Day 5 Immunology Flashcards
Does the innate or adaptive immune system have a quick response?
Does the innate or adaptive immune system have B and T cells?
Does the innate or adaptive immune system self distinguish and find cancer cells?
Innate
Adaptive
Adaptive
What do the epithelial cells do?
What do the natural killer cells do?
What do neutrophils do?
Produce local antibiotics, signal local T lymphocytes.
Cause apoptosis, activate macrophages, respond to local cytokines.
primary workhoses, large response.
What do mast cells do?
What do dendritic cells do?
What do macrophages do?
Vasodilation, increased capillary permeability, bacteria/toxic inactivation, prostaglandin and cytokine release inflammation.
Detecting microbes, transfrom to APC, T cell activation and proliferation, initiate inflammation.
Inhale foreign bodies, stay in body for a long time.
What are the cells of the adaptive immune system?
How do T lymphocytes get activated?
Can B cells also act as APC’s for T cell activation?
B lymphocytes and plasma cells, T lymphocytes, abtibodies, interleukins, MHC.
Naive T cells–> Binding with APC stimulates clonal expansion, differention, and activation–> release of cytokines by activated T cell. Does not occur without co-stimulation.
YES.
What does Belatacept(Nulojix) do?
What are the Calcineurin inhibitors?
Can B cells and T cells recognize protein and non protein antigens?
blocks costimulation by binding to the CD80 and CD86 receptors on APC in order to prevent T cell activation. Used in kidney transplant. It is administered with other immunomodulating medications early in the kidney transplantation process.
Cyclosporine, Tacrolimus(these 2 used for preventing rejection of transplanted organs), Picrolimus(atopic derematitis)
NO, only B cells can recognize both. B for both.
What do Th1 cells do?
What do Th2 cells do?
What do Th17 cells do?
Stimulate macrophage function and fight myobacteria.
support B cells and therefore humoral immunity through the production of IL-4.
found in high numbers in patients with autoimmune diseases, IL-6 makes this.
What Ig cell causes inflammation?
What 2 CD’s are required for co-stimulation?
What diseases are you more susceptible to when you have spleen damage?
IgE activation of mast cells–> TNF, IL-4, IL-5–> neutrophils and eosinophils–> leukotriene release.
CD-80 or CD-86.
encapsulated bacteria, damage caused by sickle cell, trauma.
What are the A/E metabolic effects of corticosteroids?
What are the A/E renal effects of corticosteroids?
What are the A/E immune system effects of corticosteroids?
Obesity, moon face, buffalo hump, poor glucose tolerance(can cause DKA or hyperosmolar coma).
Hypertension and peripheral edema.
Inhibit cytokine formation, induce eosinophil apoptosis and reduce vascular peremeability, increase neutrophil numbers but have poor chemotaxis, do very little with humoral immunity.
Can corticosteroids cause osteoperosis?
What are the A/E CNS effects of corticosteroids?
What are the non-biologic DMARD’s that affect purine nucleotide function or synthesis?
Yes because they inhibit sex hormones(amenorrhea), can also cause adrenal crisis upon abrupt cessation.
mood swings, psychosis, sleep disturbance, depression, euphoria.
Azathioprine(false nucleotide), Methotrexate(decreased purine synthesis), Cyclophosphamide(alklyating).
What are the A/E’s of the purine non biologic DMARD’s?
What is the main side effect of the calcineurin inhibitor?
What are the MTOR inhibitors?
Teratogenic, folic acid can help with methotrexate, blood cells, bladder cells, skin/hair cells, gut cells most susceptible.
vasoconstriction–> hypertension.
Sirolimus, Everolimus.
What are the main side effects of the MTOR inhibitors?
How does mycophenolate work?
What is mycophenolate’s ADR’s?
Inhibited T cell function=infection suscept. All inhibit VEGF–>formation of blood vessels, hypertension, edema, N/V/D/C, wound healing.
by reversibly inhibiting inosine monophosphate dehydrogenase, which is involved in the synthesis of guanine nucleotides.
Teratogenic, increased infection risk, GI side effects.
What drugs block JAK inhibitor?
What drugs block CD80/86 inhibitors?
What is the JAK inhibitor A/E’s?
Tofacitinib.
Abtacept/Belatacept.
infection, liver toxicity, dyslipidemia.
What are the CD80/86 inhibitors A/E’s?
What is the PDE-4 inhibitor?
What is the PDE-4 inhibitor A/E’s?
Infection, cancer.
Apremilast(Otezla). Increase cAMP and therefore release of proinflammatory mediators.
N/V w initial therapy(goes away), depression, weight loss.
What is the old biologic DMARD?
What are the anti TNF drugs?
What are the anti TNF A/E’s?
Infliximab(human/mouse mix).
Infliximab,adalimumab, certolizumab, golimumab, etanercept.
Infection, tuberculosis reactivation black box warning, cancer, heart failure, autoimmune disease.
What drugs are the IL-6 inhibitors?
What are the IL-6 inhibitors A/E’s?
What are the anti IL-17 agents?
Toclizumab, Sarilumab
Respiratory infections, neutropenia, thrombocytopenia, liver enzymes.
Secukinumab, ixekiumab, brodalumab.
What are the A/E’s of Anti-IL-17 agents?
What drugs are the IL-23 drugs?
What are the IL-23 drug A/E’s?
Inflammatory bowel disease exacerbation, mucocutaneous candida.
Ustekinumab, guselkumab
Upper respiratory infections.
What to know about polyclonal antibodies?
What are the polyclonal A/E’s?
Does your body make antibodies to biologics?
recognize a variety of site on antigen, primarly used for transplanted organ rejection, create a vaccine against human T lymphocytes.
Infusion reactions due to cytokine release, serum sickness, immune glomerulonephritis.
YES, could make antidrug antibody. Primary concern is neutralizing drug activity.
What is the small molecule generic approval?
What is the biosimilar regulatory process?
What are some challenges of biosimilars?
Absorption rate(Ka) and bioavailability(F), No in vivo studies(animals), no clinical studies.
Invivo pharmacodynamic studies, post approval clinical studies of 1+ years.
Interchangeability(can’t have reduced efficay, no increased safety concerns, regulated by state law).
What is basiliximab’s MOA?
What is the new immunization for this year?
What to know about this new immunization?
IL-2 receptor complex inhibitor.
Herpes Zoster Subunit Vaccine.
Inactivated, IM in 2 doses, protective for 4 years, no serious A/E’s.
Which vaccines were removed?
Is flumist recommended for 2016-2017?
What other 3 recommendations from 2018 ACIP do we have?
Meningococcal polysaccharide, meningococall hemophilaius.
Nope, no reduction in total flu vaccine.
recommending 3rd MMR group, new zoster vaccine will be preferred over old and abbreviation changed to ZVL(no CI’d in pregnancy but no data, appropriate to give to someone already immunized with Zostavax), Hep A vaccine in adults with risk factors(including pregnancy), in certain settings or outbreaks.
What is the Hep B recommendation?
What is the Hep B catch up recommendation?
How do you determine whether a child should get 2 or 3 doses of HPV?
Dose #1 at birth(within 12-24 hours)–> Dose #2 at 4-8 weeks(no less than 4 weeks)–> Dose #3 at 24 weeks(6 months) or later.
4 weeks between 1&2–> Between 2 and 3 you need at least 8 weeks from dose #2 and at least 16 weeks from doses #2 AND at least 24 weeks(6 months) of age.
If one dose was given before age 15 give just one more, if one dose was given at age 15 or later give 2 more doses.
What are some exceptions to simultaneous administration of vaccines?
When do you give 2 doses to a toddler of influenza in a single season spaced 4 weeks apart?
What to know if someone refuses child vaccination?
Pneumococcus and meningococcus in patients with asplenia–> give PCV13 1st and wait 4 weeks before meningococcal. PCV13 and PPSV23–> give PCT 13 1st and wait one year before giving PPSV23(seperate by a year if PPSV23 given 1st). This applies if they are older than 65. Immunocompromised give PCV 13 and then wait 8 weeks before giving PPSV23.
Not needed if 2 doses were given in the same season during 16-17 OR if 1 dose was given during 15-16 and 1 dose was given during 16-17. Needed if no doses in 16-17, if 1 dose given during 16-17 or unknown.
Recommendation from healthcare professional can go a long way. Visit immunize.org for other stuff, use form that states consequences.
How do you administer Intradermal stuff?
When do you not give live vaccines?
When do you give additional inactivated vaccine doses or vaccines?
shake before injecting, hold between middle finger and thumb, insert perpendicular in deltoid, maintain pressure and press needle do not aspirate, remove needle from skin and put in sharps.
Combined immunodeficiency syndromes IF decreased lymphocyte counts, HIV if the CD4 lymphocyte count is <200, Any primary or acquired condition including cancer that affects the bone marrow or lymphatics, Graft vs host disease post bone marrow transplant.
Complement deificency, nephrotic syndrome, chronic granultomatous disease, HIV if CD4 > or equal to 400. No spllen or sickle cell, all types of cancer, anatomic barrier defects(cochlear implants, CSF leak), 2-6 months post solid organ transplant.
In what medications do we not give live vaccines?
When do we give additional doses of inactivated vaccines?
When are inactivated vaccines may be ineffective (additional doses required)?
B-lymphocyte depleting therapies(rituxamab), Any antirejection medications for solid organ transplant, cancer chemotherapy(and 3 months after), high level immunosuppresion medications for chronic inflammatory diseases.
B-lymphocyte depleting therapy, antirejection medications for solid organ transplant, cancer chemotherapy or radiation, low and high level immunosuppresion.
B-lymphocyte depleting, antijrection induction medications for solid organ transplant, cancer chemotherpay, patients taking immunoglobulin therapies for immunodeficiency syndromes.
