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Immunology Flashcards

1
Q

primary immune system organs

A

Bone Marrow - B cell maturation

Thymus - T cell differentiation and maturation

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2
Q

secondary immune system organs

A

Spleen, lymph nodes, tonsils, peyer patches allow immune cells to interact with antigens

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3
Q

Lymph node

A

nonspecific filtration by macrophages
Storage of B and T cells
Immune response activation

Follicle - B cells

Paracortex- T cells. Endothelial venules which allow T and B cells to enter from blood. Enlarges in extreme immune response

Medulla - medullary cords (lymphocytes and plasma cells) and medullary sinus (reticular cells and macrophages, also communicates with efferent lymphatics)

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4
Q

Spleen

A

Red pulp - sinusoids which are long vascular channels

White pulp - T cells in Periarteriolar lymphatic sheath (PALS). B cells are found in follicles (White pulp -> white blood cells)

Marginal zone - between red and white pulp contains macrophages and specialized B cells. This is where antigen presenting cells (APCs) capture blood borne antigens for recognition by lymphocytes

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5
Q

Splenic dysfunction/postsplenectomy findings

A

decrease IgM –> decrease complement activation –> decrease C3b opsonization –> increase susceptibility to encapsulated organisms

Postsplenectomy: Howell -jolly bodies, target cells, thrombocytosis, lymphocytosis

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6
Q

opsonization

A

Antibody opsonization is the process by which the pathogen is marked for ingestion and eliminated by the phagocytes.

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7
Q

Thymus

A

THymus = THird pharyngeal pouch

Cortex - immature T cells

Medulla- mature T cells and hassal corpuscles containing epithelial reticular cells

Normal neonatal thymus is “sail shaped” on CXR

Thymoma - myasthenia gravis and superior vena cava syndrome

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8
Q

Innate immunity

A

neutrophils, macrophages, monocytes, dentritic cells, natural killer cells, complement, physical epithelial barriers, secreted enzymes

Resistance does not change throughout organisms lifetime

nonspecific, rapid, no memory response

secretes lysozymes, complement, c reactive protein (CRP), defensins

Pathogen recognition via toll like receptors (TLRs) - recognize pathogen associated molecular patterns (PAMPs) and lead to activation of NK-kB (i.e. LPS in gram -)

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9
Q

Adaptive immunity

A

T cells, B cells, Circulating antibodies

Variations through the V(D)J recombination during lymphocytes development

Resistance is not heritable, highly specific, refined over time, memory response

Secretes immunoglobulins

Memory cells: activated B and T cells

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10
Q

Major histocompatibility complex I

A

1 loci: encoded by the HLA-A,B, and C genes

Binds T cell receptors (TCRs) and CD8 on CD8+ cytotoxic T cells

1 long chain and 1 short chain ( 3 alpha, 1 Beta)

Antigen loaded onto MHC I in RER after delivery via TAP (transporter associated with antigen processing)

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11
Q

Major histocompatibility complex II

A

2 loci: encoded by HLA-DP, DQ, and DR

Binds TCRs and CD4 on CD4+ helper T cells

Antigen laoded following release of invariant chain in an acidified endosome

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12
Q

MHC I diseases

A

HLA-A3 : Hemochromatosis
HLA-B8 : addison disease, myasthenia gravis, graves disease (dont be l8te dr. addison, or youll send my patient to the grave)
HLA-B27: Psoriatic arthritis, Ankylosing spondylitis, IBD-associated arthritis, Reactive arthritis

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13
Q

MHC II diseases

A

HLA-DQ2/DQ8: Celiac disease (cant eat DQ ice cream)
HLA-DR2: multiple sclerosis, hay fever, SLE, goodpasture (2-3 SLE)
HLA-DR3- DM type I, SLE, Graves disease, hashimoto , addison disease (2-3 SLE)
HLA-DR4: Rheumatoid arthritis, diabetes mellitus type 1, Addisons disease “ 4 walls in the rheum”
HLA-DR5: hashimoto thyroiditis (Hashimoto is an odd doctor DR3 and DR5)

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14
Q

Natural killer cells

A

perforin and granzymes induce apoptosis

Also by anibody dependent cell mediated cytotoxicity (CD16 binds Fc region of bound Ig activating the NK cells)

enhanced by IL2, IL12, IFN alpha, IFN beta

induce to kill when exposed to nonspecific activaion signal or absence of MHC I

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15
Q

B cells

A

humoral immunity
recognize antigen, produce antibody by differentiating into plasma cells to secrete specific immunoglobulins, maintain immunological memory

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16
Q

T cells

A

Cell mediated immunity

CD4+ t cells help B cells
CD8+ T cells directly kill

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17
Q

Differentiaton of T cells

A

1) T cell precursor in the bone marrow
2) in the cortex of the thymus we have positive selection where T cells expressing TCR capable of binding self-MHC on coritcal epithelial cells survive
3) In the medulla of the thymus we have negative selection where T cells with TCRS that have high affinity for self antigens undergo apoptosis or become regulatory T cells
4) move to lymph nodes where CD8+ T cells become cytotoxic T cells and CD4+ T cells become Helper T cells
5) Helpter T cells –> Th1, Th2, Th17, Treg

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18
Q

TH1

A

+ IL 12 and IFN gamma
- IL 4 and IL 10

secretes IFN gamma

Activates macrophages and cytotoxic T cells to kill phagocytosed microbes

THis is enhanced by the T cell CD40L interacting with CD 40 on macrophages

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19
Q

TH2

A

+ IL 2 and IL 4
- IFN gamma

Secretes IL-4, IL-5, IL-6, IL 10 , IL 13

activates eosinophils and promotes production of IgE for parasite defense

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20
Q

TH17

A

+ TGF beta and IL-6
- IFN gamma and IL 1 and IL6

secrete sIL 17, IL 21 IL 22

immunity against extracellular micorbes through induction of neutrophilic inflammation

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21
Q

Treg

A

+ TGF beta
- IL-6

Secretes TGF beta and IL 10 and IL 35

Regulatory T cells that produce anti antiinflammatory cytokines

prevents autoimmunity by maintaining tolerance to self antigens

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22
Q

Regulatory T cells

A

are identified by expression of CD3, CD4, and CD25, and FOXP3

IPEX syndrome ( Immune dyregulation, polyedocrinopathy, enteropathy, X linked) - geneticdeficiency in FOXP3

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23
Q

T cell activation

A

Dendritic cell migrates to the lymph nodes to present the antigen

T cell activation (signal 1) : antigen is presented on the MHC and recognized by the TCR of the Th Cell.

Proliferation and survival (signal 2) : B7 protein (CD80/86) on the dendritic cell and the CD28 on the naive T cell interact

Th cell activates and produces cytokines

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24
Q

B cell activation

A

After the Th cell activates

B cell is an antigen presenting cell

Foreign antigen is present on the MHC II and recognized by the TCR on the Th cell

CD40 receptor on the B cell binds CD40 ligand on the Th cell

Th cell secretes cytokines that determine Ig class switching of B cell –> B cell begins antibody production

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25
Q

Antibody structure

A

Fab consists of light and heavy chains and recognizes antigens

Fc region of igM and IgG fixes complement. All heavy chain

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26
Q

Fab region of antibody

A

Fragment, antigen binding

Variable and hypervariable regions

Unique antigen binding pocket

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27
Q

Fc region of antibody

A

constant region, carboxy terminal, complement binding, carb side chains, determines iso type (igM, IgD)

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28
Q

Mature naive B cells prior to activation express?

A

IgM and IgD

they eventually isotype switche in lymph nodes into plasma cells that secrete IgA, IgE, or IgG

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29
Q

IgG

A

secondary response to an antigen

Fixes complement
Opsonizes bacteria
neutralizes toxins and viruses

ONLY isotype that crosses the placenta and provides infants with passive immunity

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30
Q

IgA

A 
prevents attachment to mucous membranes
does not fix complement
Monomer in circulation
Dimer with J chain when secreted
Gi tract, tears, saliva, mucus, and breast milk
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31
Q

IgM

A

Primary response to an antigen (immediate)

Fixes complement

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32
Q

IgE

A

binds mast cells and basophils

Immediate (type I) hypersensitivity

immunity to parasites b activating eosinophils

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33
Q

thymus independent vs thymus dependent antigens

A

independent lacks a peptide component

dependent contains a protein component

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34
Q

Complement

A

plays a role in innate immunity and inflammation

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35
Q

C3b
C3a,C4a,C5a
C5a

A

C3b binds bacteria (opsonization)
C3a,C4a,C5a - anaphylaxis
C5a-neutrophil chemotaxis

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36
Q

MAC?

A

membrane attack complex defends against gram _ bacteria

Cytolysis

C5b-9

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37
Q

Opsonins

A

C3b and IgG are the two primary ones in bacterial defense

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38
Q

Inhibitors

A

decay accelerating factor (DAF aka CD55) and C1 esterase inhibitor help prevent complement activation on self cells

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39
Q

Paroxysmal nocturnal hemoglobinuria

A

defect in PIGA gene

prevents formation of anchors for complement inhibitors such as DAF/CD55 and membrane inhibitor of reactive lysis )MIRL/CD59)

Causes complement mediated lysis of RBCs

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40
Q

IL 1

A

“Hot T-Bone stEAK” for 1,2,3,4,5,6

IL 1 is HOT for fever

Secreted by macrophages

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41
Q

IL 2

A

“Hot T-Bone stEAK” for 1,2,3,4,5,6

IL 2 is for T cells stimulation

Secreted by T cell

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42
Q

IL3

A

“Hot T-Bone stEAK” for 1,2,3,4,5,6

IL3 is for bone marrow stimulation

Secreted by T cell

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43
Q

IL4

A

“Hot T-Bone stEAK” for 1,2,3,4,5,6

IL4 is for IgE

secreted by Th2 cells to induce differenciation of T cells into Th2 cells

Promotes growth of B cells and enhances class switching to IgE and IgG

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44
Q

IL5

A

“Hot T-Bone stEAK” for 1,2,3,4,5,6

IL4 is for IgA production

Growth and stimulation of eosinophils

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45
Q

IL6

A

“Hot T-Bone stEAK” for 1,2,3,4,5,6

aKute phase protein production

secreted by macrophages

46
Q

IL8

A

neutrophils

secreted by macrophages

47
Q

IL 12

A

T cells into Th1 cells
activates NK cells

secreted by macrophages

48
Q

TNF alpha

A

causes WBC recruitment and vascular leak. activates the endothelium

granulomas in TB

mediates fever and sepsis along with IL1 and IL6

49
Q

IL 10

A

decreases expression of MHC class II and Th1 cytokines

TGF beta and IL10 both attenuate the immune response

50
Q

Respiratory burst

A

rapid release of reactive oxygen species from different types of cells

activation of phagocyte NADPH oxidase complex which utilizes O2 as a substrate

NADPH plays a key role in both CREATION and NEUTRALIZATION Of ROS

51
Q

Respiratory burst rxn

A

Inside phagolysosome

O2 + NADPH — NADPH oxidase –> O2*-

O2*- is super oxide anion –superoxide dismutase —> H2O2

H2O2 + Cl- —Myeloperoxidase–> HClO*

NOTE: myeloperoxidase contains a blue-green heme containing pigment that gives sputum its color

HClO* is hydroxyl- halide radicals which degrades bacteria

52
Q

Patient with whose phagocytes cannot kill some types of bacteria and fungi due to a deficieny of what enzyme in the oxidative burst/respiratory burst?

A

NADPH oxidase

phagocytes of patients with chronic granulomatous disease can utilize H2O2 generated by invading organisms and convert it to ROS

Increased risk of infection by catalase + species because they neutralize their own H2O2 leaving phagocytes without ROS for fighting infections

53
Q

Interferons

A

INTERFERE with RNA and DNA viruses

synthesized by cirus infected cells that act on local cells to prime them for viral defense

how?

  • downregulating protein synthesis to resist potential viral replciation
  • upregulating MHC expression
54
Q

T cell surface proteins

A

TCR
CD3
CD28 binds B7 on APC

55
Q

Helper T cells surface protiens

A

CD4
CD40L
CXCR4/CCR5 (coreceptor for HIV)

56
Q

cytotoxic surface proteins

A

CD8

57
Q

Regulatory T cells surface proteins

A

CD4

CD25

58
Q

B cell surface proteins

A 
Ig
CD19
CD20
CD21 (receptor for EBV - "bar" drinking age is 21)
CD40
MHC II
B7
59
Q

MAcrophage surface proteins

A 
CD14 (receptor for PAMPS like LPS)
CD40
CCR5
MHC II
B7 (CD80/86)
Fc and C3b receptors (enhance phagocytosis)
60
Q

NK cell surface proteins

A

CD16

CD56 (marker for NK)

61
Q

Hematopoietic stem cells

A

CD34

62
Q

Anergy

A

state where a cell cannot become activated by exposure to its antigen (i.e. no costimulatory signal)

example of self tolerance

63
Q

Passive immunity

A

By receiving preformed antibodies from someone else to protect from infection (i.e. IgA in breast milk, materla IgG, antitoxin etc)

Rapid and short lived protection

Give preformed antibodies to pt afer exposure to tetanus toxin, botulinum toxin, HBV, Varicella, Rabies virus, or diphtheria toxin

64
Q

Active immunity

A

Exposure to foreign antigens (i.e. natural infection, vaccines etc.)

Slow but long lasting protection/memory

65
Q

Live attenuated vaccine

A

No pathogenicity but retains ability for growth

Induces cellular and humoral responses

Given for “Attention! Please Vaccinate Small Beautiful Young Infants with MMR Regularly”

1) adenovirus
2) Polio virus
3) Varicella
4) Smallpox
5) BCG
6) Yellow Fever
7) Influenza
8) MMR
9) Rotavirus

66
Q

Killed or inactivated vaccine

A

Pathogen is inactivated but maintains epitope structure on surface antigen

Induces humoral response

Safer but weaker and rewures booster shots

RIP Always = Rabies, Influenza, Polio, Hep A

67
Q

Subunit

A

Includes only the antigens that best stimulate the immune system

HBV via HBsAg
HPV (types 6,11,16,18)
etc.

68
Q

Toxoid

A

Denatured bacterial toxin with intact receptor binding site

protects against bacterial toxins without risk of disease

i.e. clostridium tetani

69
Q

Type I hypersensitivity

A

ABCD 1234

Type 1 –> A –> Anaphylactic and Atopic

Two phases:

1) Immediate (minutes) - antigen crosslinks preformed IgE on presensitized mast cells
2) Late (hours): chemokines (attract inflammatory cells/WBCs) and cytokines cause inflammation and tissue damage

Example: allergen specific IgE test

70
Q

Type II hypersensitivity

A

ABCD 1234

Type 2 –> AntiBody mediated

Antibodies bind to cell surface antigens causing cellular destruction (cell is opsonized and then either phagocytosis, complement activation, or Nk cell killing occurs), inflammation due to complement system activation and Fc receptor mediated inflammation, Cellular dysfunction due to abnormal blockade of activation of downstream process

Direct coombs test - detects Ab DIRECTLY attached to RBC surface

Indirect coombs test- detects Ab unbound in the serum

71
Q

Type III hypersensitivity

A

ABCD 1234

3–> immune Complex

antigen antibody (mostly IgG) complexes activate complement

complement attracts neutrophils which release lysosomal enzymes

Examples: SLE, polyarteritis nodosa (systemic necrotizing inflammation of small and medium BV), poststrococcal glomerulonephritis

Serum sickness- antibodies to foreign proteins
Arthus reaction - local subacute immune complex mediated hypersensitivity reaction after intradermal injection of antigen into presensitized individual

72
Q

Type IV hypersensitivity

A

ABCD 1234

4–> Delayed (also technically last one)

Two mechanisms involving T cells ( DOES NOT INVOLVE ANTIBODIES):

1) direct cell cytotoxicity: CD8+ cytotoxic T cells kill targeted cells
2) inflammatory reaction: effector CD4+ T cells recognize antigen and release inflammation inducing cytokines

4 Ts: T cells,Transplant rejection, TB skin test, Touching (contact dermatitis)

73
Q

Blood transfusion rxn: allergic/anaphylactic rxn

A

Type I hypersensitivity

If IgA deficient then must receive blood products without IgA

74
Q

Blood transfusion rxn: Febrile nonhemolytic transfusion reaction

A

1) Due to type II hypersensitivity rxn to donor HLA and WBCs

OR

2) Due to Cytokines that are created and accumulate during the storage of blood products

75
Q

Blood transfusion rxn: Acute hemolytic transfusion rxn

A

Type II hypersensitivity rxn

intravascular hemolysis due to ABO blood group incompatibility

Extravascular hemolysis due to foreign antigen on donor RBCs

76
Q

Blood transfusion rxn: Transfusion related acute lung injury

A

Donor anti-leukocyte antibodies against recipient neutrophils and pulmonary endothelial cells

77
Q

Autoantibody: Myasthenia gravis

A

Anti-Ach receptor

78
Q

Autoantibody: Lambert Eaton Myasthenic syndrome

A

Anti-presynaptic voltage gated calcium channel

79
Q

Autoantibody: SLE

A

ANA (non specific)
Anti-cardiolipin
Anti-dsDNA
Anti-smith

80
Q

Autoantibody: Rheumatoid arthritis

A 
Rheumatoid factor (Igma against IgG Fc region)
Anti-CCP (more specific)
81
Q

Autoantibody: Sjogren syndrome

A

(Body’s immune system attacks its own healthy cells that produce saliva and tears)

Anti-Ro/SSA
Anti-La/SSB

82
Q

Autoantibody: Scleroderma (diffuse)

A

Anti-Scl-70 (anti DNA topoisomerase I)

83
Q

Autoantibody: Microscopic polyangiitis, eosinophilic granulomatosis with polyangiitis (churg strauss syndorome), uncerative colitis

A

MPO-ANCA/ PANCA

84
Q

Autoantibody: granulomatosis with polyangitis (Wegener)

A

PR3-ANCA/CANCA

85
Q

Autoantibody: Hashimoto thyroiditis

A

Antimicrosomal
antithyroglobulin
antithyroid peroxidase

86
Q

Autoantibody: Graves disease

A

Anti-TSH receptor

87
Q

Autoantibody: Celiac disease

A

IgA anti-endomysial
IgA anti-tissue transglutaminase
IgA and IgG deamidated gliadin peptide

88
Q

Autoantibody: Type 1 diabetes mellitus

A

Anti glutamic acid decarboxylase

Islet cell cytoplasmic antibodies

89
Q

Autoantibody: Pernicious anemia

A

Antiparietal cell, anti-intrinsic factor

90
Q

Autoantibody: Goodpasture syndrome

A

Anti-glomerular basement membrane

91
Q

Pt is a 8 month old baby boy that present with recurrent bacterial and enteroviral infections. He has no B cells and no Lymph nodes. He was healthy for the first 6 months

A

X linked (Bruton) agammaglobulinemia –> Boys

Defect in BTK gene (tyrosine kinase)

No B cell maturation

Live vaccines contraindicated

92
Q

Pt presents with Giardiasis and low IgA but normal IgG and IgM levels

A

Selective IgA deficiency

Asymptomatic
Airway and GI infections
Autoimmune
Atopy
Anaphylaxis to IgA
93
Q

Pt is a 2 year old and presents with low plasma cells and low immunoglobulins

A

Common Variable immunodeficiency

Defect in B cell differentiation

94
Q

Pt presents with tetany and recurrent infections. His labs show low T cells, low PTH, and low Calcium. Also has conotruncal abnormalities.

A

Thymic aplasia (DiGeorge syndrome)

22q11 deletion

Failure to develop 3rd and 4th pharyngeal pouches resulting in absent thymus and parathyroids

95
Q

Pt received the BCG vaccine and now has disseminated mycobacterial and fungal infections. He is also noted to have low IFNγ levels

A

IL-12 receptor deficiency which decreases the Th1 response

IFNγ - functions as the primary activator of macrophages, in addition to stimulating natural killer cells and neutrophils.

96
Q

Upon examination it is noted that the patient has a cold/noninflamed staphylococcal abscess and retained primary teeth. He also has dermatologic problems like eczema. His labs show increased IgE and eosinophils.

A

Job syndrome - Autosomal Dominant hyper-IgE syndrome

STAT3 mutation
Deficiency of Th17 cells and thus impaired recruitment of neturophils to sites of infections

97
Q

Pt presents with noninvasive candida albicans infections of skin and mucous membranes. However, he has no T cell proliferation or cutaneous reaction to it.

A

Chronic mucocutaneous candidiasis

T cell dysfunction - defects in IL17 and IL17 receptor

98
Q

Pt presents with failure to thrive, chronic diarrhea, and thrush. Also has recurrent viral, bacterial, fungal, and protozoal infections. On CXR he lacks a thymic shadow. On lymph node biopsy he lacks germ cells. On flow cytometry there are no T cells

A

Severe Combined Immunodeficiency (SCID)

Defective IL-2R gamma chain
OR
adenosine deaminase deficiency

Bone marrow transplant curative because no concern for rejection.

99
Q

Pt presents with cerebellar defects (Ataxia). On physical exam its noted that he has spider angiomas/telangiectasia. His labs show low IgA levels

A

Ataxia-telangiectasia

Defect in the ATM gene –> failure to detect DNA damage and halt profession of cell cycle. Mutations accumulate

Pt presents with the triad (AAA) of Ataxia, spider Angiomas, IgA

Labs show high AFP but low IgA IgG and IgE

100
Q

Pt presents with severe pyogenic infections early in life. Also noted to have opportunistic infections with pneumocystitis, cryptosporidium, CMV. Labs show high IgM but very low IgG, IgA, IgE

A

Hyper IgM syndrome

Defective CD40L on Th cells –> class switching defect

Failure to make germinal centers

101
Q

Pt presents with thrombocytopenia, eczema, and recurrent (pyogenic) infections

A

Wiskott-aldrich syndrome

Think WATER -
Wiskott-Aldrich syndrome
Thrombocytopenia
Eczema
Recurrent infections

low to normal IgG or IgM but high IgE and IgA

102
Q

Pt is a newborn that presents with recurrent skin and mucosal bacterial infections. Pus is absent. It has been over 30 days and his umbilical cord has not yet seperated

A

Leukocyte adhesion deficiency (type 1)

Defect in LFA-1 integrin (CD 18) protein on phagocytes

Increased neutrophils in blood but absent in infection sites

103
Q

pt is partialy albino and presents with progressive neurodegeneration, lymphohistiocytosis, recurrent infections by staph and strep, peripheral neuropathy.

A

Chediak Higashi syndrome

Defect in lysosomal trafficking regulator gene (LYST)

microtubule dysfunction in phagosome lysosome fusion

Giant granules in granulocytes and plateletes. Pancytopenia

104
Q

pt that is increasingly susceptible to catalase + organisms and has a positive dihydrohodamine (flow cytometry) test (decreased green fluorescence)

A

Chronic granulomatous disease

Defect of NADPH oxidase that decreases reactive oxygen species and thus decreases respiratory burst in neutrophils

105
Q

Immunodeficiency in B cells tends to produce recurrent ?

A

bacterial infections

especially encapsulated ones (Please SHINE my SKiS)

Pseudomonas aeruginosa
Streptococcus pneumo
Haemophilus Influenza type b
Neisseria meningitidis
Escheridchia coli
Salmonella
Klebsiella pneumoniae
Group B strep
106
Q

Immunodeficiency in T cells tends to produce more?

A

fungal and viral infections

107
Q 
Grafts-
Autograft
Syngeneic graft (isograft)
Allograft
Xenograft
A

autograft is from self
syngeneic graft (isograft) is from twin or clone
Allograft is from same species
Xenograft is from different species

108
Q

Hyperacute transplant rejection

A

within minutes

Type II hypersensitivity

pre-exiting recipient antibodies react to donor antigen

MUST remove graft

109
Q

Acute transplant rejection

A

Weeks to months

cellular response: Type IV hypersensitivity reaction. CD4+ and CD8+ T cells activate against donor MHCs

Humoral: antibodies that develop after transplant

prevent/reverse with immunosuppressants

110
Q

Chronic transplant rejection

A

Months to years

Type II and type IV hypersensitivity reactions

CD4+ T cells respond to recipient APC presenting donor peptides (including MHC)

Dominated by arteriosclerosis

111
Q

Graft vs host disease

A

Varying onset

Grafted immunocompetent T cells proliferate in the immunocompromised host and reject host cells with “foreign bodies” –> severe organ dysfunction

Type IV hypersensitivity reaction

pt presents with maculopapular rash, jaundice, diarrhea, hepatosplenomegaly

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