Term
| What CNS structures are involve din the dopamine reward pathway? |
|
Definition
| Ventral tegmental area -> dopamine producing neurons -> activation of mesolimbic dopamine system (Dopamine reward pathway) |
|
|
Term
| What is metabolic tolerance? |
|
Definition
| Stimulation of metabolism allows for increased drug elimination with long-term use |
|
|
Term
| What is pharmacodynamic tolerance? |
|
Definition
| Cellular tolerance: biochemical adaptation-changes in neurotransmitter levels and receptor numbers and activity |
|
|
Term
| What metabolizes ethanol? |
|
Definition
| Alcohol dehydrogenase and the microsomal ethanol oxidizing system (MEOS) |
|
|
Term
| ADH has a fixed capacity to metabolize ethanol at what rate? |
|
Definition
|
|
Term
| How does ethanol tolerance develop? Ethanol tolerance increases the tolerance for what other substances? |
|
Definition
CNS adaptation and increased rate of ethanol metabolism
Cross tolerance to sedative-hypnotic drugs (benzodiazepines and barbiturates) |
|
|
Term
| What are the toxic effects of ethanol? |
|
Definition
Progressive loss of liver function
Inhibition of gluconeogenesis: Hypoglycemia
Pancreatitis
Peripheral neuropathies
Wernicke-Korsakoff syndrome
Gynecomastia, testicular atrophy, edema
GI irritation and inflammation
Fetal Alcohol Syndrome |
|
|
Term
| What are the characteristics of fetal alcohol syndrome? |
|
Definition
Mental retardation (most common)
Growth deficiencies
Microcephaly
Underdevelopment of the midface region
Facial abnormalities associated w/heavy consumption during 1st trimester |
|
|
Term
| What is the MoA of Disulfuram use in the treatment of alcoholism? |
|
Definition
Inhibits acetaldehyde dehydrogenase
Minimal amounts of alcohol will cause “disulfiram reaction” |
|
|
Term
| What is the MoA of Acamprosate use in the treatment of alcoholism? |
|
Definition
| Lowers the activity of receptors for glutamate for maintenance of abstinence |
|
|
Term
| What are benzodiazepines used for in the treatment of alcoholism? |
|
Definition
| Used for alcohol withdrawal to prevent delirium or seizures |
|
|
Term
| How is propanolol used for in the treatment of alcoholism? |
|
Definition
| Used for alcohol withdrawal to reduce tremors and reduction of heart rate and blood pressure |
|
|
Term
| What is the MoA of cocaine? |
|
Definition
Blocks dopamine transporter that recovers DA from the synapse-buildup of DA in the synapse, contributes to the pleasurable effects
Blocks both NE and serotonin re-uptake |
|
|
Term
| What are the short term physiological effects of cocaine? |
|
Definition
Increased energy
Decreased appetite
Mental alertness
Increased heart rate and blood pressure
Constriction of blood vessels
Increased temperature
Dilated pupils |
|
|
Term
| What are the potential cardiovascular effects of cocaine use? |
|
Definition
Arrhythmias
Myocardial infarction
Increased heart rate
Increased BP |
|
|
Term
| What are the potential respiratory effects of cocaine use? |
|
Definition
Chest pain
Respiratory failure |
|
|
Term
| What some notable signs that a patient has been abusing cocaine? |
|
Definition
Loss of smell sensation, nosebleeds, problems with swallowing, hoarseness, irritation of the nasal septum, chronically inflamed runny nose, IV users-allergic reactions
Auditory hallucinations |
|
|
Term
| Ingested cocaine causes what? |
|
Definition
| Severe bowel gangrene due to vasoconstriction |
|
|
Term
| What maternal complications are associated with cocaine abuse? |
|
Definition
| Malignant hypertension, cardiac ischemia, cerebral infarction, and sudden death |
|
|
Term
| What are the fetal effects of cocaine abuse during pregnance? |
|
Definition
Spontaneous abortion and death in utero
High risk of premature rupture of membranes, preterm labor and delivery, IUGR, abruptio placentae
Newborns display tremulousness, irritability and suckling problems
Cognitive and neurobehavioral problems
Lack of coordination
Visual problems |
|
|
Term
|
Definition
| Stimulation or presynaptic and postsynaptic serotonin receptors. |
|
|
Term
|
Definition
| Blocks NMDA-type glutamate receptors in cortex and limbic structures (ion channels) |
|
|
Term
| What is the MoA of methamphetamines? |
|
Definition
Dopaminergic and adrenergic reuptake inhibitor, similar to cocaine |
|
|
Term
| What are the side effects of methamphetamine abuse? |
|
Definition
Drug craving
Weight loss
Depression
Tooth decay (“meth mouth”)
Neurotoxicity
Paranoia, hallucinations |
|
|
Term
| What are the side effects of MDMA abuse? |
|
Definition
| In high doses, can interfere with the body’s ability to regulate body temperature (resulting in liver, kidney and CV system failure) |
|
|
Term
| How is methamphetamine differentiated from cocaine? |
|
Definition
| Lasts much longer (8-24hrs vs. 20-30min) 1/2 life is 12hrs vs 1hr Is man made (cocaine is plant derived) |
|
|
Term
| Methadone is indicated for what use? |
|
Definition
Treatment of opioid withdrawal
Short-term detoxification (30 days) or long-term detoxification (180 days) |
|
|
Term
| What is the most obvious sign that someone has been abusing marijuana? |
|
Definition
| Reddening of the conjunctiva |
|
|
Term
| Buprenorphine is indicated for what use? |
|
Definition
Initial treatment of opiate withdrawal
Can also use Buprenorphine + Naloxone for maintenance treatment for addiction |
|
|
Term
| What is the "date rape drug? |
|
Definition
| Flunitrazepam (Benzodiazepine) |
|
|
Term
| How is Alpralozam used as a party drug? |
|
Definition
Z-bars, Zandy bars, Zannies
Used to curb the need for alcohol
However, mixing with alcohol can be disasterous |
|
|
Term
| What is used to treat benzodiazepine intoxication? |
|
Definition
|
|
Term
| What is used to treat benzodiazepine withdrawal or detoxification? |
|
Definition
| Chlordiazepoxide or lorazepam tapered over 5-7days |
|
|
Term
| What drug characteristics increase the chance it will be secreted in breast milk? |
|
Definition
Lower molecular weight
Lower protein binding
Weakly basic
Greater lipid solubility |
|
|
Term
| Generally, likelihood of adverse reaction to maternal medication declines with what? |
|
Definition
| Increasing age of the infant |
|
|
Term
| Why should breastfeeding mothers avoid quinolones? |
|
Definition
| Greater concentration in breast milk than in serum; associated with arthropathy and photosensitivity |
|
|
Term
| What medications can be passed in breast milk to can induce hemolytic reactions in cases of infant G6PD deficiency? |
|
Definition
| Nitrofurantoin, sulfamethoxazole |
|
|
Term
| What are the galactogogues? |
|
Definition
Domperidone
Metoclopramide |
|
|
Term
| What are the lactation suppressors? |
|
Definition
Estrogrens
Cabergoline
Levodopa
Bromocriptine
Antihistamines
Pseudoephedrine
Alcohol
Nicotine
Bupropion
Diuretics
Testosterone |
|
|
Term
| How does drug absorption change within the first few days of life? |
|
Definition
Stomach pH drops within 24 hours of birth
Gastric emptying is delayed for first few days
Both passive and active transport probably developed by 4 months |
|
|
Term
| How does protein binding differ in newborns? |
|
Definition
Lower protein concentration, lower affinity for drug binding, competition with endogenous compounds (bilirubin)
Even lower in premature infants |
|
|
Term
| How does protein binding affect drug dosage in newborns? |
|
Definition
| Lower plasma protein concentration requires larger loading dose |
|
|
Term
| What can displace bilirubin and cause Kernicterus? |
|
Definition
|
|
Term
| How does body fat composition in neonates impact drug distribution? |
|
Definition
Significantly less body fat than children and adults
Lipophilic medications may require smaller loading dose due to lower volume of distribution
Relevant also in breastfed infants since highly lipid-soluble medications are deposited in breastmilk |
|
|
Term
| How is drug metabolism different in infants? What pathways are delayed? |
|
Definition
Generally slower in infants
Glucuronidation and oxidation pathway activity is delayed up to one year
Sulfation pathway is well-developed |
|
|
Term
| How does metabolism in infants impact the effective dosages of morphine? |
|
Definition
| Greater concentrations of morphine due to decreased metabolism to the active 6-glucuronide metabolite |
|
|
Term
| More than 2/3 of dosing errors occur in what demographic? |
|
Definition
Children
More common in sicker patients, and those with urgent or complex medical conditions |
|
|
Term
| What are the consequences of Floroquinolone administration to neonates? |
|
Definition
Permanent lesions in the cartilage of weight-bearing joints
Reversible arthralgia +/- synovial effusion |
|
|
Term
| Despite the dangerous side effects, floroquinolones are still used in infants for what treatments? |
|
Definition
Post-exposure inhalation anthrax
Complicated UTI/pyelonephritis (E.coli) |
|
|
Term
| What are pharmacokinetics? |
|
Definition
“What the body does to the drug”
Impacted by absorption, body distribution, metabolism, and elimination |
|
|
Term
| How does absorption change with age? |
|
Definition
No direct significant change with age but affected by changes in :
Achlorhydria
Prolonged transit time in gut
Competing compounds, especially OTC’s |
|
|
Term
| How does body distribution changes with age impact drug distribution? |
|
Definition
Decreased water and lean muscle mass as % of body weight decreases Vd of hydrophilic drugs
Increased fat as % of body weight Increases Vd of lipophilic drugs |
|
|
Term
| The changes in body distribution with age due to decreased body water and increased body fat mainly affects what dosages? |
|
Definition
| Loading dose of drugs like digoxin or warfarin |
|
|
Term
| How does live function change with age? |
|
Definition
| Variable decline in the ability to metabolize drugs, mainly related to change in liver size and blood flow |
|
|
Term
| What metabolic functions remain preserved or increase with age? |
|
Definition
Acetylation and conjugation
Phase I metabolism (creation of active metabolites via oxidation/reduction) is increased |
|
|
Term
| What metabolic functions decrease with age? |
|
Definition
Oxidative metabolism (cytochrome P450 system), resulting in variably decreased clearance of drugs
Phase II metabolism (creation of inactive metabolites via conjugation) |
|
|
Term
| What factors have a far greater effect on drug metabolism than age alone? |
|
Definition
| Genetics, nutrition, environmental exposure, disease, and other drugs |
|
|
Term
| What are the characteristics of an ideal drug for an older adult? |
|
Definition
| Undergoes phase II metabolism and does not compete for, induce or suppress its own metabolism |
|
|
Term
| How does elimination change with age? |
|
Definition
Kidney is main organ of elimination
One third of older adults have truly preserved creatinine clearance (means 2/3 of older adults do not)
Serum creatinine tends NOT to change with age but this is falsely encouraging due to changes in muscle mass, etc. |
|
|
Term
| What are pharmacodynamics? |
|
Definition
“What the drug does to the body”
Affected by transmitters, receptors, and second messengers |
|
|
Term
| What homeostatic mechanisms diminish with age? |
|
Definition
Postural blood pressure control
Posture control
Extrapyramidal functions
Cognitive function
Thermoregulation |
|
|
Term
| Why is it difficult to account for pharmacodynamic changes with age? |
|
Definition
Difficulty in accounting for baseline differences
Dependence on cultural/educational differences
Assumes mean changes between age groups reflect changes in the individual over time
Birth cohort effects confound those of age
Selective mortality effects |
|
|
Term
| What causes the change in response to CNS active drugs with age? |
|
Definition
Altered neurotransmitters/receptors
Hormonal changes (sex and growth hormones)
Impaired cerebral glucose metabolism
Decreased oxygen with cerebrovascular changes
Better CNS penetration with age (reduced p-glycoprotein activity |
|
|
Term
| Why are Benzodiazepines rarely prescribed to the elderly? |
|
Definition
Association with falls, hip fractures
Caused by changes in CNS response, demonstrated by EC50 of midazolam decreased by 50% in older adults |
|
|
Term
| How does the response to anesthetics change with age? |
|
Definition
|
|
Term
| How does the response to neuromuscular blockers change with age? |
|
Definition
| No change in sensitivity but decreased dosing requirements due to changes in pharmacokinetics |
|
|
Term
| How does the response to opioids change with age? |
|
Definition
| Increased sensitivity as well as changed pharmacokinetics |
|
|
Term
| How does the response to ACE-inhibitors change with age? |
|
Definition
No direct change with age but there is a decrease in sensitivity after repeated dosing (seen in both age groups, enzyme induction)
Older adults more likely to be orthostatic, lightheaded |
|
|
Term
| How does the response to dihydropyridines Ca++ blockers change with age? |
|
Definition
| greater response observed in treatment-naïve elderly, diminishes in as little as three months |
|
|
Term
| How does the response to non-dihydropyridines Ca++ blockers change with age? |
|
Definition
Decrease in sensitivity of PR response (which is prolonged in the young)
Enhanced HR and BP responses |
|
|
Term
| How does Beta-sensitivity change with age? |
|
Definition
Decreases with age, may be related to G proteins
Exception: activity of β-blockers in elderly with very high blood pressure |
|
|
Term
| How does the pharmacodynamic response to diuretics change with age? |
|
Definition
| No change in drug sensitivity with age |
|
|
Term
| What is the greatest predictor of the response to diuretics? |
|
Definition
GFR
Diuretics further ↓ GFR |
|
|
Term
| HCTZ is not an effective anti-hypertensive if CrCl is what value? |
|
Definition
|
|
Term
| How does the response to anticoagulants change with age? |
|
Definition
Increased risk of pathologic bleeding
Warfarin – no pharmacokinetic effect but greater decrease in K-dependent clotting factor synthesis |
|
|
Term
| What is one of the greatest predictor of anticoagulant response? |
|
Definition
|
|
Term
| What is the primary prevention of serotonin syndrome? |
|
Definition
|
|
Term
| What are the symptoms of serotonin syndrome? |
|
Definition
Agitation, confusion, tachycardia, headache, diaphoresis, diarrhea
Mydriasis*, hyperactive bowel sounds*, hyperreflexia*
Develops in minutes to hours |
|
|
Term
| What are the symptoms of neuroleptic malignant syndrome? |
|
Definition
*Muscle rigidity – “lead pipe”
Autonomic dysregulation
Hyperthermia (hours to days after exposure)
Altered mental status (even coma)
Normal/decreased bowel sounds*, bradyreflexia*, elevated aminotransferases* and rhabdomyolysis*
Usually develops within first two weeks of treatment |
|
|
Term
| What causes neuroleptic malignant syndrome? |
|
Definition
|
|
Term
| How do you treat neuroleptic malignant syndrome? |
|
Definition
Mild: benzodiazepine
Moderate: dopaminergic agonist (bromocriptine)
Severe: dantrolene to address muscle rigidity
Use atypical antipsychotics in future |
|
|
Term
| What causes Parkinsonism-hyperpyrexia syndrome |
|
Definition
| Withdrawal/decrease, dopaminergic medications*, amantadine, and anticholinergics |
|
|
Term
| How is Parkinsonism-hyperpyrexia syndrome treated? |
|
Definition
Dopaminergics, supportive care +/- methylprednisolone
Important that patients going into surgery still receive their Parkinson’s Disease medications |
|
|
Term
| What causes Parkinsonian dyskinesia? |
|
Definition
Levodopa-induced
Related to disease severity and dose
Use of dopamine agonist as initial therapy can delay
Exhausting if prolonged, risk of rhabdomyolysis |
|
|
Term
| How is Parkinsonian dyskinesia treated? |
|
Definition
| Lower dose of dopaminergics, mild benzodiazepine for dyskinesia; amantadine |
|
|
Term
| What causes acute dystonic reactions? |
|
Definition
Neuroleptics/antiemetics
Usually occurs ≤ 24 hrs after medication
Rx: Stop ppt’ing medication, use anticholinergics |
|
|
Term
|
Definition
| Opiate toxicity or withdrawal |
|
|
Term
| What are the severe consequences of Baclofen withdrawal? |
|
Definition
|
|
Term
| What are the primary uses of biologic induction therapy? |
|
Definition
Delay the use of the nephrotoxic calcineurin inhibitors
Intensify the initial immunosuppressive therapy in patients at high risk of rejection |
|
|
Term
| While polyclonal antibodies are highly effective immunosuppressive agents, they have what drawback? |
|
Definition
| Vary in efficacy and toxicity from batch to batch |
|
|
Term
| What are the pros and cons of monoclonal antibodies compared to polyclonal antibodies? |
|
Definition
| Do not have the problems of variability in efficacy and toxicity but are more limited in their target specificity |
|
|
Term
| What is the MoA of Antilymphocyte Antibodies (ALG)? |
|
Definition
Primarily act on small, long-lived lymphocytes
With continued use “thymus dependent” lymphocytes are depleted
Destruction or inactivation of T cells can impair DTH and cellular immunity |
|
|
Term
| What are the important potential toxic effects of ALGs? |
|
Definition
Histocytic lymphomas
Increased risk of cancer
Risk of anaphylaxis and serum sickness |
|
|
Term
| What is the MoA of Antithymocyte Antibodies (ATG)? |
|
Definition
Contains cytotoxic antibodies that bind to CD markers and HLA class I and II molecules on the surface of human T lymphocytes
Deplete circulating lymphocytes by direct cytotoxicity (both complement and cell-mediated)
Block lymphocyte function by binding to cell surface molecules involved in the regulation of cell function |
|
|
Term
| What are ATGs indicated for? |
|
Definition
Acute renal transplant rejection
Acute rejection of other types of organ transplants and for prophylaxis of rejection
Reducing the severity of GVHD after BMT
Mean T-cell counts fall by day 2 of therapy |
|
|
Term
| What are the important potential toxic effects of ATGs? |
|
Definition
Leukopenia and thrombocytopenia
Increased risk of infection and malignancy |
|
|
Term
| What is the MoA of Muromonab-CD3 mAb? |
|
Definition
Binds to the e chain of CD3 on the T-cell receptor complex involved in antigen recognition, cell signaling, and proliferation
Induces rapid internalization of the T-cell receptor, preventing antigen recognition
Rapidly depletes T cells and reduces function by decreasing IL-2 production |
|
|
Term
| Muromonab-CD3 mAb is indicated for what use? |
|
Definition
| Acute organ transplant rejection |
|
|
Term
| What are the drawbacks of repeated Muromonab-CD3 mAb use? |
|
Definition
| Results in the immunization of the patient against the mouse determinants of the antibody which can neutralize and prevent efficacy |
|
|
Term
| What are the important potential toxic effects of Muromonab-CD3 mAb? |
|
Definition
Cytokine release syndrome
Attributed to increased serum levels of cytokines |
|
|
Term
| What can help prevent cytokine release syndrome associated with Muromonab-CD3 mAb? |
|
Definition
| Administration of glucocorticoids (prednisone) before injection, now a standard procedure |
|
|
Term
| What is the significant about the structure of Daclizumab? |
|
Definition
| Chimeric monoclonal antibody that binds to CD25 |
|
|
Term
| What is the MoA of Daclizumab? |
|
Definition
| Binds CD25, blocks IL-2 from binding to activated lymphocytes |
|
|
Term
| Daclizumab is indicated for what use? |
|
Definition
| Prophylaxis of acute organ rejection in renal transplants |
|
|
Term
| What are the side effects of Daclizumab (IL-2 blocking chimeric monoclonal ab)? |
|
Definition
| Diarrhea, vomiting, fever, prutitus, respiratory tract infections, and UTI |
|
|
Term
| What is the MoA of Basiliximab? |
|
Definition
Chimeric human-mouse IgG1 monoclonal antibody similar to Daclizumab
Binds to IL-2 receptor alpha chain on activated lymphocytes
Used for prophylaxis of acute organ rejection in renal transplants |
|
|
Term
| What types of drugs are involved in maintenance immunotherapy? |
|
Definition
A calcineurin inhibitor
Glucocorticoids
Mycophenolate mofetil
Each are directed at a discrete site in T-cell activation |
|
|
Term
| What are the calcineurin inhibitors? |
|
Definition
Cyclosporine
Tacrolimus
Sirolimus |
|
|
Term
| What is the MoA of Cyclosporine? |
|
Definition
Forms a complex with cyclophyilin that inhibits calcineruin, which is required for the transcription factor (NF-AT) involved in the synthesis of IL-2 by activated T cells
Inhibits the gene transcription of IL-2***, IL-3, IFN-γ, and other factors stimulated by antigen-stimulated T cells |
|
|
Term
| What are the potential side effects of Cyclosporine? |
|
Definition
Nephrotoxicity
Hirsutism
Hypertension |
|
|
Term
| What is the MoA of Tacrolimus? |
|
Definition
Binds to cyclophilin and also binds to immunophilin FK-binding protein (FKBP)
Inhibits calcineurin in order to prevent the production of IL-2 |
|
|
Term
| Tacrolimus is indicated for what use? |
|
Definition
Used mostly in organ transplantation
Atopic dermatitis and psoriasis |
|
|
Term
| What is the MoA of Sirolimus? |
|
Definition
Works downstream of the IL-2 receptor to binds FKBP, creating a complex that inhibits the mammalian target of rapamycin (mTOR), a kinase involved in cell-cycle progression (proliferation
Does NOT** block interleukin production by T-cells |
|
|
Term
| Sirolimus is indicated for what use? |
|
Definition
Solid organ transplantation
Topical preparations used in dermatologic disorders and uveoretinits |
|
|
Term
| What are the important toxic side effects of Sirolimus? |
|
Definition
| Myelosuppression, especially thrombcytopenia |
|
|
Term
| What are the effects of glucocorticoids on the immune response? |
|
Definition
Rapid, transient decrease in peripheral lymphocyte count
Increased apoptosis of activated cells by increasing IkB expression, thereby inhibiting activation of NF-kB
Neutrophils and monocytes display poor chemotaxis and decreased lysosomal enzyme release
Key proinflammatory cytokines such as IL-1 and IL-6 are downregulated
T cells are inhibited from making IL-2 and proliferating |
|
|
Term
| What is the MoA of Mycophenolate mofetil? |
|
Definition
Inhibits de novo synthesis of purines and thus inhibits a series of T and B lymphocyte responses
Hydrolyzed to mycophenolic acid (active immunosuppressant) |
|
|
Term
| Mycophenolate mofetil is indicated for what use? |
|
Definition
Solid organ transplant recipients (refractory rejection)
Steroid-refractory GVHD
Maintenance immunotherapy
Lupus nephritis, RA, dermatologic disorders |
|
|
Term
| What are the important toxic side effects of Mycophenolate mofetil? |
|
Definition
| Myelosuppression, especially neutropenia*** |
|
|
Term
| What is the MoA of Azathioprine? |
|
Definition
Slowly converted to 6-mercaptopurine, which is then metabolized to 6-thioinosinic acid
6-thioinosinic acid inhibits inosinic acid, required in purine nucleic acid metabolism |
|
|
Term
| Azathioprine is indicated for what use? |
|
Definition
Renal allografts and other transplant tissues
Acute glomerulonephritis, renal component of SLE, RA, Crohn’s disease, and MS
Prednisone-resistant antibody-mediated idiopathic thrombocytopenia purpura and autoimmune hemolytic anemia |
|
|
Term
| Azathioprine should have its dose reduced to 1/3 or 1/4 normal dosage when taken alongside what drug? |
|
Definition
| Allopurinol, metabolite inhibits xanthine oxidase, a key enzyme for renal excretion |
|
|
Term
| What is the MoA of Cyclophosphamide? |
|
Definition
Alkylating agent
Destroys proliferating lymphoid cells
At high doses this medication can induce apparent specific tolerance to a new antigen (can "reboot" the immune system) |
|
|
Term
| Cyclophosphamide is indicated for what use? |
|
Definition
MS, SLE autoimmune hemolytic anemia, antibody-induced pure red cell aplasia, and Wegener’s granulomatosis
DOES NOT prevent GVHD |
|
|
Term
| What are the significant toxic side effects of Cyclophosphamide? |
|
Definition
| Pancytopenia and hemorrhagic cystitis |
|
|
Term
| What is the MoA of methotrexate? |
|
Definition
| Interferes with thymidine synthesis and block DNA synthesis |
|
|
Term
| Methotrexate is indicated for what use? |
|
Definition
|
|
Term
| What therapies are used for treated established transplant rejection? |
|
Definition
Glucocorticoids in high doses (pulse therapy)
Polyclonal ALGs
Muromonab-CD3 mAb |
|
|
Term
| Patients with high levels of anti-HLA antibodies should receive what treatments in order to avoid transplant rejection? |
|
Definition
Plasmapheresis
IV immunoglobulin |
|
|
Term
| Prednisone is the drug of choice for the treatment of what autoimmune diseases? |
|
Definition
ITP
Autoimmune Hemolytic Anemia
Acute Glomerulonephritis |
|
|
Term
|
Definition
| Chimeric IgG1 monoclonal antibody |
|
|
Term
| What is the MoA of Infliximab? |
|
Definition
| Binds to TNF-α to suppress inflammatory cytokines IL-1, IL-6, and adhesion molecules involved in leukocyte activation and migration |
|
|
Term
| Infliximab is indicated for what use? |
|
Definition
| Crohn’s disease of the colon and RA (used in combo with methotrexate) |
|
|
Term
| What are the potential toxic side effects of Infliximab? |
|
Definition
Increased incidence of lymphoma
Development of antinuclear antibodies, and development of new absscess (Crohn’s disease) |
|
|
Term
| Infliximab is contraindicated in patients with what co-morbidity? |
|
Definition
|
|
Term
| What is the MoA of Etanercept? |
|
Definition
Binds to both TFN-α and TFN-β
Similar to Infliximab, suppresses inflammatory cytokines IL-1, IL-6, and adhesion molecules involved in leukocyte activation and migration |
|
|
Term
| Etanercept is indicated for what use? |
|
Definition
RA
Polyarticular course juvenile RA
Psoriatic arthritis
Administration SQ twice weekly |
|
|
Term
| Etanercept can cause what toxic side effects? |
|
Definition
| Positive ANA, postive anti-double-stranded DNA antibodies (lupus-like syndrome) |
|
|
Term
| What is the MoA of Adalimumab? |
|
Definition
Blocks the interaction of TNF-α with TNF receptors on the cell surfaces
Lyses cells expressing TNF-α in the presence of complement
Reduced levels of C-reactive protein, erythrocyte sedmentation rate, serum IL-6, and matrix metalloproteinases MMP-1,3 |
|
|
Term
| Adalimumab is indicated for what use? |
|
Definition
RA
Has a 1/2 life of TWO WEEKS, can be increased further by combining with methotrexate |
|
|
Term
|
Definition
Recombinant fusion protein composed of extracellular domain of CTLA-4 fused to human IgG Fc
CTLA-4 is analogous to CD152 |
|
|
Term
| What is the MoA of Abatacept? |
|
Definition
| CTLA-4 is a costimulatory molecule found on T cells that binds to CD80/86 on APCs to inhibit T cell activation and cytokine release |
|
|
Term
| Abatacept is indicated for what use? |
|
Definition
| Severe rheumatoid arthritis who have failed other DMARDS |
|
|
Term
| Abatacept is contraindicated alongside what drug? |
|
Definition
| Other anti-TNF drugs or Anakinra |
|
|
Term
| What co-stimulatory signals are required for T cell activation? |
|
Definition
Signal 1 is via the T-cell receptor (TCR) and signal 2 is via a costimulatory receptor-ligand pair
Both signals are required for T-cell activation |
|
|
Term
What is the Multiple Sclerosis?
What are it's triad of symptoms? |
|
Definition
Demyelinating inflammatory disease of the CNS white matter
Mononuclear cell infiltration
Demyelination
Scarring (gliosis) |
|
|
Term
| What are the different classifications of MS? |
|
Definition
Acute MS (an acute attack)
Relapsing-remitting MS
Secondary progressive MS (progressive neurologic deterioration following a long period of relapsing-remitting disease)
Primary progressive MS (about 15% of patients, wherein deterioration with relatively little inflammation is apparent at onset) |
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|
Term
| What is the most common form of MS? |
|
Definition
|
|
Term
| What is recommended for treatment of MS? |
|
Definition
IFN-beta for RRMS
Mitroxantrone for worsening RRMS or SPMS, intercalates DNA |
|
|
Term
| What are the limitations of immunostimulation therapy? |
|
Definition
| Systemic (generalized) effects at one extreme and limited efficacy at the other |
|
|
Term
| What is the MoA of Levamisole? |
|
Definition
Increased magnitude of delayed hypersensitiviy or T cell-mediated immunity
Killing residual tumor cells by activating macrophages |
|
|
Term
| Levamisole is indicated for what use? |
|
Definition
Hodgkin's disease*
Dukes class C colorectal cancer after surgery |
|
|
Term
| Levamisole can cause what toxic side effects? |
|
Definition
Severe agrnulocytosis (stops when discontinued)
Monitor CBC with platelets prior to treatment and LFT’s every 3 months |
|
|
Term
| What is the MoA of Thalidomide? |
|
Definition
Inhibits TNF-α and angiogensis
Reduces phagocytosis by neutrophiles
Increase the production of IL-10
Paradoxically enhances cell-mediated immunity by interacting with T cells** |
|
|
Term
| Thalidomide is indicated for what use? |
|
Definition
Multiple Myeloma - can be combined with dexamethasone
Erythema nodosum leprosum |
|
|
Term
| Thalidomide can cause what toxic side effects? |
|
Definition
Teratogenesis
Increased risk of DVT, thrombosis (beware warfarin)
Hypothyroidism |
|
|
Term
|
Definition
| Activation of macrophages to created more effective killer cells as well as lymphoid cells of the immune response |
|
|
Term
| BCG is indicated for what use? |
|
Definition
TB immunization
Cancer therapy (bladder cancer) |
|
|
Term
| GMCSF (sargrmostim) and GCSF cytokines are indicated for what use? |
|
Definition
Pre-term neonates to combat infections
Netropenic patients |
|
|
Term
| IFN-alpha can be given for the treatment of what? |
|
Definition
Several neoplasms (hairy cell leukemia, chronic myelogenous leukemia, malignant melanoma, Kaposi’s sacroma)
Hep B and C* |
|
|
Term
| IFN-gamma can be given for the treatment of what? |
|
Definition
| Chronic granulomatous disease |
|
|
Term
| IL-2 can be given for the treatment of what? |
|
Definition
Metastatic renal cell carcinoma
Malignant Melanoma |
|
|
Term
| Alemtuzumab is given for the treatment of what? |
|
Definition
| Chronic lymphocytic leukemia |
|
|
Term
| Ibritumomob tuxetan is given for the treatment of what? |
|
Definition
| Rituximab resistant cases |
|
|
Term
| What is the MoA of Trastuzumab? What is it given for? |
|
Definition
Binds to the extracellular domain of HER-2/neu
Blocks the natural ligand from binding and down-regulates the receptor
Given for metastatic breast cancer |
|
|
Term
| Patients receiving Trastuzumab for breast cancer treatment should be monitored for what? |
|
Definition
Cardiac dysfunction during infusion
Dosage adjustment in renal impairment |
|
|
Term
| What is the MoA of Rituximab? |
|
Definition
Binds to the CD20 molecule on normal and malignant B lymphocytes
Complement-mediated lysis of the cell
Antibody-dependent cellular cytoxicity |
|
|
Term
| Rituximab is indicated for what use? |
|
Definition
| Follicular B cell or Non-Hodgkin’s lymphoma |
|
|
Term
| Rituximab can cause what toxic side effects? |
|
Definition
B cell depletion
Synergistic with chemotherapy |
|
|
Term
| What is the MoA of Palivuzumab? What is its indicated use? |
|
Definition
Binds to the fusion protein of respiratory syncytial virus (RSV) to prevent infection in at risk neonates
Preventional only |
|
|
Term
| What is the MoA of Abciximab? |
|
Definition
Binds to the GPIIb/IIIa receptor on activated platelets to inhibit fibrinogen, Von Wilebrand factor, and other adhesive molecules from binding to activated platelets
Prevents platelet aggregation |
|
|
Term
| Abciximab is indicated for what use? |
|
Definition
Prevention of acute cardiac ischemic complications
Patients at risk for restenosis
Can be given with heparin |
|
|
Term
| What should be monitored when taking Abciximab? |
|
Definition
| CBC, PT, aPTT, platelet count, fibrogen |
|
|
Term
| What metabolizes Acetaminophen? |
|
Definition
| CyP-450 oxidation to NAPQI which reacts with glutathion (GSH) to form an inactive product |
|
|
Term
| How does Acetaminophen cause hepatic and renal injury? |
|
Definition
| GSH depletion causes NAPQI accumulation, destroys hepatocytes and renal tubular cells |
|
|
Term
| How does Acetaminophen toxicity progress? |
|
Definition
Presents 12-24 hrs after ingestion
Nausea/vomitting -> hepatitis, malaise, -> liver injury, metabolic acidosis, hypoglycemia, renal failure, pancreatitis |
|
|
Term
| How is Acetaminophen toxicity treated? |
|
Definition
Activated charcoal (recent overdose)
N-acetylcysteine (NAC)- glutathione precursor
Antiemetic therapy if needed (metoclopramide, droperidol, ondanestron) |
|
|
Term
| Ethylene Glycol and Methanol poisoning initially resembles what other condition? |
|
Definition
|
|
Term
| How does Ethylene Glycol cause renal failure? |
|
Definition
| Calcium oxalate crystalluria |
|
|
Term
| What is antidotal for Ethylene Glycol and Methanol poisoning? |
|
Definition
| Fomepizole competitively inhibits ADH |
|
|
Term
| Ethylene Glycol poisoning should be given Fomepizole and supplemented with what? |
|
Definition
|
|
Term
| Methanol poisoning should be given Fomepizole and supplemented with what? |
|
Definition
|
|
Term
| How do Organophosphates cause toxicity? What kinds of products contain organophosphates? |
|
Definition
Irreversible acetylcholinesterase inhibitors
Found in insecticides |
|
|
Term
| What are the symptoms of organophosphate poisoning? |
|
Definition
DUMBBELSS: diarrhea, urination, myosis, bronchoconstriction, bradycardia, excitation, lacrimation, salivation, sweating
Respiratory failure can be fatal |
|
|
Term
| How is organophosphate poisoning treated? |
|
Definition
Atropine is a competitive inhibitor of Ach (symptomatic control)
Pralidoxime (2-PAM) breaks covalent bond between organophosphates and ACh-esterase (for regeneration of Ach-E) |
|
|
Term
| What substances can cause anti-cholinergic poisoning? |
|
Definition
Benztropine
Antihistamines
Phenothiazines
Jimson weed
Some mushrooms |
|
|
Term
| What are the symptoms of anti-cholinergic poisoning? |
|
Definition
HTN, tachycardia, fever, dry mouth urinary retention, hallucinations, confusion
"Dry as a bone, red as a beet, hot as a pistol, blind as a bat, mad as hatter" |
|
|
Term
| How is anti-cholinergic poisoning treated? |
|
Definition
| Physostigmine to inhibit acetylcholine degradation |
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|
Term
| What are the symptoms of lead poisoning? |
|
Definition
Dysregulation of signal transduction*, inhibition of heme synthesis*
Seizures, abd cramping, anemia, hepatitis, neuropathy, fatigue |
|
|
Term
| At what toxic levels does lead illicit its effects? |
|
Definition
Biochemical toxicity: 5-10 ug/dL
Neurobehavioral effects: 10-20 ug/dL
Encephalopathy & Neuropathy: >100 ug/dL |
|
|
Term
| How is lead poisoning treated? |
|
Definition
Treat seizures with benzodiazepines
Corticosteroids and mannitol for reduction of intracranial pressure
Whole bowel irrigation
Chelation therapy with EDTA
Dimecaprol* is ANTIDOTAL |
|
|
Term
| Arsenic is found in what products? |
|
Definition
| Rodenticides, insecticides, herbicides, paints, folk remedies |
|
|
Term
| How does Arsenic cause toxicity? |
|
Definition
Cellular toxin-disruption of enzymes required for oxidative phosphorylation
Acute poisoning > 1000 ug/L |
|
|
Term
| What are the symptoms of Arsenic toxicity? |
|
Definition
Garlic breath & rice water stools**
Abd pain, GI symptoms and hemorrhaging, hypotension, shock, edema, convulsions, delirium, polyneuropathy |
|
|
Term
| How is Arsenic poisoning treated? |
|
Definition
Gastric lavage* is ANTIDOTAL
Dimecaprol highly effective if administered promptly
Endotracheal intubation for unstable patients
IV fluids, cardiovascular support |
|
|
Term
| How does iron overdose cause toxicity? |
|
Definition
Free ferric iron disrupts oxidative phosphorylation & catalyzes formation of oxygen free radicals
Causes transferritin saturation
Lipid peroxidation & cell death
Increased capillary permeability
Shift to anerobic metabolism |
|
|
Term
| How is iron poisoning treated? |
|
Definition
Deferoxamine mesylate chelates iron to form water soluble ferrioxamine complex for renal excretion
Volume resuscitation
Whole bowel irrigation |
|
|
Term
| What are the asphyxiants? |
|
Definition
|
|
Term
| How does CN and H2S cause asphyxiation? |
|
Definition
| Inhibit the formation of ATP |
|
|
Term
| What is required for treatment in patients with CO poisoning? |
|
Definition
| Hyperbaric oxygen therapy |
|
|
Term
| How is asphyxiant poisoning (CO, CN, H2S) treated? |
|
Definition
Maximal oxygen therapy
Treat seizures with benzodiazepines
Treat acidemia with NaHCO3 (IV)
Activated charcoal(minimal effect) |
|
|
Term
| CN poisoning is specifically treated with what? |
|
Definition
| Sodium Nitrate IV* followed by Sodium Thiosulfate |
|
|
Term
| What do you do if IV access is delayed in a CN poisoning patient that is spontaneously breathing? |
|
Definition
| Hold amyl nitrite pearls under nose |
|
|
Term
| How do antidepressants cause toxicity? |
|
Definition
Excessive CNS serotonergic activity, reuptake inhibition of 5-HT, inhibited 5-HT metabolism
Causes Serotonin Syndrome |
|
|
Term
| How is serotonin syndrome treated? |
|
Definition
Cyporheptadine** (antagonist)
Charcoal
Benzos for seizure
Treat hypoxia, axidosis, hypokalemia, and hypotension |
|
|
Term
| Buproprion SR induced serotonin syndrome may require what treatment? |
|
Definition
|
|
Term
| What are alternative routes of cocaine toxicity? |
|
Definition
| “Body packing” & “body stuffing” |
|
|
Term
| What cocaine metabolite is detectable in the urine? |
|
Definition
|
|
Term
| Cocaine taken with Ethanol creates what dangerous metabolite? |
|
Definition
|
|
Term
| Cocaine users will have what distinct sign of use in the urine? |
|
Definition
Tea colored urine due to rhabdomyolysis
Benzoylecgonine metabolite |
|
|
Term
| Severe hypertension due to cocaine toxicity should be treated with what? |
|
Definition
Nitroglycerin or phentolamine
Avoid Beta-blockers!! |
|
|
Term
| Cocaine body packers & stuffers should be treated with what? |
|
Definition
| Multiple dose charcoal plus whole bowel irrigation & endoscopic removal of intact packets |
|
|
Term
| How is the ingestion of corrosives treated? |
|
Definition
Endoscopy, radiography, barium contrast
Endotracheal intubation for patients with respiratory distress
Gastric lavage via nasogastric tube
Dilution with water or milk
Corticosteroids for burns + short term antibiotics
DO NOT induce emesis or give charcoal |
|
|
Term
| How do you treat envenomations? |
|
Definition
If minimal, observe, if moderate, Crofab 4g over 60min, if severe, Crofab 5g over 60min
With every treatment of Crofab, monitor and give additional doses if needed
If severe, maintain dosing at 2g every 6hrs x 3 |
|
|
Term
| What four abnormalities lead to acne? |
|
Definition
Hyperkeratinization
Sebum production
Propionibacterium Acnes
Inflammation |
|
|
Term
| Hyperkeratinization and sebum production are both increased under the influence of what? |
|
Definition
|
|
Term
| What is the MoA of Benzoyl Peroxide? |
|
Definition
*Keratolytic – solubilizes cell surface proteins
*Bactericidal due to formation of benzoyl peroxide radicals
Is also comedolytic |
|
|
Term
| Benzoyl Peroxide is often combined with what when used to treat acne? |
|
Definition
| Erythromycin or clindamycin enhances formation of active compound |
|
|
Term
| What are the side effects of Benzoyl Peroxide? |
|
Definition
Irritation, dryness, peeling & erythema (redness)
Bleaching of hair / clothing
Contact dermatitis (1-2%) |
|
|
Term
| What is the MoA of Siacylic Acid? |
|
Definition
Keratolytic ONLY*
Solubilizes intercellular cement, causes desquamation and is comedolytic |
|
|
Term
| What are the side effects of Siacylic Acid? |
|
Definition
Salicylism
Very rare with topical salicylates, syndrome is due to excessive systemic absorption |
|
|
Term
| What is the MoA of Sulfur Compounds used for acne treatment? |
|
Definition
Keratolytic*
Possibly anti-bacterial but unproven |
|
|
Term
| What are the side effects of using sulfur compounds for acne treatment? |
|
Definition
Stain
Odor (newer reduced-odor formulations)
Comedogenic with long-term use |
|
|
Term
| What is the MoA of Azelaic Acid? |
|
Definition
A scavenger of oxygen free-radicals**, making it a weak anti-inflammatory
Keratolytic**
INDIRECTLY** bactericidal via inhibiting thioredoxin reductase and tyrosinase (inhibits DNA synthesis) |
|
|
Term
| What are the side effects of Azelaic Acid? |
|
Definition
Hypopigmentation
Anti-tyrosinase and anti-mitochondrial enzymatic activities may interrupt the activity of normal melanocytes |
|
|
Term
| How does Retinoic Acid (vit A is a precursor) mediate its effects? |
|
Definition
Endogenous ligand for Retinoic acid receptors (RARs) and retinoic X receptors (RXRs) – nuclear receptors
Binds directly to DNA gene promoter regions to regulate gene transcription |
|
|
Term
| Retinoic Acid has what overarching effects? |
|
Definition
Bone Growth
Immune function
Reproductive function
Regulation of cellular proliferation and differentiation (epithelial cells) |
|
|
Term
| What are the characteristics of 1st and 2nd gen retinoids? |
|
Definition
Flexible backbone imparted by alternating single and double bonds
May bind to several retinoid receptors
This relative lack of receptor specificity may lead to greater side effects** |
|
|
Term
| What areWhat are the characteristics of 3rd gen retinoids? |
|
Definition
Much less flexible than those of earlier-generation retinoids
Interact with fewer retinoid receptors
Generally milder side effect profile |
|
|
Term
| What is the MoA of Tretinoin? |
|
Definition
1st gen retinoid
Binds RAR's to increase mitosis and thymidine incorporation into DNA to increase turnover, exfoliation, desquamation, keratolysis**, and decrease inflammation** |
|
|
Term
| What are the side effects of Tretinoin? |
|
Definition
Irritation, Erythema, Peeling, Dryness
“Appearance” of Worsening Acne
UV-reactive, apply at bedtime
Anti-wrinkle effects via vasodilation and collagen |
|
|
Term
| What is the MoA of Adapalene? |
|
Definition
3rd gen retinoid derivative of naphthoic acid
Similar to Tretinoin: Karatolytic* & anti-inflammatory* |
|
|
Term
| What are the side effects of Adapalene? |
|
Definition
| Similar to Tretinoin but more mild due to being 3rd gen, resistant to UV degredation |
|
|
Term
| What is the MoA of Tazarotene? |
|
Definition
3rd gen retinoid, prodrug converted by esterases
Binds RAR's, exfoliative, cellular differentiation
Blocks ornithine decarboxylase to prevent mitosis and normalize growth of keratinocytes*
Anti-inflammatory* |
|
|
Term
| What are the side effects of Tazarotene? |
|
Definition
| Similar to Tretinoin but UV stable and pregnancy category X* |
|
|
Term
| What is the MoA of Isotretinoin (Accutane) |
|
Definition
Binds RAR, MoA unknown
Corrects ALL FOUR abnormalities found in acne**
Keratolytic, anti-inflammatory, bactericidal, lowers sebum |
|
|
Term
| What are the common side effects of Isotretinoin (Accutane)? |
|
Definition
| Dry Skin / Peeling, pruritis, dry eyes, conjunctivitis, nosebleeds, alopecia (Hair Loss) |
|
|
Term
| What are the more severe side effects of Isotretinoin (Accutane)? |
|
Definition
Inflammatory Bowel Disease*
Joint pain and poor lipid profile
Depression/Suicide ideation*
Pregnancy category X*
Avoid sunlight*
Interacts with Tetracycline to cause pseudotumor cerebri
Has been removed from the market |
|
|
Term
| What was always required prior to prescribing Isotretinoin (Accutane)? |
|
Definition
| 2 forms of birth control and a negative pregnancy test |
|
|
Term
| Isotretinoin (Accutane) has what drug interaction? |
|
Definition
| Tetracycline causes pseudotumor cerebri |
|
|
Term
| What is the MoA of Erythromycin? |
|
Definition
Macrolide
Binds 50s ribosomal subunit to inhibit translocation |
|
|
Term
| What are the side effects of Erythromycin? |
|
Definition
Liver enzyme inhibitor
Increased concentration when given with theophylline, caffeine, coumadin, digoxin, warfarin, corticosteroids |
|
|
Term
| What is the MoA of Clindamycin? |
|
Definition
NOT A MACROLIDE
Binds 50s ribosomal subunit to inhibit translocation |
|
|
Term
| What are the side effects of Clindamycin? |
|
Definition
| Psuedomembranous Colitis (with systemic use) |
|
|
Term
| What is the MoA of Tetracycline? |
|
Definition
| Binds to 30s Ribosomal Subunit to inhibit elongation |
|
|
Term
| What are the side effects of Tetracycline? |
|
Definition
Alters normal GI flora causing GI disturbance, opportunistic infection, and potential Pseudomembranous colitis
Binds to Ca++ ions** to affect teeth and bones
Photosensitization |
|
|
Term
| Tetracycline interacts with what other substances? |
|
Definition
Absorption decreases with antacids, avoid dairy and iron
Decreases oral contraceptive effectiveness |
|
|
Term
| How does Doxycycline differ from Tetracycline? |
|
Definition
Same class
2x potency
Increased side effects* except Ca++ binding |
|
|
Term
| How does Minocycline differ from Tetracycline? |
|
Definition
Same class
2-4x potency
DECREASED side effects* but with ototoxicity and CNS effects |
|
|
Term
| What is the MoA of Ortho-Tri-Cyclen? |
|
Definition
| Increases sex hormone binding globulin to decrease free androgens and in turn decreasing sebum production and hyperkeratinization |
|
|
Term
| What is is Ortho-Tri-Cyclen indicated for? |
|
Definition
Moderate inflammatory acne in females
2-4 months to see effectiveness
Relapse once med is d/c |
|
|
Term
| What are the side effects of Ortho-Tri-Cyclen? |
|
Definition
Estrogens promote clotting (dose-related)
Increase risk of Breast Cancer
Stroke and MI risk increase |
|
|
Term
|
Definition
T-cells are stimulated in a lymph node by an antigen presenting cell (APC)
The activated T-cells migrate through the blood, finally migrating into the dermis
The T-cells (specifically TH1-cells) are re-activated by an APC within the dermis
Characteristic plaques are a result of chemokines
Is considered a disorder of keratinocyte hyperproliferation* |
|
|
Term
| What causes keratinocyte hyperproliferation in psoriasis? |
|
Definition
Triggered by infection, trauma, drugs, UV light, hypocalcemia
Normal epidermal turnover (56 days) and psoriasis (7 days)
Connected to a disruption in arachidonic acid metabolism (30-fold increase) |
|
|
Term
| What keratolytics can be used to treat psoriasis? |
|
Definition
Salicylic acid with emollients (lotion)
Coal Tar, Vitamin D analogs, Retinoids |
|
|
Term
| What immunosuppressants are used to treat psoriasis? |
|
Definition
Corticosteroids
Cyclosporine A
Alefacept, Adalimumab |
|
|
Term
| What systemic agents are used to treat psoriasis? |
|
Definition
|
|
Term
| How should corticosteroid treatment of psoriasis be approached? |
|
Definition
Start with high potency followed by less potent
Very high potency should NEVER be used on the face
With high potency, you can use on the face for short periods
Always use on small areas to decrease systemic effects |
|
|
Term
| What are the potential side effects of corticosteroid therapy? |
|
Definition
Suppression of the pituitary-adrenal axis (less with topicals)
Iatrogenic Cushing’s Syndrome
Topicals can cause petechiae, purpura, ecchymosis, steroid rosacea, contact dermatitis, and persistent erythema, skin atrophy |
|
|
Term
| What is the MoA of Alefacept? |
|
Definition
Interferes with lymphocyte activation, prevents interaction with APC
Reduces active T lymphocytes involved in psoriasis, other T-cells are largely unaffected |
|
|
Term
| Alefacept is indicated for what use? |
|
Definition
| Treatment of moderate to severe chronic plaque psoriasis |
|
|
Term
| What are the side effects of Aledacept? |
|
Definition
CD4+ lymphocyte count should be monitored weekly
Discontinue if count is below 250 cell/µL
Avoid with infections (duh!) |
|
|
Term
| What is the MoA of Acitretin? |
|
Definition
A retinoid prodrug, converts to etritinate
Specific MoA unknown but can normalize kertainocyte growth |
|
|
Term
| Acitretin is indicated for what use? |
|
Definition
| Moderate to severe psoriasis |
|
|
Term
| What are the side effects of Acitretin? |
|
Definition
| Similar to Isotretinoin (Accutane) but even more teratogenic, must avoid pregnancy for 3yrs and donating blood for 1mo |
|
|
Term
| What is the MoA of Calcipotriene? |
|
Definition
Vit D3 derivative available as an ointment
Inhibit keratinocyte differentiation and proliferation
Decreases TH1-stimulating cytokines (IL-2, etc) |
|
|
Term
| Calcipotriene is indicated for what use? |
|
Definition
| Moderate plaque type psoriasis |
|
|
Term
| What are the side effects of Calcipotriene? What should be avoided? |
|
Definition
Burning, itching, mild irritation, with drying and erythema around treated areas
Avoid mucous membranes and contact with eyes to avoid systemic effects |
|
|
Term
| What is the MoA of methotrexate? |
|
Definition
Inhibits dihydrofolate reductase (DHFR) which is required for thymidine synthesis, causes cell death
*Ant-inflammatory due to decreased IL-1 production and death of active T cells
Primarily affects rapidly dividing cells such as immune cells |
|
|
Term
| What are the side effects of methotrexate? |
|
Definition
Hepatic fibrosis
Should not be used with drugs that will compete for serum binding proteins
Bone marrow depression, megaloblastic anemia, alopecia, mucositis |
|
|
Term
| hich of the following correctly describes an agerelated physiologic alteration that affects the pharmacokinetics of medications in geriatric patients? |
|
Definition
| Decline in creatinine clearance with an increase in age |
|
|
Term
| Which of the following statements regarding renal function and pharmacokinetics in geriatric patients is most accurate? |
|
Definition
| Decreased muscle mass (sarcopenia) is the basis for normal or low creatinine levels in older patients, despite a decrease in renal function |
|
|
Term
| What is detectable in the meconium of neonates whose mothers consumed alcohol during pregnancy? |
|
Definition
|
|
Term
| What is the definition of a prescription drug? |
|
Definition
Drug that requires a prescription because it is considered potentially harmful if not used under the supervision of a licensed health care practitioner
Known synonymously as a legend drug |
|
|
Term
| What is the definition of a controlled or scheduled drug? |
|
Definition
A prescription drug whose use and distribution is tightly controlled because of its abuse potential or risk
Prescriptions for controlled substances have additional requirements by law |
|
|
Term
| What is included with the date of a prescription? |
|
Definition
Date the prescription is issued or written
Allows the determination of the life of the prescription to validate refills |
|
|
Term
| How long are legend drug prescriptions valid? |
|
Definition
| Expire 1 year from date issued |
|
|
Term
| How long are controlled drug prescriptions valid? |
|
Definition
CIII-CV – expire 6 months from date issued
CII – expire 7 days from date issued |
|
|
Term
| What are the benefits of having prescriptions expire? |
|
Definition
Ensures continual patient supervision
Promotes patient follow-up |
|
|
Term
| What does bioequivalent mean? |
|
Definition
The same amount of active ingredient is delivered to body and will produce identical effect in terms of duration and intensity (the difference between brand vs. generic)
If practitioner prefers brand, must indicate in print |
|
|
Term
|
Definition
| These are the directions to the patient |
|
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Term
| What is the purpose of refills on prescriptions? |
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Definition
To avoid interrupting maintenance therapy, practitioners can authorize refills on a written prescription
Refills are not required |
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Term
| Which substances have no limit to the number of refills allowed? |
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Definition
| Non-controlled substances |
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Term
| How long are refills in prescriptions valid? |
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Definition
| Authorized are valid only for life of the prescription – 1 year |
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Term
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Definition
| Refill as needed for 1 year |
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Term
| What are the characteristics of Schedule I (C-I) substances? |
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Definition
| Highest abuse risk. No safe medical use in U.S. Examples: heroin, marijuana, LSD, PCP, and crack cocaine |
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Term
| What are the characteristics of Schedule II (C-II) substances? |
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Definition
| High abuse risk but have safe and accepted medical use. Examples: morphine, oxycodone, methylphenidate, dextroamphetamine |
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Term
| What are the characteristics of Schedule III (C-III) substances? |
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Definition
| Abuse risk less than C-II and safe and accepted medical use. Examples: Acetaminophen/Codeine (Tylenol #3), acetaminophen/hydrocodone (Vicodin), Butalbital (Fiorinal) **Note: FioriCET is NOT scheduled |
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Term
| What are the characteristics of Schedule IV (C-IV) substances? |
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Definition
| Abuse risk less than C-III and safe and accepted medical use. Examples: diazepam (Valium), alprazolam (Xanax), phenobarbital, chloral hydrate, Darvocet (propoxyphene) |
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Term
| What are the characteristics of Schedule V (C-V) substances? |
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Definition
| Abuse risk less than C-IV and safe and accepted medical use. Mainly consist of preparations containing limited quantities of certain stimulant and narcotic drugs for antitussive and antidiarrheal purposes |
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Term
| What additional law requirements are there for CII prescription drugs? |
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Definition
Every practitioner must register with DEA and DPS
Exemptions do not apply for outpatient prescriptions
Special prescriptions required: Triplicate and an Official Prescription Form
No refills allowed
Expires 7 days after issuance |
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Term
| How do you maximize patient safety when writing prescriptions? |
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Definition
ALWAYS write legibly
ALWAYS space out words and numbers to avoid confusion
ALWAYS complete medication orders
AVOID abbreviations
When in doubt, ask to verify |
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Term
| What are the characteristics of Wernicke-Korsakoff Syndrome? |
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Definition
Wernicke: Gout, opthalmological problems, cognitive deficiencies, all are reversible
Korsakoff: Irreversible memory loss |
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Term
| What are all the way ethanol causes damage on a biochemical level? |
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Definition
Ester synthetase forms fatty acid ethyl esters which damages the myocardium, pancrease, and liver
Release of free radicals worsens myocardial damage. Progresses to fatty liver and hypoxic damage
Acetaldehyde causes protein adduct formation which can cause allergic reactions, cell damage, and breakdown of cell tissue and lysosomal enzyme release which induces inflammation
Induction of xenobiotic metabolism leads to carcinogenesis and enhanced toxicity |
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Term
| How do methampthetamines and cocaine differ? |
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Definition
Cocaine is plant derived, high lasts 20-30min, is metabolized quickly by plasma cholinesterasees, 1/2 life is 1hr
Meth is man made, high lasts 24hrs, 1/2 life is 12 hrs, is not metabolized in the same fashion |
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Term
| What are the determinants of toxicology? |
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Definition
Dose
Dose rate
Duration of exposure
Route of exposure |
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Term
| What are the factors affecting toxicity? |
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Definition
Biotransformation
Genetics
Immune Status
Photosensitivity
Age
Gender
Protein Binding
Interactions
Nutritional Status |
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Term
| A patient was given succinylcholine and later presented with delayed paralysis. Why? |
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Definition
| An atypical succinylcholine esterase or succinylcholine esterase is nonexistant. This is a high yield example of genetics affecting toxicity |
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Term
| What are the high yield antimicrobials that cause photosensitivity? |
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Definition
FAST
Fluoroquinolones
Aminoglycosides
Sulfonamides
Tetracyclines |
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Term
| What are the different types of toxic reactions? |
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Definition
Pharmacological (ex. CNS depression)
Pathological (ex. hepatic injury)
Genotoxic (ex. neoplasms via nitrogen mustard) |
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Term
| What high yield agents are likely to cause seizures? |
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Definition
TCA's
Cocaine
Amphetamines
Meperidine (metabolite causes serotonin syndrome and lowering of seizure thershold) |
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Term
| What high yield agents are likely to cause hypokalemia? |
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Definition
Diuretics (particularly by fluorsomide diuretics)
Barium salts |
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Term
| What high yield agents are likely to cause hyperkalemia? |
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Definition
Spironolactone
Beta-blockers
Cardiac glycosides |
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Term
| What high yield agents are likely to cause hypocalcemia? |
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Definition
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Term
| Digoxin will likely cause what ECG finding? |
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Definition
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Term
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Definition
| Serum Cl + HCO3 - Serum Na+ |
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Term
| Stimulants generally mediate their effects via what means? |
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Definition
| Dopamine and possible activation of glutamate receptors |
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Term
| Depressants generally mediate their effects via what means? |
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Definition
| GABAergic neurotransmission |
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Term
| What opioid uniquely causes mydriasis (dilated pupils) instead of miosis (pinpoint pupils) like other opioids? |
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Definition
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Term
| Why must you monitor drug abuse patients for rebound and clinical toxicity? |
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Definition
Metabolites can become stuck in adipose tissue and released later, causing delayed toxicity
Amiodarone is the classic example |
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Term
| What is the drawback of using NAC to treat Acetaminophen poisoning? |
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Definition
Will not reverse hepatic damage, must be given quickly, acts as a glutathione precursor
Mist be given given IV because of foul smell |
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Term
| What are the side effects of charcoal? |
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Definition
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Term
| The effectiveness of gastric lavage is dependent on what? |
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Definition
| Time since toxin exposure, sooner is better |
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Term
| What are the risks associated with gastric lavage? |
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Definition
Mechanical damage to the esophageal tract
Aspiration pneumonitis
Laryngeal spasms |
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Term
| Methanol can cause what irreversible injury? |
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Definition
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Term
| How does methanol cause injury? |
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Definition
| Metabolized to formic acid which causes metabolic acidosis and tissue injury |
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Term
| What can you give in the absence of Fomepizole in cases of ethylene glycol or methanol poisoning? |
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Definition
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Term
| What is the general (non-antidotal) treatment for ethylene glycol or methanol poisoning? |
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Definition
Gastric aspiration (nasogastric tube)
Activated charcoal
IV glucose
Sodium bicarbonate (metabolic acidosis) |
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Term
| How do you reverse renal failure due to heavy metal toxicity? |
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Definition
Thiazide
Fluids
ACE-inhibitors
Mannitol (only the diuretic that increases excretion of water relative to the electrolytes) |
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Term
| What is the most common cause of iron overdose? |
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Definition
| Overdose of prenatal vitamines |
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Term
| What is the most common cause of cyanide poisoning? |
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Definition
| Nitroprusside used beyond 2days or infused too quickly |
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Term
| How does cyanide poisoning present and progress? |
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Definition
| Headache, nausea vomiting, followed by sudden coma |
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Term
| Other than anti-venom, how should you approach treating an envenomation? |
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Definition
Endotracheal intubation for airway protection
IV fluids for hypotension
Tetanus prophylaxis and antibiotics
Corticosteroids, antiinflammatories & antihistamines if required |
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