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Boards 23' > Immunology/Allergy > Flashcards

Immunology/Allergy Flashcards

1
Q

PAMPs

A

“pathogen-associated molecular patterns” - present on many microbes and not present on human cells

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2
Q

Endotoxin (LPS) binds what complex on macrophages?

A

CD14 - triggers TLR4 and cytokine release: IL-1, IL-6, IL-8 and TNF

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3
Q

Mannose (polysaccharide found in bacteria and yeast) binds which receptor to trigger an immune reaction?

A

mannose-binding lectin (MBL) from liver - activates the lectin pathway on complement activation

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4
Q

Phagocytosis of macrophage components?

A

reactive oxygen species (O2-) - produced by *NADPH Oxidase and reactive nitrogen intermediates (ONOO-) = peroxynitrate

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5
Q

how does TB block the process of phagocytosis in macrophages?

A

TB modifies the phagosome so that it is unable to fuse w/ the lysosome leading to proliferation inside the macrophage and protection from antibodies

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6
Q

Chediak-Higashi Syndrome

A

immune deficiency syndrome that results in failure of lysosomes to fuse with phagosomes - kids will have recurrent pyogenic bacterial infections - also oculocutaneous albinism and progressive neurological dysfunction

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7
Q

Surface receptors on macrophages

A

CD14 - LPS on gram (-)
Fc receptor - FC on antibodies
C3b receptor - complement
MHCII - CD4 on T cells
B7 - CD28 on T cells
CD40 - CD40L on T cells

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8
Q

the major cytokines release of macrophages

A

IL-1 = “endogenous pyrogen” act on the hypothalamus and causes fever

TNF-alpha = “cachectin” inhibits lipoprotein in fat tissue reducing FA and leading to *cachexia; also kills tumors in animals and can cause intravascular coagulation - DIC

Both cytokines increase synthesis of endothelial adhesions (allows neutrophils to enter inflamed tissues)

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9
Q

IL-6, IL-8 and IL-12 cytokines released by macrophages

A

IL-6 - fever and stimulates acute phase protein production in the liver (CRP)

IL-8 - attracts neutrophils

IL-12 - promotes TH1 development

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10
Q

neutrophils rolling mechanism

A

Rolling - Selectin ligand neutrophils (Silly-Lewis X) binds to E-selectin or P-selectin

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11
Q

neutrophils crawling mechanism

A

Crawling (tight binding) - neutrophils express integrins and bind ICAM on endothelial cells

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12
Q

neutrophils transmigration

A

Transmigration - neutrophils bind PECAM-1 between endothelial cells and migrate to the site w/ help from chemokines C5a and IL-8

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13
Q

small granules in neutrophils

A

alkaline phsophatase, collagenase, lysozyme, lactoferrin; they fuse w/ phagosomes and kill pathogens and also be released into the extracellular space

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14
Q

large granules in neutrophils

A

acid phosphatase and myeloperoxidase; these fuse w/ the phagosome ONLY (do not get released in extracellular space)

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15
Q

Major contrast w/ neutrophils and macrophages w/ antigen presentation

A

neutrophils do NOT present antigen (not an APC) and macrophages do present antigen

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16
Q

natural killer cells

A

CD16 binds to IgG
CD56 aka NCAM (identifying)
MHC I that presents to CD8 T cells

NK cells destroys human cells w/ reduced MHC I

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17
Q

ADCC

A

antibody-dependent cellular toxicity (ADCC) - antibodies coat pathogen and pathogen is then destroyed in a non-phagocytic process

ex: NK cells (CD16 on NK and Fc of IgG - NK kills cells) and eosinophils (IgE and Fc of IgE - release of toxic enzymes onto parasite)

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18
Q

Eosinophils

A

stain red due to major basic protein that has a (+) charge; activated by IgE and stimulated by IL-5 from Th2; increased in helminth infections and also seen in many allergic diseases

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19
Q

mast cells and basophils

A

appear blue
basophils = blood stream
mast cells = tissues

bind the Fc portion of IgE antibodies - cross-linking and *aggregation leads to degranulation of histamine and tryptase

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20
Q

transplant rejections within minutes to hours

A

hyperacute rejection: due to preformed antibodies (IgG) against graft antigens (ABO or HLA) - this is prevented by cross-matching

will see “white rejection”
gross motting and cyanosis, arterial fibrinoid necrosis and capillary thrombotic occlusion

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21
Q

transplant rejection within 6 months

A

acute rejection: exposure to donor antigens induces activation of naive immune cells - this is predominantly *cell-mediated (CD8)

biopsy: cellular - lymphocytes/mononuclear infiltrates

tx: immunosuppression

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22
Q

transplant rejection months to years later

A

chronic rejection: chronic low-grade immune response refractory to immunosuppression will see mixed cell-mediated and humoral response

Hallmark = fibrosis especially in vessels

kidneys: fibrosis of capillaries and glomeruli
heart: narrowing coronary arteries
lung: bronchiolitis obliterans

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23
Q

the most important cytokine mediator in septic shock

A

TNF-alpha
stimulates systemic inflammation and recruitment of additional leukocytes

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24
Q

HLA-DP, HLA-DQ and HLA-DR genes encode for with protein?

A

genes on chr 6
MHC class II which are expressed on APCs (B cells, macrophages and dendritic cells)

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25
Q

HLA-A, HLA-B and HLA-C genes encode for which protein?

A

genes on chr 6
MHC class I which are expressed on all nucleated cells (if not expressed then will be killed by NK cells)

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26
Q

C1 inhibitor (C1INH) deficiency

A

C1INH prevents C1 mediated cleavage of C2 and C4 thereby limiting activation of complement and it also blocks kvllikrein-induced conversion of kininigen to bradykinin

pt w/ this deficiency leads to elevated bradykinin (bradykinin-associated angioedema) NOTE: ACEi are contraindicated in these pts because they can lead to angioedma as well (precipitate disease episodes)

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27
Q

Adverse effects of corticosteroids on the immune system

A

neutrophilia (increase in neutrophils) - due to neutrophil demargination: neutrophil recruitment to fight infection is decreased leading to increased risk in infections

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28
Q

CD40L activity

A

expressed on helper T cells and important in costimulatory for APC

activates macrophages by binding CD40 and secreting TNF-alpha

stimulates class switching in B cells by binding CD40 and secreting IL-2/4

because CD40L is important for B cell class switching a deficiency will lead to hyperIgM syndrome

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29
Q

Sympathetic ophthalmia

A

traumatic injury in one eye that results in granulomatous inflammation of BOTH the injured and noninjured eye - occurs due to robust T-cell response to previously sequestered antigens in the eye that display *immune privilege

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30
Q

age-related immune decline

A

also called immunosenescence - loss of telomere length affects rapidly dividing cells such as immune cells leading to decreased production of naive B and T lymphocytes - these changes impair the adaptive immune response to novel (new) antigens such as pathogens or vaccinations - can predispose pts to vaccine failure and increases susceptibility to infections

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31
Q

skin test

A

delayed-type hypersensitivityskin test to screen for cellular immunodeficiency. the predominate cell responsible for a positive test would be T cells

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32
Q

mellatoproteinases

A

zince-containing enzymes that degrade components of the ECM and basement membrane, which is composed of laminin and collagens IV and VII

facilitate basement membrane penetration (invasion of malignancies)

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33
Q

type I hypersensitivity

A

immediate reaction to antigens (mins) due to preformed IgE antibodies from primary exposure: antibodies bind and cross-link and aggregate to mast cells and cause mast cell degranulation

all because IgE antibodies (IgG is normal response) **IL-4 is the key cytokine for IgE

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34
Q

Type I hypersensitivities reactions

A

Skin: urticaria (hives)
Resp: rhinitis or wheezing
Eyes: conjunctivitis (itchy red eyes)
GI: diarrhea
Anaphylaxis - can lead to shock and death tx: epinephrine

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35
Q

Type I hypersensitivities examples

A

asthma
penicillin drug allergy
seasonal allergies
allergic conjunctivitis
peanut allergy
shellfish allergy

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36
Q

type II hypersensitivity

A

antibodies IgG or IgM directed against OWN tissue antigens - they are binding normal structures, there are 3 mechanisms:

  1. phagocytosis (Fc receptors or C3b)
  2. complement-mediated lysis (classical complement)
  3. antibody-dependent cytotoxicity (ADCC)
37
Q

Type II hypersensitivities examples

A

Rheumatic fever - strep antibodies cross-react w cardiac myocytes

Exposure to wrong blood type - RBC lysis by circulating IgG (erythroblastosis fetalis Rh- mothers w/ Rh+ babies)

Autoimmune hemolytic anemia - methyldopa and penicillin: drugs bind to surface of RBCs or w mycoplasma pneumonia: induces RBC antibodies

38
Q

Type III hypersensitivities

A

antigen-antibody (IgG) complex forms and deposits in tissues; two types:

  1. generalized - serum sickness
  2. localized - Arthus reaction
39
Q

Serum sickness form of type III hypersensitivity reaction

A

immune complexes (IC) deposits in lots of places (skin, kidneys, joints) causes systemic disease - trigger complement activation (Fc receptors)

40
Q

Arthus reaction form of type III hypersensitivity reaction

A

local tissue reaction (unlike serum sickness - systemic)

injection of antigen will bind w/ preformed antibodies and form immune complexes (IC) locally; 4-10 hours later (not mins like type I)

41
Q

Type IV delayed type hypersensitivity

A

classic example: PPD test for TB
also contact dermatitis - poison ivy or chemical/oils/dyes that attach to skin cells

12-48 hours after exposure

42
Q

What is the likelihood of a sibling with the same mother and same father being a perfect MHC match for transplant donation?

A

25%

43
Q

Graft vs. Host Disease

A

mostly a complication of bone marrow transplant but can also occur in organ rich in lymphocytes - liver; the donated (grafted) *T cells (CD8) react to recipient cells, they see the recipient as foreign (the opposite of rejection - here the tissue is rejecting the body)

symptoms:
Skin: rash
GI: diarrhea, abdominal pain
Liver: increased LFT and bilirubin

44
Q

X-linked agammaglobulinemia

A

X-linked defect in BTK gene resulting in failure of B cells to mature (light chains not produced); recurrent bacterial infections and enteroviral infection after 6 months due to loss of maternal antibodies (IgG)

Findings: loss of mature B cells (CD19, CD20 and BCR), underdeveloped germinal centers

Tx: IV Igs

45
Q

Selective IgA deficiency

A

defective IgA - most pts are Asymptomatic but symptomatic pts will have Airway and GI infections from Giardiasis; associated w Autoimmune disease (SLE and RA), Atopy, and Anaphylaxis to IgA containing products (blood transfusions)

labs: low IgA but IgM and IgG will be normal

Special features: false positive B-HCG pregnancy test

46
Q

Common variable immunodeficiency (CVID)

A

defective in B cell maturation - loss of plasma cells and antibodies; often sporadic - no family hx

Normal B cell count but absence of antibodies (usually IgG but can be IgM to IgA - it is variable)

majority of 20-45 yr old pt (contrast w. X-linked agammaglobulinemia when baby after 6 months - infancy)

47
Q

DiGeorge Syndrome

A

22q11 deletion failure of 3/4th pharyngeal pouches to form leading to thymus and parathyroids

Classic triad:
loss of thymus (loss of T cells)
loss of parathyroid glands (hypocalcemia)
congenital heart defects

can also see facial abnormalities - cleft palate

**DO NOT confuse w/ SCID - calcium will be normal

48
Q

Hyper-IgE Syndrome

A

aka Job’s syndrome
deficiency in Th17 cells due to a STAT3 mut leading to an impaired recruitment of neutrophils

Labs: overproduction of IgE (eosinophils/histamine) and decreased IFN-gamma

FATED
coarse Facies, cold (noninflamed) staph Abscesses, retained primary Teeth, increased IgE and Derm probs (eczema)

49
Q

Classic case: newborn baby w/ deformed face or teeth, a diffuse rash (eczema) with a skin abscesses that are “cold” and also recurrent infections without fever, what should you suspect?

A

Hyper-IgE Syndrome aka Job’s syndrome

deficiency in Th17 cells due to a STAT3 mut leading to an impaired recruitment of neutrophils

Labs: overproduction of IgE (eosinophils/histamine) and decreased IFN-gamma

50
Q

Chronic mucocutaneous candidiasis

A

T cell dysfxn defects in AIRE genes; AIRE associates w lectin-1 and this responds to Candida antigens - defect = recurrent candida infections

noninvasive Candida albicans infections of skin and mucous membranes (thrush); associated w endocrine dysfunction

51
Q

Classic case: child w/ recurrent thrush and diaper rash with endocrine dysfunction should make you suspect what?

A

Chronic mucocutaneous candidiasis; T cell dysfxn defects in AIRE genes; AIRE associates w lectin-1 and this responds to Candida antigens - defect = recurrent candida infections

52
Q

Severe Combined Immunodeficiency (SCID)

A

loss of T cells and B cells; loss of thymus shadow; loss of germinal centers in nodes

due to either X-linked defective IL-2R or AR adenosine deaminase deficiency (ADA) - fins to convert adenosine to inosine

susceptible to many infections screen w: TRECs tx: bone marrow transplant

53
Q

Ataxia Telangiectasia

A

AR defective ATM gene in chr 11; repairs dsDNA breaks via non homologous end-joining (NHEJ) defective = failure to repair DNA mut

pts will have hypersensitivity of DNA to ionizing radiation

triad:
Ataxia, spider Angiomas and IgA deficiency

Labs: increased AFP, decreased IgA, IgG and IgE, increased risk of lymphoma and leukemia

54
Q

Hyper IgM Syndrome

A

class switching disorder due to failure of B cells (CD40) to T cells (CD40L) binding so B cells make IgM only (70% of cases are T cell prob w/ CD40L)

Labs: increased IgM and other antibodies are absent

55
Q

Wiskott-Aldrich Syndrome

A

X linked disorder of WAS gene leading to WASp absence/dysfxn which is necessary for T cell cytoskeleton - T cells cannot properly react to APCs

Immune dysfxn - decreased platelets and eczema, elevated IgE and IgA tx: bone marrow transplant

WATER: Wiskott-Aldrich, Thrombocytopenia, Eczema, Recurrent infections

56
Q

Leukocyte Adhesion Deficiency

A

defect in LFA-1 integrin (CD18) protein on phagocytes - impaired migration (roll) and chemotaxis

delayed separation of the umbilical cord (>30 days) and presents w/ a umbilical stump infection

increased neutrophils in blood (neutrophilia) but absence at infection site (no pus/delayed wound healing)

57
Q

Chediak-Higashi Syndrome

A

failure of lysosomes to fuse w phagosome due to mut in lysosomal trafficking regulator (LYST) gene; causes microtubule dysfxn

PLAIN: Peripheral neurodegeneration, Lymphohistiocytsis, Albinism,
Recurrent infections, and peripheral Neuropathy (often wheelchair bound)

58
Q

Chronic Granulomatous Disease (CGD)

A

loss of NADPH oxidase leads to decreased ROS and respiratory burst in neutrophils needed to kill catalase (+) organisms

catalase (+) organisms:
Staph aureus
Pseudomanas
Serratia
Nocardia
Aspergillus (fungi)

Test: Nitroblue tetrazolium test - absence of NADPH oxidase - cells do not turn blue (more blue = more NADPH present)

59
Q

NSAIDs

A

agents that reversibly inhibit COX 1 and COX 2

60
Q

Acute interstitial nephritis caused by NSAIDs

A

hypersensitivity reaction triggered by drugs; inflammation of the interstitum “space between cells” (not the nephron itself)

classic finding: urine eosinophils

61
Q

Classic case: pt takes NSAID then days to weeks later they present w fever and rash, oliguria and increased BUN/Cr and then eosinophils in the urine

A

Acute interstitial nephritis caused by NSAIDs; hypersensitivity reaction triggered by drugs; inflammation of the interstitum “space between cells” (not the nephron itself)

62
Q

COX-2 inhibitors

A

celecoxib
reversibly inhibits COX-2 only so there is less risk of GI ulcers/bleeding

Adverse effects of increased CV events (MI/strokes) and sulfa allergy

63
Q

Glucocorticoids

A

steroids that easily diffuse across cell membranes, bind glucocorticoid receptor (GR) the complex translocates into the nucleus and then alters gene expression

64
Q

MOA of Glucocorticoids

A
  1. inactivation of NF-kB: controls synthesis inflammatory mediators

Other effects: neutrophilia (increased WBCs) - more neutrophils in blood and less at infection

65
Q

Side effects of chronic glucocorticoids use

A

skin: skin thinning (paper thin) and easy bruising; Cushingoid appearance/weight gain - truncal obesity, buffalo hump and moon facies; Osteoporosis and hyperglycemia - increased liver gluconeogenesis; cataracts, myopathy and gastritis/peptic ulcers and avascular necrosis

66
Q

Avascular necrosis

A

osteonecrosis - associated with long tern steroid use - bone collapse of the femoral head

67
Q

Abrupt discontinuation in long-term steroid use

A

Adrenal insufficiency due to long term suppression of the HPA axis; symptoms (adrenal crisis):
hypotension/shock, anorexia, n/v, abdominal pain, weakness, fever and confusion or coma

68
Q

Cyclosporine and Tacrolimus

A

immunosuppressive drugs that both inhibit calcineurin (which activates NFAT - nuclear factor of activated T cells) - this is important to transcription of many cytokines (IL-2)

Adverse effect: Nephrotoxicity (most important) - vasoconstriction of afferent/efferent arterioles

69
Q

two unique side effects of cyclosporine

A

these are not reported w tacrolimus - gingival hyperplasia and hirsutism

70
Q

Sirolimus

A

kidney transplant immunosuppressive; inhibits mTOR (does NOT inhibit calcineurin); blocks response to IL-2 in B and T cells: the cell cycle arrest in the G1-S phase so there is no growth/proliferation

71
Q

Adverse effects of Sirolimus

A

anemia, thrombocytopenia and leukopenia, hyperlipidemia (inhibition of lipoprotein lipase) and hyperglycemia (insulin resistance)

72
Q

Coronary Stents

A

“drug-eluting stents” (DES) coated with anti-proliferating drug that blunts scar tissue growth (restenosis)

73
Q

Methotrexate

A

used as a chemotherapy and to tx some autoimmune disease; mimics folic acid - inhibits dihydrofolate reductase

74
Q

Side effects of Methotrexate

A
  • myelosuppression - reversible w leucovorin “leucovorin rescue”
  • stomatitis/mucositis (mouth soreness)
  • abnormal LFTs and GI upset
75
Q

Mycophenolic acid (mycophenolate)

A

aka CellCept
immunosuppressive drug that inhibits IMP dehydrogenase; the rate limiting step in purine synthesis in lymphocytes ONLY - decreased nucleotides leads to decreased DNA synthesis in T and B cells

76
Q

Cyclophosphamide

A

power immunosuppressant agent used in vasculitis and glomerulonephritis; it is a prodrug that requires activation by the liver (P450); it is an “alkylating agent” that causes DNA to cross link to inhibit DNA replication and cause cell death

Unique side effects of hemorrhagic cystitis - acrolein is toxic to the bladder and SIADH - hyponatremia that leads to seizures

77
Q

Azathioprine

A

immunosuppressive that is used in transplants and autoimmune disease; prodrug that is converted to 6-Mercaptopurine (6-MP) which competes for binding to HGPRT

77
Q

Azathioprine

A

immunosuppressive that is used in transplants and autoimmune disease; prodrug that is converted to 6-Mercaptopurine (6-MP) which competes for binding to HGPRT

78
Q

Muromonab-CD3

A

monoclonal antibody that is used in organ transplants binds to CD3 and blocks T cell activation; leads to T-cell depletion from circulation

Unique side effects: cytokine release syndrome - occurs after 1st or 2nd dose - fevers, rigors, n/v, diarrhea and hypotension

79
Q

Infliximab

A

antibody against TNF-alpha used in RA and Crohn’s; “chimeric” - both mouse and human components

there is a risk of reactivation of TB - PPD screening is done prior to tx

80
Q

Etanercept

A

TNF-alpha inhibitor made by recombinant DNA; it is an “decoy receptor” that binds TNF binds instead of binding the actual TNF-alpha receptor

81
Q

pt w Common variable immunodeficiency (CVID) have an increased risk of developing which other disorders?

A

autoimmune disorders and lymphoma

82
Q

Which GI disease has a high association with IgA deficiency?

A

Celiac’s disease

83
Q

Autoimmune diseases are caused by what broad defect in the immune system?

A

loss of self-tolerance (central - thymus/bone marrow or peripheral - lymph nodes)

NOTE: negative selection is very important for T cells so they do not attack self tissue

84
Q

Effects of IL-2

A

produced by CD4, CD8 and NK cells and has strong proinflammatory and some anti-inflammatory effect; high-dose IL-2 therapy can be used for advanced renal cell carcinoma and metastatic melanoma; this can lead to long-lasting remission due to increased cytotoxic activity of NK cells against the tumor

85
Q

Programmed cell death protein 1 (PD-1)

A

PD-1 is an immune checkpoint inhibitor that down-regulates the T-cell response; neoplastic cells and chronic viral infections often exploit this receptor via over expression of PD-1 ligand; PD-1 ligand inhibits restore the T-cell response, allowing cytotoxic T-cells to kill infected or neoplastic cells

86
Q

X-linked agammaglobulinemia

A

X-linked agammaglobulinemia is characterized by low or absent circulating mature B cells (CD19, CD20, Cd21) and pan-hypogammaglobulinemia; affected pts have increased susceptibility to pyogenic bacteria, enteroviruses, and Giardia lambda due to the absence of opsonizing and neutralizing antibodies

87
Q

Splenectomy

A

the spleen acts as both a blood filter capable of removing circulating pathogens and as a major site of opsonizing antibody synthesis; splenic pts are prone to infections caused by encapsulated organisms (Strep pneumonia, H. influenza and Neisseria meningitidis)

Boards 23' (29 decks)

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