missed questions Flashcards

1
Q

high molecular weight bacterial polysaccharides stimulate _____ complement pathway, which begins with _____

A

high molecular weight bacterial polysaccharides stimulate ALTERNATIVE complement pathway, which begins with C3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

C1 and C2 are part of which complement pathway

A

classical, activated by antigen-bound Ab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

biological agents ending in “-cept” contain ____

A

receptor moieties as part of their molecule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

abatacept inhibited _____ by binding _____

A

abatecept: inhibits T CELL ACTIVATION by binding CD80 and CD86 on APC (aka B7), preventing APC from binding CD28 on T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

difference between plasma and serum

A

PLASMA has CLOTTING factors

serum does NOT

both have antibodies, neither have RBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

____ domains of Ab differentiate isotypes

A

CONSTANT domains of HEAVY chain (part on the bottom in Fc region)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

haptens

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

molecules that require a carrier to be immunogenic, even if they are antigenic

A

haptens - can bind antibody (antigenic) but too small to cause immune response (immunogenic) on their own

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

when do T cells begin producing effector cytokines like IL-4, IFN-y?

A

after differentiation from naive cells into effector/memory cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

how do NK cells kill

A

via granules!! extracellularly!! target virus infected cells or tumor cells!!

secretory lysosomes contain perforins, defensiones, proteases —> induce apoptosis or lysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

TH1 produce ___, which activates ____
TH2 produce ____, which activates ____

A

TH1 —> IFNy —> macrophages
TH2 —> IL-4 —-> B cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

_____ cells of cortex and medulla of thymus assist in selection of immunocompetent T cells

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

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

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

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

A

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

17
Q

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?

A

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

18
Q

How would you set up a RAST assay for a patient’s allergy to dog dander? (the steps of the assay)

A
  1. dog dander antigen is covalently linked to the insoluble matrix
  2. IgE anti-dander is added (patient’s serum)
  3. amount bound is determined by radio-labeled anti-human IgE
19
Q

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

A

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]

20
Q

after an intradermal injection of an allergen, a visible and immediate hypersensitivity reaction usually occurs in…

A

1 to 15 minutes

21
Q

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

A

d. glucocorticoids

bronchial hyper-responsiveness associated with chronic asthma is caused by chronic inflammation of peribronchial tissues - glucocorticoids are most effective therapy for inflammation

22
Q

by what mechanism does cromolyn sodium prevent mast cell degranulation?

A

stabilizes the membrane

23
Q

Explain why desensitization by a series of injections would be less effective for ragweed allergic rhinitis than it would be for a bee sting?

A

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

24
Q

____ is a rare autosomal recessive diseased caused by mutation in the LYST gene

A

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)

25
Q

What is the mechanism behind the oculocutaneous albinism seen in Chediak Higashi syndrome?

A

melanocytes are not properly transferred to keratinocytes or epithelial cells - cannot exocytose melanin from melanosomes

26
Q

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?

A

Hemophagocytic Lymphohistocytosis (HLH): infiltration of many organs by non-neoplasticism lymphocytes (extended activity of APC) —> increase in immunodeficiency, pancytopenia, bleeding disorders, multi-organ inflammation

27
Q

What would you see in a peripheral blood smear that would distinguish Chediak-Higashi Syndrome from Griscelli Syndrome?

A

laboratory analysis of blood from patients with CHS would show WBC with giant purple-stained granules

28
Q

the only cure for Chediak-Higashi Syndrome is…

A

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

29
Q

how does Chediak-Higashi Syndrome present clinically?

A

partial albinism, susceptibility to bruising/bleeding (low platelets), recurrent bacterial infections, photosensitivity, progressive neurodegeneration (neuropathy, sensory loss, cerebellar ataxia, cognitive impairment, muscular weakness)