (increases CVD risk)
Breakthrough bleeding during non-menstrual periods |
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Term
| Adverse effects of Norplant? |
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Definition
Changes in menstrual bleeding & breakthrough bleeding
Acne
Weight gain
Muscle pain
Breast discharge |
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Term
| Adverse effects of combination contraceptives (mild symptoms)? |
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Definition
Nausea, Edema, Headache
Change in libido
Decreased menstrual flow; amenorrhea after stopping
Weight gain
Increased pigmentation
Jaundice
Increased glucose tolerance
Decreased folate absorption |
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Term
| Severe adverse effects of combination contraceptives? |
|
Definition
Increased risk of thromboembolic disease (increased clotting)
Clotting leads to increased risk of MI, CVA
HTN development (if over 35)
Decrease risks of endometrial & ovarian cancer, may cause hepatic adenomas |
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Term
| What is mifepristone (contraceptive)? |
|
Definition
It is an anti-progestin; blocks effect of progesterone on endometrium to cause sloughing
Can be taken after "missed period" to cause menstruation |
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Term
| Examples of post coital contraceptives? What do they contain? |
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Definition
Preven, Plan B
Contain large dose of estrogen (3x amount in oral contraceptive) to either delay or inhibit ovulation; taken within 24 hrs, and no later than 72 hours |
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Term
Pregnancy rate of ....
IUD
Diaphragm/spermicidal jelly
Male condom
Female condom |
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Definition
IUD = 3/100
Diaphragm = 10/100
Male condom = 15/100
Female condom = > 15/100 |
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Term
| What appears to be the least effective form on contraceptive? |
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Definition
| Rhythm method (abstain during ovulation) |
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Term
| Roles of FSH and LH in men? |
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Definition
FSH - stimulates spermatogenesis in seminiferous tubules
LH - stimulates Leydig cells to produce testosterone |
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Term
| Where is gossypol obtained from? |
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Definition
Phenolic compound obtained from cottonseed
Used to decrease sperm production by destroying seminiferous tubules |
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Term
| Major problem reported with Gossypol? |
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Definition
| Hypokalemia - leads to transient paralysis |
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Term
| Use of estrogens as a contraceptive in men? |
|
Definition
Causes GNRH suppression and decreases spermatogenesis
However, too many adverse effects (loss of libido, female characteristics)
Tried to add androgens, but it become ineffective then |
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Term
|
Definition
Surgeon in Long; described cancer of the scrotum in young chimney sweeps
Soot-wart - due to chronic soot exposure |
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Term
|
Definition
In 1910, showed X-rays could cause cancer in rats
In 1914, others showed the same was true for humans |
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Term
|
Definition
| Produced cancer of the skin due to coal tar exposure to rabbit ears |
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Term
|
Definition
| Isolated polycyclic hydrocarbons that were carcinogens from coal tar |
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Term
|
Definition
| Showed bladder cancer in anniline dye workers |
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Term
| English poultry deaths in 1961? |
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Definition
Saw deaths of poultry due to liver cancer
Traced back to fungus, A. flavus, which produced aflatoxin (potent hepatic carcinogen) |
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Term
| What can cancer of the liver be attributed to in most developing countries? |
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Definition
Hepatitis B infection
Contamination of foods with aflatoxin |
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Term
| Why is colo-rectal cancer more common in the developed world? |
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Definition
| Due to western diet - high in saturated fat, low in fiber, fruit & veggies |
|
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Term
| Prevalence of liver cancer vs. colo-rectal cancer in the world? |
|
Definition
Liver - more prevalent in developing world
Colo-rectal - more prevalent in developed world |
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Term
| Causes of cancer death table, what are the top 2? |
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Definition
|
|
Term
| What percentage of cancer deaths is caused by tobacco? Nutrition? |
|
Definition
|
|
Term
| What caused the deaths of English poultry in the 1960s? |
|
Definition
| Aflatoxin - produced by the fungus A. flavus |
|
|
Term
| What does the effect smoking has on cancer development depend on? |
|
Definition
| Depends on the tar content of cigarettes, frequency, and duration of habit |
|
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Term
| What is the latent period between smoking & lung cancer? |
|
Definition
|
|
Term
| When did smoking habits increase in women vs. men? |
|
Definition
Men - from 1900-1960
Women - from 1920-30 |
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Term
| What dietary items are linked to cancer of the colo-rectal area & prostate? |
|
Definition
| Saturated animal fat & red meat |
|
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Term
| What do diets high in fruits and vegetables produce in our body? |
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Definition
| Cause blockage of cancer-causing chemicals produced in the body |
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Term
| Which viruses can cause liver cancer? |
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Definition
| Hep B virus and Hep C virus |
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Term
| Viral infections leading to cancer? |
|
Definition
HBV and HCV can cause liver cancer
HIV can cause Kaposi's sarcoma
HPV can cause cervical cancer
Epstein-Barr virus can cause a variety of cancers |
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Term
| In general, it can be said that carcinogens are.... |
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Definition
| Inactive; they are metabolically activated within the body |
|
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Term
| In terms of cancer, what must occur so that the change in DNA is permanent? |
|
Definition
|
|
Term
| What are 3 classes of carcinogens? |
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Definition
Initiators
Promoters
Progressors |
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Term
| Difference in carcinogenic function of initiators, promoters, and progressors? |
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Definition
Initiators - cause DNA damage to induce mutation
Promoter - favour growth of cancer cells in early stages; DO NOT damage DNA
Progressors - aid in tumor proliferation after it has already been established |
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Term
| What is the Delaney Amendment? |
|
Definition
| Added to food & drug act; prohibits use of any substance that has been shown to produce cancer in any experimental animals |
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Term
| What organism is used in the Ames test? |
|
Definition
| Mutant S. typhimurium that has lost the ability to synthesize histidine |
|
|
Term
|
Definition
Use mutant S. typhinurium which cannot synthesize His
Place in His free medium with a chemical
When the bacterium can grow, means mutation has occurred, therefore the chemical is a mutagen |
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Term
| What are the 6 categories of cancer treatment? |
|
Definition
Surgery
Chemotherapy
Radiation
Hormone-blocking or supplementing
Bone marrow transplantation
Biological therapies |
|
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Term
| Goals of cancer treatment? |
|
Definition
Primary goal = CURE
Other goals = reduce symptoms, prolong survival, provide support |
|
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Term
| Principles of cancer chemotherapy? |
|
Definition
Benefit-risk assessment
Mechanism of action of therapy
Adverse effects
Dosage & schedule
Combination chemotherapy |
|
|
Term
| What is the rational behind combination chemotherapy? |
|
Definition
Cancer cells less likely to defend against variety of drugs
Select drugs with different toxicities, so dose can be more effective |
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Term
|
Definition
| Nitrogen mustard used as an alkylating agent in chemotherapy |
|
|
Term
|
Definition
| Folic acid antimetabolite used in chemotherapy |
|
|
Term
|
Definition
Isolated from the Periwinkle plant
Natural product used to arrest cell division in chemotherapy |
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Term
|
Definition
| Cancer chemotherapeutic ANTIBIOTIC that damages DNA |
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|
Term
|
Definition
| Used to suppress the effects of estrogen; used in prevention of high risk breast cancer |
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|
Term
| What is prednisone used for in chemotherapy? |
|
Definition
| Hormone used to suppress cell division |
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|
Term
|
Definition
| Damages DNA; used in cancer chemotherapy |
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