missed questions Flashcards
high molecular weight bacterial polysaccharides stimulate _____ complement pathway, which begins with _____
high molecular weight bacterial polysaccharides stimulate ALTERNATIVE complement pathway, which begins with C3
C1 and C2 are part of which complement pathway
classical, activated by antigen-bound Ab
biological agents ending in “-cept” contain ____
receptor moieties as part of their molecule
abatacept inhibited _____ by binding _____
abatecept: inhibits T CELL ACTIVATION by binding CD80 and CD86 on APC (aka B7), preventing APC from binding CD28 on T cells
difference between plasma and serum
PLASMA has CLOTTING factors
serum does NOT
both have antibodies, neither have RBC
____ domains of Ab differentiate isotypes
CONSTANT domains of HEAVY chain (part on the bottom in Fc region)
haptens
molecules that are too small to stimulate immune response (be immogenic), even if bound by an antibody (antigenic) - must be bound by a carrier to stimulate response
molecules that require a carrier to be immunogenic, even if they are antigenic
haptens - can bind antibody (antigenic) but too small to cause immune response (immunogenic) on their own
when do T cells begin producing effector cytokines like IL-4, IFN-y?
after differentiation from naive cells into effector/memory cells
how do NK cells kill
via granules!! extracellularly!! target virus infected cells or tumor cells!!
secretory lysosomes contain perforins, defensiones, proteases —> induce apoptosis or lysis
TH1 produce ___, which activates ____
TH2 produce ____, which activates ____
TH1 —> IFNy —> macrophages
TH2 —> IL-4 —-> B cells
_____ cells of cortex and medulla of thymus assist in selection of immunocompetent T cells
epithelial reticular cells (ERC’s): large, pale, stellar (star) shaped, support thymocytes
roles - thymocytes selection/deletion, contribution to blood-thymus barrier, secretion of hormones/cytokines, degeneration into thymic (Hassell’s) corpuscles
A 25yo medical student has had 4 injections of DPT in their first year of life and a booster at age 5. They are bitten by a mouse while doing an experiment in the lab. They should be given:
a. tetanus toxoid
b. tetanus immune globulin (human)
a. tetanus toxoid
the toxoid will enhance their immune response before the toxin can cause harm - they don’t have enough antibody already present in serum for protection, but toxoid will activated memory lymphocytes
not immune globulin because it is both expensive and unnecessary in previously immunized patients, and passive immunity will not provide protection for more than several months. Toxoid will provide protection for 5-10 years
A 10yo girl receives a deep laceration. She has no previous immunizations against tetanus. The best next steps would be:
a. mixture of tetanus toxoid and tetanus immune globulin (human) as one injection
b. a tetanus toxoid injection this visit, with an injection of tetanus immune globulin (human) 3 weeks later
c. separate injections of tetanus toxoid and tetanus immune globulin (human) in different sites in one visit
d. a tetanus immune globulin (human) injected this visit, with an injection of tetanus toxoid 3 weeks later
c. separate injections of tetanus toxoid and tetanus immune globulin (human) in different sites in one visit
patient may not return if you advise a booster in a different visit, and injections should be in separate sites so they don’t cross react (passive antibodies would just bind toxoid)
note that she should also return for 2 tetanus toxoid booster injections after this
A 3yo patient received the standard DPT immunization series starting at 3 months old, but they have no detectable antibodies to diphtheria, pertussis, or tetanus. He has a deep puncture wound in his foot. You should give:
a. tetanus toxoid for active immunity
b. tetanus immune globulin (human) for passive immunity
b. tetanus immune globulin (human) for passive immunity
the patient has an immune deficiency and cannot produce antibodies - tetanus toxoid will not induce active immunity (there are no memory cells to be activated)
Your 10yo pt comes in with a deep puncture wound on his foot. He has had a standard DPT series as a baby, a booster at age 5, and another booster 6 months ago for a previous wound. That proper treatment is:
a. tetanus toxoid
b. tetanus immune globulin (human)
c. tetanus toxoid + tetanus immune globulin (human)
d. nothing
d. nothing
the patient has adequate immunity from prior immunization
*Public Health Service suggests a booster when the last booster was given 5+ years ago
A patient’s RAST test comes back as 4+, indicated the patient has IgE antibodies, but their skin test is negative for a reaction, indicating a lack of in vivo sensitivity to the allergen. What could explain this discrepancy?
the patient has received desensitization shots for the allergen
antihistamine therapy or blocking antibody can suppress skin test reaction
note that IgE myeloma would cause suppression of all skin-test reactions (for a whole panel of antigens), but this is extremely rare
How would you set up a RAST assay for a patient’s allergy to dog dander? (the steps of the assay)
- dog dander antigen is covalently linked to the insoluble matrix
- IgE anti-dander is added (patient’s serum)
- amount bound is determined by radio-labeled anti-human IgE
Which of these will block binding of reaginic antibody to mast cells?
a. cromolyn sodium
b. antihistamine
c. epinephrine
d. blocking antibody
e. none of the above
e. none of the above
none of these can block antibody binding mast cell
[remember that blocking antibody is IgG, which binds allergen and prevents it from binding IgE on mast cells]
after an intradermal injection of an allergen, a visible and immediate hypersensitivity reaction usually occurs in…
1 to 15 minutes
Which of the following drugs are most effective for treating patients with chronic asthma and bronchial hyper-responsiveness?
a. antihistamines
b. cromolyn sodium
c. epinephrine
d. glucocorticoids
e. leukotrienes inhibitors
d. glucocorticoids
bronchial hyper-responsiveness associated with chronic asthma is caused by chronic inflammation of peribronchial tissues - glucocorticoids are most effective therapy for inflammation
by what mechanism does cromolyn sodium prevent mast cell degranulation?
stabilizes the membrane
Explain why desensitization by a series of injections would be less effective for ragweed allergic rhinitis than it would be for a bee sting?
bee venom must travel via blood from site of sting to target tissue (respiratory tract), so along the way it is likely it would combine with serum IgG blocking antibody
ragweed allergen can reach mast cells easily through nasal submucosa and would have less exposure to blocking IgG antibody
____ is a rare autosomal recessive diseased caused by mutation in the LYST gene
Chediak Higashi syndrome: mutation in LYST gene results in defective cytoplasmic protein that regulates lysosomal trafficking
leads to improper fusion of phagosomes and lysosomes in phagocytes
giant cytoplasmic granules are seen in affected leukocytes in blood and bone marrow smears (result of aberrant lysosomal fusion)
What is the mechanism behind the oculocutaneous albinism seen in Chediak Higashi syndrome?
melanocytes are not properly transferred to keratinocytes or epithelial cells - cannot exocytose melanin from melanosomes
85% of patients with Chediak-Higashi Syndrome enter the accelerated phase of the disease in their first decade of life. What is this phase called and how is it characterized?
Hemophagocytic Lymphohistocytosis (HLH): infiltration of many organs by non-neoplasticism lymphocytes (extended activity of APC) —> increase in immunodeficiency, pancytopenia, bleeding disorders, multi-organ inflammation
What would you see in a peripheral blood smear that would distinguish Chediak-Higashi Syndrome from Griscelli Syndrome?
laboratory analysis of blood from patients with CHS would show WBC with giant purple-stained granules
the only cure for Chediak-Higashi Syndrome is…
hematopoietic stem cell transplantation (HSCT) - should be done as soon as diagnosis is established (early in life)
*note that HSCT corrects immunological and hematologic manifestations, but does not prevent progressive neurological deterioration or oculocuteaneous albinism
*ideally before HLH accelerated phase is reached, if not, then after HLH is in remission
how does Chediak-Higashi Syndrome present clinically?
partial albinism, susceptibility to bruising/bleeding (low platelets), recurrent bacterial infections, photosensitivity, progressive neurodegeneration (neuropathy, sensory loss, cerebellar ataxia, cognitive impairment, muscular weakness)
