Term
| Characterisistics of psychosis |
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Definition
Delusions
Hallucinations
Disorganized behavior and speech |
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Term
| The most common illness in which psychosis is observed |
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Definition
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Term
| Psychosis is seen in dementia, depression, severe metabolic disturbances |
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Definition
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Term
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Definition
| symptoms include psychosis, cognitive difficulties such as problems with memory and concentration, and negative symptoms such as apathy and low mood. |
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Term
| Prevalence of schizophrenia |
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Definition
| 1% in the general population |
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Term
| First antipsychotic used clinically |
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Definition
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Term
| One problem with current antipsychotics |
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Definition
| they still have trouble treating the negative and cognitive symptoms of schizo |
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Term
| Mechanism of action of antipsychotics |
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Definition
| most act on dopamine receptors |
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Term
| Evidence that antipsychotics act on DA receptors |
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Definition
Reserpine depletes brain DA and has antipsychotic actions
Amphetamines act to release DA which induces psychosis and antipsychotics blocks this
Antipsychotics block the peripheral and central actions of L-dopa, apomorphine, and bromocriptine DA receptor agonists |
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Term
| The dopaminergic system consists of cells in the |
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Definition
| midbrain and hypothalamus |
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Term
| The cells arising from the substantia nigra (midbrain) |
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Definition
| ascend to the striatum and are involved in motor control. Think of how striatum sounds like stride. In Parkinson's patients these cells die |
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Term
| Dopaminergic cells arising from the ventral tegmental area (VTA) project to |
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Definition
| the limbic and cortical regions |
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Term
| Two major families of dopamine receptors |
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Definition
D1-like
D2-like
Receptors are GPCRs and are localized pre and post synaptically |
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Term
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Definition
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Term
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Definition
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Term
| Which dopamine receptor family is more closely linked to antipsychotic action? |
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Definition
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Term
| Reasons antipsychotics are more closely linked to D2-like receptors |
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Definition
At clinically-effective concentrations, they only block D2 receptors
Selective D2 blockers are better antipsychotics
There's a good correlation between in vitro D2 affinities and their potencies as antipsychotics in vivo
There is a correlation between percentage of D2 receptors blocked and the antipsychotic response |
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Term
| The antipsychotic drug that resembles dopamine |
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Definition
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Term
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Definition
| has a higher affinity for D4 than D2 receptors and doesn't have the parkinsonian side effects |
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Term
| Functional effects of antipsychotics |
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Definition
decrease bizarre behaviors, delusions and hallucinations.
As a side effect, they block D2 receptors in the chemoreceptor trigger zone which induces anti-nausea and anti-vomiting effects |
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Term
| Side effects of antipsychotics |
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Definition
Parkinsonism such as akinesia (decreased bodily movement)
Akathisis - tremendous urge to move around
Pseudopregnancy
Neuroleptic malignant syndrome (NMS)
Tardive dyskinesia
Seizure at high doses |
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Term
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Definition
| decreased bodily movement |
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Term
|
Definition
| tremendous urge to move around |
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Term
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Definition
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Term
| Neuroleptic malignant syndrome (NMS) |
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Definition
| a life threatening disorder that consits of muscle rigidity, fever, delirium |
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Term
| If the GABA receptor is activated by acetlycholine (ACh), ie dopamine is blocked by antipsychotics, then |
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Definition
| then Parkinsonian symptoms can occur. Movement is affected |
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Term
| If the GABA receptor is activated by anticholinergic agents, ie Ach is blocked, then |
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Definition
| then you will not see Parksinsonian symptoms. Movement is not affected |
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Term
| Two disorders antidepressants are used to treat |
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Definition
| major depression and bipolar disorder |
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Term
| Diagnosis criteria for bipolar disorder |
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Definition
Must have depression for at least 2 weeks or mania for 1
Must have depressed mood, loss of interest in pleasurable activities, change in appetite, loss of energy
In mania, signs must be inflated self-esteem, decreased sleep, racing thoughs, excessive talkativeness |
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Term
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Definition
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Term
| Mechanism of action of affective disorders |
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Definition
| It's believed that affective disorders arise from defects in neurotransmission due to the underactivity of serotonin, dopamine and norepinephrine |
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Term
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Definition
| The monoamine hypothesis is a biological hypothesis stating that depression is caused by the underactivity in the brain of monoamines, such as dopamine, serotonin, and norepinephrine. |
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Term
| Classes of antidepressant drugs |
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Definition
Tricyclic compounds
Monoamine oxidase (MAO) inhibitors
Selective serotonin reuptake inhibitors (SSRIs)
Serotonin-norepinephrine reuptake inhibitors (SNRIs)
Dopamine reuptake inhibitors (DRIs) |
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Term
| Antidepressant drugs have a delayed onset of action of 2-4 weeks. This is due to |
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Definition
| the slowness of adapting to the biochemical changes caused by these drugs |
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Term
| Tricyclic antidepressants |
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Definition
3 ring shape obviously
Doesn't elevate mood in healthy individuals but does in 2-4 weeks in depressed individuals
These inhibit the uptake of norepinephrine and serotonin. A consequence of this is that they downregulate brain beta-adrenoreceptors and sensitize postsynaptic serotonergic receptors (i guess they're basically saying this makes it more likely for the nuerotransmitter to bind to the beta-adrenoceptor since there's a higher concentration of neurotransmitter now)
examples include Tofranil |
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Term
| Monoamine oxidase inhibitors (MOA inhibitors) |
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Definition
example is Iproniazid
Works by (like its name) inhibiting the monamine oxidase enzyme. There are two MAOs (A and B) and the A one is the one more important in relieving depression. This inhibition leads to an increase of NE, DA, and serotonin(the most important)
Results aren't seen until 2-3 weeks later |
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Term
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Definition
| A monoamine oxidase inhibitor anti-depressant drug that was originally designed to treat tuberculosis but it was noticed that patients with tuberculosis showed an improvement in their mood |
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Term
| Side effects of MAOIs and TCAs |
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Definition
excessive CNS stimulation
Peripheral vascular effects
Atropine-like effects (dry mouth, constipation, g.i. disturbances) |
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Term
| Notable drug interactions with MAOIs and TCAs |
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Definition
| patients shouldn't take cough/cold medicines and should avoid foods high in tyramine such as cheese, alcohol and yeast.. Tyramine causes the release of monoamines and so this can cause a crisis (the cheese effect) |
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Term
| Selective serotonin reuptake inhibitors (SSRIs) |
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Definition
Obviously act on the 5-HT (serotonin) system
Because it has a greater selectivity, it has fewer side effects because they have little effect on DA and NE uptake
They all inhibit 5-HT uptake
Takes several weeks for them to act
examples include Zoloft and Prozac
Side effects: loss of appetite, sleep problems, loss of interest in sex) |
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Term
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Definition
Acts by inhibiting norepinephrine and serotonin uptake
Used to treat major depression, anxiety, OCD and ADHD
examples: Cymbalta, Effexor
Side effects: loss of appetite, sleep problems, loss of interest in sex)
MOST WIDELY USED ANTIDEPRESSANTS |
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Term
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Definition
Acts by inhibiting dopamine reuptake (excess dopamine...yeah!!)
Has a high abuse liability because it has stimulant effects and is reinforcing.
Used to treat major depression, narcolepsy, ADHD and smoking
Side effects: psychosis if overdosed, seizures, hypertension
Example: Wellbutrin, has a slow onset and long half life |
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Term
| Antipsychotics used to treat depression |
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Definition
Abilify and risperidone
Helps treat residual symptoms so it can't be prescribed alone to treat depression
Acts by blocking serotonin-2A, affects 2C and is a partial agonist to D2 receptors |
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Term
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Definition
used to treat manic patients. stabilizes their mood without causing drowsiness or motor incoordination
Acts by blocking adenylyl cyclase and the inositol cycle. So it basically antagonizes second messenger systems |
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Term
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Definition
| patients with panic disorder respond will to MAOIs, TCAs, and SSRIs |
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Term
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Definition
| SSRIs are useful in the treatment of OCD |
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Term
| First clinically useful antibiotic |
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Definition
| penicillin discovered by Fleming |
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Term
| Selective toxicity for antibiotics |
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Definition
| Basically antibiotics need to be able to attack targets present in bacteria but won't affect humans |
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Term
| Pathogen/Host interaction |
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Definition
| A pathogen infects the host and the host will respond with an immune response, a defense reaction, or disease |
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Term
| Pathogen/Drug interaction |
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Definition
| A drug acts on pathogens and a pathogen can respond by resisting |
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Term
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Definition
| A drug is administered by selective toxicity and the host may respond with allergy or toxic effects |
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Term
| Sites of action of antibiotics |
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Definition
Bacterial cell wall
Bacterial cell membrane
Bacterial cell proteins
Bacterial nucleic acids |
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Term
| Antibiotics can be either bacteriostatic, bactericidal, or both |
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Definition
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Term
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Definition
| describes antibiotics that don't kill bacteria but rather stops their growth |
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Term
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Definition
| describes antibiotics that kill bacteria |
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Term
| Antibiotics that act on cell walls |
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Definition
Cycloserine
Bacitracin
Vancomycin
Penicillin
Cephalosporins - binds to the active site of the enzyme responsible for cross-linking thus inhibiting its function |
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Term
| Antibiotics that act on cell membranes |
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Definition
polymyxins
amphotericin B
nystatin
Mostly used topically since they can affect human cell membranes |
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Term
| Antibiotics that affect the synthesis of bacterial cell proteins |
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Definition
aminoglycosides
tetracylines
chloramphenicol
Macrolides |
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Term
| Antibiotics that act on nucleic acids |
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Definition
5-fluorocytosine
Bacteria have to make their on folic acid and so these antibiotics interfere in that process |
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Term
| Antibiotics affecting cell walls result |
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Definition
| During bacteria growth, the bacteria cell elongates, a cross wall forms, and the cell divides at this wall creating a new cell. Antibiotics act by making cross wall formation defective which either results in an abnormally elongated cell which is genetically inferior, or a cell that ruptures due to excessive internal pressure (sheroplast) |
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Term
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Definition
| an antibiotic that binds to the 30s subunit which interferes with the binding of the tRNA to the mRNA |
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Term
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Definition
| blocks 'A' site binding and also interferes with the binding of the tRNA to the mRNA |
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Term
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Definition
| interferes with the peptidyl transferase so the amino acid won't bind to the growing peptide chain |
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Term
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Definition
| L-alanine is converted to D-alanine in the cytoplasm and these two link up to form 2 D-alanine molecules. The next step is two link this dipeptide to 3 other amino acids and a sugar. This whole complex is then linked to a lipid carrier molecule and transported through the cell membrane to the cell wall where it is added. Final step is the cross-linking of the polymer strands |
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Term
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Definition
| antibiotic that inhibits the linking of two D-alanine molecules in cell wall formation |
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Term
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Definition
| antibiotic that acts by interfering with the carrier molecule in cell wall formation |
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Term
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Definition
| antibiotic that acts by preventing the transfer of the sugar pentapeptide (two D-alanine molecyles, 3 other amino acids, and an amino sugar) from the carrier molecule to the growing cell wall |
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Term
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Definition
| binds to the active site of the enzyme responsible for cross-linking thus inhibiting its function in cell wall formation |
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Term
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Definition
| antibiotics that bind to the active site of the enzyme responsible for cross-linking thus inhibiting its function in cell wall formation |
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Term
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Definition
| antibiotics that are large polypeptides with polar and hydrophobic environments. Because of this they can act as cationic detergents and bind to the phospholipid groups of cell membranes. This leads to disorganization of cell membranes and eventually cell death |
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Term
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Definition
| Has the same mechanism of polymyxins except they act on fungi |
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Term
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Definition
| Has the same mechanism of polymyxins except they act on fungi |
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Term
|
Definition
| similar mechanism to chloramphenicol |
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Term
| Antibiotic resistance example |
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Definition
| penicillin once being effective towards treating staph infection but not anymore |
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Term
| Bacteria can develop resistance to more than one antibiotic |
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Definition
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Term
| Mechanism of antibiotic resistance |
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Definition
| basically it's the inheritance of resistance plasmids. Usually these plasmids will have 6-7 resistance genes |
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Term
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Definition
| extra-chromosomal genetics elements that arose from collections of foreign genes |
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Term
| Examples of products of genes on R-plasmids |
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Definition
Products in the cell walls that prevent antibiotics from entering
Enzymes that modify the site of drug action so antibiotic can no longer bind
Enzymes that destroy the antibiotic
Enzymes that are resistant to the antibiotic
Active transport systems that remove antibiotic from the bacterium |
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Term
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Definition
| transfer of resistance genes through a sex pilus betweeen 2 bacteria cells |
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Term
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Definition
| resistance genes is transferred to bacteria by a bacteriophage (virus) |
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Term
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Definition
| resitance genes in the environment is uptaked by the bacteria |
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Term
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Definition
| when genes change their positions in plasmids and chromosomes |
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Term
| Why antiviral medication development has been slow |
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Definition
| Viruses use the host's metabolic machinery so it's hard to be selective because you're using human parts. So the primary approach has become to just prevent viral infections |
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Term
| Viruses are either single or double stranded DNA or RNA |
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Definition
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Term
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Definition
Infection
Replication
Release |
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Term
| Infection of a virus in the viral infection process |
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Definition
virus binds to plasma membrane receptors, it gets absorbed in by phagocytosis, and the protein coat of the viral cell is uncoated so it's nucleic acids are exposed to start the replication process
For RNA viruses, this process is facilitated by Hemagglutinin. Additionally, a low pH will cause the M2 protein to uncoat |
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Term
| Replication of a virus in the viral infection process |
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Definition
Viral DNA is replicated obviously and Viral DNA-dependent RNA polymerase and RNA-dependent RNA polymerase catalyze the synthesis of mRNAs to make viral proteins. These proteins become structural proteins, viral enzymes and regulatory proteins which are packaged into a virion
For an RNA virus, the process is similar except the RNA is replicated |
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Term
| Release of a virus in the viral infection process |
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Definition
| virus particles either leak or burst out the cell |
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Term
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Definition
responsible for Spanish flu, swine flu, Asian flu, Hong Kong flu, and Russian flu
has different strands (H1N1, H2N2, H3N2, etc)
which vary in the Hemagglutinin and neuraminidase proteins
swine flue is a reassortment of several strains of H1N1 |
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Term
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Definition
produces acute encephalitis (inflammation of the brain) if not treated in time. Alters behavior to maximize chances for transmission (aggression, biting)
Enters brain by following peripheral nerves
Produces flu-like symptoms initially, later confusion, paranoia, terror
Antivirals are useless against rabies
Post-exposure vaccinations are effective until the virus gets into the nervous system |
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Term
| Factors that determine success of antiviral therapy |
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Definition
Age
type of disease and immune system of patient
stage of illness
dose
ability of virus to remain latent
ability of virus to penetrate CNS
ability of virus to develop resistance |
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Term
| 3 Major groups of antiviral chemotherapeutics |
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Definition
virucidal - directly inactivate viuses
antiviral - inhibit viral replication
immunomodulating - changes host's response to infection |
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Term
| How do antiviral drugs work? |
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Definition
Decreases viral penetration or uncoating, inhibits enzymes specific for viral genome replication, inhibits viral mRNA translation, interferes with viral regulatory proteins, interferes with viral assembly, interfers with viral release from cell.
So basically, they interfere with every step of viral infection |
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Term
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Definition
Amantadine
Tamiflu
Acyclovir
Lamivudine |
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Term
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Definition
| inhibits the function of the viral envelope ion channel (M2) of influenza A which interferes with viral cell uncoating |
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Term
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Definition
used to treat influenza A and B
inhibits the enzyme neuraminidase which decreases the release of viral particles |
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Term
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Definition
a nucleoside analogue that inhibits viral DNA polymerase and leads to chain termination once it's inserted
It gets activated by herpes thymidine kinase |
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Term
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Definition
| acts as a nucleoside analogue reverse transcriptase inhibitor so basically you can't make DNA from RNA |
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Term
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Definition
| a protein used to help the viral cell leave the cell membrane |
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Term
| Highly active antiretoviral therapy (HAART) |
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Definition
| involves giving patients 3-4 drugs concurrently with different classes of drugs acting at different phases of the HIV life cycle |
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Term
| Drug cocktails used against HIV |
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Definition
| include: nRTIs, non-nucleotide reverse transcriptase inhibitors (NNRTI), protease inhibitors, integrase inhibitors, entry inhibitors, maturation inhibitors |
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Term
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Definition
| inhibit reverse transcription |
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Term
| NNRTIs (non-nucleotide reverse transcriptase inhibitors) |
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Definition
| bind to enzyme and affect its function |
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Term
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Definition
inhibits the enzyme activity of HIV-protease.
HIV protease creates mature protein components of the HIV virus so this is inhibited |
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Term
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Definition
| affect integration of viral DNA into host DNA |
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Term
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Definition
| affect binding, fusion or entry of virus |
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Term
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Definition
| interfere with creation of mature capsid |
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Term
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Definition
proteins released by host cells to trigger the immune system after infection. Also communicates with other host cells about the attack
Have antiviral, immunomodulatory and antiproliferative activities
Can increase p53 activity in virus-infected cells to trigger apoptosis
Act through |
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