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STEP1 2015 > Immunology > Flashcards

Immunology Flashcards

1
Q

primary lymphoid organs

A

bone marrow

thymus

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2
Q

Secondary lymphoid organs

A

spleen, lymph nodes, MALT

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3
Q

Peyer patches

A

only found in the lamina propria and submucosa of the ileum, made of unencapsulated lymphoid tissue and containing M cells, which sample ans present antigens to immune cells.
Peyer patch germinal center B cells make IgA.

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4
Q

LN

A

where macrophages filter lymph, B and T cells are stored, and where immune response activation/ proliferation/ differentiation take place.

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5
Q

LN- follicle

A

B cell localization

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6
Q

Medulla (middle, medial to paracortex)

A

Medullary sinuses house macrophages

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7
Q

Paracortex

A

Paracortex houses T cells (between follicles and medulla. high endothelial venules through which T and B cells enter from blood, not well developed in patient with DiGeorge, expands when cellular immune reponse (viral infection)

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8
Q

arm, lateral breast

A

axillary nodes

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9
Q

lateral dorsum of foot

A

popliteal nodes

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10
Q

thighs

A

superficial inguinal nodes

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11
Q

stomach

A

celiac nodes

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12
Q

duodenum, jejunum

A

superior mesenteric nodes

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13
Q

sigmoid colon

A

inferior mesenteric

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14
Q

upper rectum

A

pararectal

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15
Q

lower rectum above pectinate line

A

internal iliac nodes

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16
Q

lower rectum below pectinate line

A

superficial inguinal nodes

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17
Q

testes

A

para-aortic lymph nodes. testes descend from within the body cavity and are not a superficial structure

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18
Q

scrotum

A

superficial inguinal nodes

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19
Q

right arm, right half of head

A

right lymphatic duct

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20
Q

everything besides the right arm and right half of the head

A

thoracic duct, which joins in at the branch of the left IJ and brachiocephalic veins

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21
Q

sigmoid colon

A

inferior mesenteric nodes

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22
Q

upper rectum

A

pararectal lymph nodes

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23
Q

lower rectum above pectinate line

A

internal iliac nodes

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24
Q

lower rectum below pectinate line

A

superficial inguinal nodes

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25
Q

HLA B27 associated with disease

A

psoriatic arthritis, ankylosing spondylitis, arthritis of inflammatory bowel disease, reactive arthritis (formerly Reiter syndrome) seronegative arthropathies

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26
Q

DR3

A

diabetes mellitus type I, SLE, Goodpasture syndrome

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27
Q

DR4

A

rheumatoid arthritis, DM1 (4 walls in a rheum)

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28
Q

DR5

A

pernicious anemia > B12 deficiency, Hashimoto thyroiditis

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29
Q

DR2

A

MS, hay fever, SLE, Goodpasture syndrome

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30
Q

DQ2/DQ8

A

celiac disease

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31
Q

A3

A

hemochromatosis

32
Q

IL2

A

T cell proliferation

33
Q

IL4

A

B cell proliferation, Th0 stimulated to become Th2

34
Q

IL5

A

B cell proliferation

35
Q

IL10

A

Th1 and macrophage inhibition

36
Q

IL12

A

Th0 is stimulated to become Th1

37
Q

IFN-gamma

A

macrophage activation, Th2 inhibition

38
Q

cytokines produced by Th1

A

IL2, IFN-gamma

39
Q

cytokines produced by Th2

A

IL2, IL4, IL5, IL10

40
Q

B cell surface markers

A

CD19, 20 21, IgM, IgD, MHCI, MHC II, B7 protein (80 or 86), CD40

41
Q

The differential diagnosis for eosinophilia

A

Collagen vascular disease (PAN, dermatomyositis)
Atopic diseases (allergy, asthma, churg- strauss, bronchopulmonary asperfillosis)
Neoplasm
Adrenal insufficiency (Addison disease)
Drugs (NSAIDs, PCN, cephalosporin)
Acute interstitial nephritis
Parasites (Strongyloides, Ascaris > Loeffler eosinophilic pneumonitis)
Other: HIV, hyper IgE, coccidiomycosis, etc.

42
Q

secreted by all T cells

A

IL2, IL3

43
Q

secreted by Th1 cells

A

IL2, IL3, IFN gamma

44
Q

secreted by Th2 cells

A

ILe, IL3, IL4, IL5, IL20

45
Q

secreted by macrophages

A

IL1, IL6, TNFa ramp up immune response and generate fever, IL6, IL8, Il12 (promotes Th2 from Th0

46
Q

hyperacute transplant rejection

A

within minutes, type 2 hypersensitivity reaction by host abs that activate complement, features widespread thrombosis of graft vessels leading to ischemia/necrosis, treat by removing the graft

47
Q

acute transplant rejection

A

weeks to months, CD8 T cells activate against foreign MHC, humoral is also possible, with abs developing after the transplant. reversible, features vasculitis of graft vessels with dense interstitial lymphocytic infiltrate. reverse with IL2 blockers and other immunosuppressants

48
Q

chronic transplant rejection

A

months to years, translplant cells present antigens to the hosts’ T cells, this is a cellular and humoral response, featuring vascular smooth muscle proliferation and parenchymal fibrosis, lots of cytokines, arteriosclerosis

49
Q

graft versus host disease

A

variable amount of time. new transplanted immune system attacks that host, as if the host is non- self, features maculopapular rash, jaundice, diarrhea, hepatosplenomegaly, bone marrow and liver transplants are most prone, potentially benefital in bone marrow transplant for leukemia (graft- versus- tumor)

50
Q

cyclosporine side effects

A

binds cyclophilins in cysotol of T cells. cyclophilin binding inhibits calcineurin and this prevents IL2 transcription,

transplant rejection, psoriasis, severe RA, other severe autoimmune

NEPHROTOXICITY because it constricts both afferent and efferent kidney arterioles, hypertension, hyperlipidemia, neurotoxicity, gingival hyperplasia, hirsutism

51
Q

Tacrolimus (FK506) and pimecrolimus

A

calcineurin inhibitor that binds FK506 binding protein, the complex blocks T cell activation by inhibiting calcineurin and transcription of IL2,

used for transplant rejection prophylaxis and topical application for eczema

nephrotoxity, increased risk of diabetes and neurotoxicity, HTN

52
Q

Sirolimus (Rapamycin)

A

Binds FK binding protein 12 (FKBP12), inhibiting mammalian target of rapamycin (mTOR). This blocks T cell activation and B cell differentiation by preventing T cell response to IL2

NOT NEPHROTOXIC
so it can be used to prevent kidney transplant rejection

synergistic with cyclosporine
can be used in drug- eluting stents

side effects include anemia, thrombocytopenia, leukopenia, insulin resistance, hyperlipidemia

53
Q

Azathioprine

A

precursor of 6-mercaptopurine (6MP), interferes with nucleic acid synthesis so that the immune cells can’t divide and proliferate

used in kidney transplants, autoimmune disorders

side effects include bone marroq suppression. It is metabolized by xanthine oxidiase. Toxic effecst are increased by allopurinol, which inhibits xanthine oxidase.

54
Q

Mycophenalate

A

Mechanism: inhibits synthesis of guanine by inhibiting inosine monophosphate dehydrogenase (IMP) and thereby prevents lymphocyte proliferation

this is how it prevents humoral response. used in transplant patients and off- label for lupus nephritis

side effects include hyperglycemia, hypercholesterolemia, hypertension, infection, LYMPHOMA, infection, teratogenic

55
Q

Thalidomide

A

sedative given to pregnant women, causes phocomyelia. mechanism is that is suppresses TNFa, increases NK cells and IL2 both suppressing and inhibiting immune response. Used for erythema nodosum leprosum (Hansen disease), multiple myeloma where it stmulates cancer cells to kill the cancer cells.

56
Q

infliximab and adalimumab

A

bind TNFa

57
Q

Rituximab

A

anti CD20 mAb that binds B cells and induces complement to lyse the B cells
useful for B cell non-Hodgkin lymphoma, CLL, RA, ITP

58
Q

Eculizumab

A

complement protein C5, mimics TNFalpha receptor decoy receptor.

use for paroxysmal nocturnal hemoglobinuria

59
Q

Adalimumab, infliximab

A

binds soluble TNFa, used for IBD, RA, ankylosing spondylitis, and psoriasis

60
Q

Abciximab

A

platelet glycoproteins IIb/IIIa. Antiplatelet agent for prevention of ischemic complications in patient undergoing percutaneous coronary intervention.

61
Q

Thymic aplasia

A

DiGeorge
90% have a chr 22q11 del (FISH)

3rd and 4th pouches fail to develop
no thymus so no mature T cells, so recurrent viral, fungal, protozoal infections

congenital defects in heart/ great vessels

no parathyroid so no PTH so tetany 2/2 hypocalcemia

62
Q

Hypocalcemia signs

A

Chvostek sign- tap on the cheep to cause a muscle spasm

Trousseau sign- tightening the BP cuff yields carpo- pedal spasm

63
Q

chronic mucocutaneous candidiasis

A

T cell dysfunction leading to problems specifically with c. albicans.
give prophylactic ketoconazole

64
Q

IL12 receptor deficiency

A

Th0 cells without IL12 R.
Macrophages still make IL12 but the Th0 don’t differentiate correctly into Th1 the way they would under normal circumstances
Increased susceptibility to mycobacterial and fungal infections

65
Q

Bruton agammaglobulinemia

A

X- linked (boys)
B-cell deficiency leading to defective tyrosine kinase gene, low levels of all immunoglobulins results, and therefore recurrent bacterial infections after 6 months (after passive immunity)

66
Q

Selective immunoglobulin deficiencies

A

Selective IgA is most common. Patient appears healthy, even unaware.
Recurrent sinus and lung infections
1/6 people of European descent, associated with atopy, asthma
important to diagnose because possible anaphylaxis to blood transfusions and blood products.
not much you can do to treat this, but you can give prophylactic treatment before blood products.

67
Q

Severe combined immunodeficiency

A 
defect in early stem cell differentiation, can be caused by at least 7 different gene defects leading to Adenosine deaminase deficiency
Last line is NK cells
Presentation triad: 
I Failure to thrive
II chronic diarrhea
III recurrent infections: 
1 .chronic mucocutaneous candidiasis
2. fatal or recurrent RSV, VZV, measles, flu, parainfluenza
3. pneumocystis jirovecii (PCP), PNA

No thymic shadow on newborn CXR (ddx DiGeorge)

68
Q

Ataxia telangiectasia

A

IgA deficiency and T cell deficiency leading to sinus and lung infections
Cerebellar ataxia
Poor smooth pursuit of moving target with eyes
Telangiectasias on face (after 5 yrs age)
Radiation sensitivity (avoid x- rays)
increased risk of lymphoma and acute leukemias
elevated AFP after 8 months of age
Average oge of death is 25yo

ATAXIA:
Ataxia
Telangiectasia
Acute leukemia and lymphoma
X- ray sensitivity
IgA deficiency
AFP
69
Q

Wiskott Aldrich

A 
WAITER
Wiskott
Aldrich
Immunodeficiency
Thrombocytopenia and purpura
Eczema (truncal)
Recurrent pyogenic infections

X- linked
No IgM against bacterial capsular polysaccharides
Low IgM, high IgA

70
Q

Hyper IgM syndrome

A

Increased IgM; other antibody isotypes decreased

The 2 most important variants include AR where there is no CD40 on B cells

More common is the X- linked version where there is no CD40L on the helper T cell

71
Q

Chronic granulomatous disease

A

X- linked (65- 70%)
Lack of NADPH oxidase so the phagocytes cannot destroy catalase- positive microbes

Patient is especially susceptible to catalase- positive pathogens, especially
staph aureus and aspergillus infections

Diagnosis is based on negative nitro- blue tetrazolium test (impotent phagocytes)

Treatment: prophylactic TMP- SMX
IFN- gamma is also helpful (mechanism unclear)

72
Q

Chediak Higashi

A

phagosome can ingest but can’t transport to lysosome for digestion due to missing LYST gene.
Defective phagocyte lysosomes leads to giant cytoplasmic granules in PMNs

Presentation triad:

  • partial albinism
  • recurrent respiratory tract and skin infections
  • neurologic disorders
73
Q

HyperIgE syndrome

Job syndrome

A

Mutation in STAT3 Jak/Stat signaling pathway gene leading to

  • impaired PMN recruitment
  • impaired Th17 differentiation (mucosal, recruit PMN)

Patient with high levels of IgE and eosinophilia

Presents with eczema
recurrent cold s. aureus abcesses (biblical Job with boils); PMNs can’t be recruited so they stay cold
Coarse facial features: broad nose, prominent forehead, deep- set eyes, and doughy skin
Retains primary teeth resulting in 2 rows of teeth

74
Q

Leukocyte adhesion deficiency syndrome

A

abnormal integrins leads to inability of phagocytes to exit circulation

delayed separation of umbilical cord

75
Q

X- linked immunodeficiencies: WATCH

A

Wiskott- Aldrich
Agammaglobulinemia (Bruton)
Chronic granulomatous disease
Hyper- IgM syndrome

76
Q

evidence of asplenia in the blood

A

thrombocytosis
Howell- Jolly bodies
Target cells

77
Q

autoabs in type 1 and type 2 autoimmune hepatitis

A

Type 1:ANA, anti-smooth muscle ab

Type 2: anti- liver- kidney microsomal ab
Anti- liver cytosol ab

STEP1 2015 (30 decks)

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