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NPLEX I (2022) > Immunology > Flashcards

Immunology Flashcards

1
Q

What is produced in bone marrow?

A

immune cell production

B cell maturation

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2
Q

What is produced in thymus?

A

T cell maturation

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3
Q

Lymph node anatomy

A

capsule: subcapsular sinuses, trabeculae of connective tissue, trabecular sinuses

outer cortex: nodules, follicles of b cells, germinal center where B cells differentiate

inner cortex (paracortex): no nodules, T cells, high endothelial venules, eosinophilic

Medulla: cords of lymphoid tissue and medullary sinuses

encapsulated, bean shaped structures, dendritic cells, plasma cells

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4
Q

Deep cervical lymph nodes

A

Drain: head, neck, oropharynx

path: Kawasaki dz

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5
Q

Supraclavicular lymph nodes

A

R: L Virchow node
L: abdomen, pelvis

path: cancer of thorax, abdomen, pelvis

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6
Q

Epitrochlear lymph node

A

Drain: hand, forearm

path: secondary syphilis

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7
Q

Spleen anatomy

A

LUQ of abdomen, anterolateral to L kidney

Periarteriolar lymphatic sheath: T cells

Follicle: B cells

Marginal zone: macrophages, specialized b cells, antigen-presenting cells

White pulp: antibody coated bacteria are filtered our and antibodies are made by B cells, filters blood

Red pulp: old RBC destroyed

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8
Q

Thymus anatomy, embryo, location, function

A

anterosuperior mediastinum

Thymus: endoderm
Thymic lymphocytes: mesoderm

cortex: immature T cells
Medulla: mature T cells
Hassall corpuscles: containing epithelial reticular cells

F: t cell differentiation and maturation

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9
Q

Innate immunity

A

Neutrophils, macrophages, monocytes, dendritic cells, NK cells, complement, physical epithelial barriers

Germline encoded, nonspecific, rapid, no memory

Protein secretion: lysozyme, complement, C-reactive protein, defensisns, cytokines

Pathogen recognition: toll-like receptors, pattern recognition receptors

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10
Q

Adaptive immunity (Protein secretion, Pathogen recognition, cells included, and what is it)

A

T, B cells, and circulating antibodies

variation through V(D)J recombination during lymphocyte development, high specific, memory, longer response

Protein secretion: immunoglobulin, cytokines

Pathogen recognition: memory cells

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11
Q

MHC 1

A

Loci: HLA-A, HLA-B, HLA-C

binding TCR and CD8
1 long and 1 short

F: Present endogenous antigens (viral or cytosolic proteins) to CD8+ cytotoxic T cells

Expression: All nucleated cells, APCs, platelets (except RBCs)

Antigen loading: Antigen peptides loaded onto MHC I in RER after delivery via TAP (transporter associated with antigen processing)
Associated proteins: B2-microglobulin

Path: B27 PAIR psoriatic arthritis, ankylosing spondylitis, IBD-arthritis, reactive arthritis

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12
Q

MHC II

A

Loci: HLA-DP, HLA-DQ, HLA-DR

TCR and CD4
2 equal length chains

Expression: APCs\Function: Present exogenous antigens (bacterial proteins) to CD4 helper T cells

Antigen loading: Antigen loaded following release of invariant chain in acidified endosome

path: DQ2/8 (celiac), DR3 (DM I, SLE, graves, Hashimoto, Addison disease), DR4 (RA, DM I, Addison disease)

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13
Q

Natural Killer (NK) cells

A

innate immune system

A: perforin and granzymes to induce apoptosis of virally infx and tumor cells and antibody-dependent cell-mediated cytotoxicity

Stim: induced to kill when exposed to nonspecific activation signal on target cell, or absence of inhibitory signal on target cell surface or CD16 binds Fc region of bound IgG

Inc activity: IL-2, IL-12, IFN-a, IFN-B

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14
Q

B cell

A

Action: recognize and present antigen, produce antibodies, and maintain immunologic memory

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15
Q

T cells

A

CD4: help B cells make Ab and produce cytokines to recruit phagocytes and activate other leukocytes

CD8: directly kill virus-infx and tumor cells

MCH II x CD4 = 8
MCH I x CD8= 8

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16
Q

Type 1 hypersensitivity

A

Immediate: Antigen crosslinks IgE on pre-sensitized mast cells -> degranulation -> histamine (runny everything), tryptase, and leukotriene release (anaphylactic)

Late: chemokines attract inflammatory cells -> inflammation and tissue damage

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17
Q

Type II hypersentivity mechanism and example

A

Antibody binds to cell-surface of antigen -> opsonize -> activate phagocytosis, complement, NK cell killing-> abnormal blockage or activation of downstream effects, destruction

path: autoimmune hemolytic anemia, immune thrombocytopenia, transfusion rxn, hemolytic dz of the newborn, Goodpasture syndrome, Rheumatic fever, transplant rejection, myasthenia gravis, graves dz, pemphigus vulgaris

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18
Q

Type III hypersentivity mechanism and example

A

Antigen-Antibody-Complement (IgG) creates complex -> deposits somewhere-> attracts neutrophils and release lysosomal enzymes -> causing localized damage where it has deposited

path: SLE, RA, reactive arthritis, polyarteritis nodosa, poststreptococcal glomerulonephritis, IgA vasculitis, vaccine booster

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19
Q

Type IV hypersentivity

A

direct cell cytotoxicity via CD8 T cells kill targeted cells

effector CD4 T cells recognize Ag and release inflammation-inducing cytokines -> macrophage

Path: contact dermatitis, graft vs host dz

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20
Q

Helper T Cell Th1

A

Reg
(+) IFN-y, IL-12
(-) IL-4, IL-10

Release: IFN-y, IL-2

Action: activate macrophages, cytotoxic T cells, infection

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21
Q

Helper T Cell Th2

A

Reg: (+) IL-2, IL-4 (-) IFN-y

Release: IL-4, 5, 6, 10, 13

Action: activate eosinophils, IgE, Parasitic, allergic

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22
Q

Helper T Cell Th17

A

Reg: (+) TGF-B, IL-1, IL-6 (-) IFN-y, IL-4

Release: IL-17, 21, 22

Action: induce neutrophil inflammation

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23
Q

Helper T Cell Treg

A

Reg: (+) TGF-B, IL-2 (-) IL-6

Release: TGF-B, IL-10, 35

ACtion: prevent autoimmunity

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24
Q

Antigen structure and function

A

Fab: determines type of ag that binds

Fc: antibody class switching

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25
Q

Cytotoxic T cells

A

kill virus-infected, neoplastic, and graft cells via apoptosis, release cytotoxic granules containing preformed proteins

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26
Q

T cell activation

A

Antigen presenting cell ingests and processes Ag -> migrates to draining lymph node -> exogenous ag presents on MHC II and recognized by T-cell receptor on CD4 cell-> co-stimulatory signal via interaction of protein on dendritic cell and naïve T cell -> activated Th cell produces cytokines

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27
Q

IgG

A

most abundant in serum
fixes complement, opsonizes bacteria, neutralizes bacterial toxins and viruses
crosses placenta

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28
Q

IgA

A

mucous membrane, breast milk, crosses epithelial cells
does not fix complement
produced in peyer patches
most produced but not in serum

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29
Q

IgE

A

binds mast cells and basophils
Type I hypersentivity
contribute to immunity to parasites by activating eosinophils

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30
Q

IgM

A

primary response to an ag
fixes complement
multiple binding site

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31
Q

Complement

A

Activation: IgG or IgM, microbe surface molecules, lectin

Opsonin’s: C3b

Anaphylaxis: C3a, C4a, C5a

Neutrophil chemotaxis: C5a

MAC: C5b-9 neutralizing Neisseria species

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32
Q

Respiratory Burst

A

ROS to kill bacteria and foreign invaders -> activates catalase/glutathione peroxidase - glutathione reductase -> glucose-6-phosphatse dehydrogenase

catalase (+) organism can neutralize H2O2

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33
Q

Live attenuated Vaccine

A

can revert to virulent form, retain capacity of transient growth w/in host
induce cellular and humoral response, strong, lifelong

ex: MMR, typhoid

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34
Q

Killed/Inactivated

A

Antibody to surface antigen
pathogen is inactivated by heat or chemicals

Ex: Influenza

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35
Q

Subunit, recombinant, polysaccharide, conjugate

A

target specific epitopes of antigen
less adverse reactions
weaker immune response and costly

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36
Q

Toxoid vaccine

A

denatured bacterial toxin w/ intact receptor binding site
stimulates immune Ab response w/ ability to cause disease
protects against bacterial toxins
antitoxin levels decrease over time, needs booster shots

ex: clostridium tetani

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37
Q

mRNA vaccine

A

lipid nanoparticle delivers mRNA
induce cellular and humoral response, side effects (myocarditis, pericarditis)
safe in pregnancy

EX: covid

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38
Q

X-linked agammaglobulinemia def

A

Defect in BTK, a tyrosine kinase gene

No B-cell maturation

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39
Q

X-linked agammaglobulinemia cause

A

genetics

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40
Q

X-linked agammaglobulinemia path

A

mutation in Burton’s Tyrosine Kinase gene on x chromosome -> ineffective BTK enzyme-> B-lymphocyte precursors fail to mature into B lymphocytes, plasma cells -> differentiation stops at pre-B cell stage -> absence of B-cells in circulation -> deficiencies of all Ig -> higher risk of developing infections

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41
Q

X-linked agammaglobulinemia RF

A

Males, 6-18 mon, FH,

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42
Q

X-linked agammaglobulinemia comp

A

live vaccines autoimmune diseases, skin infections, lymphoma

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43
Q

X-linked agammaglobulinemia clinical

A

Recurrent bacterial and enteroviral infections after 6 months (decreased maternal IgG)
Absent B cells in peripheral blood
Decreased IgG
Absent/scanty lymph nodes and tonsils

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44
Q

Selective IgA deficiency def

A

isolated deficiency of IgA

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45
Q

Selective IgA deficiency cause

A

idiopathic

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46
Q

Selective IgA deficiency path

A

IgA deficiency

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47
Q

Selective IgA deficiency RF

A

FH

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48
Q

Selective IgA deficiency comp

A

Higher risk for giardiasis

Can cause false-positive B-hCG test

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49
Q

Selective IgA deficiency clinical

A

asymptomatic

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50
Q

Common Variable Immunodeficiency def

A

defect in B-cell differentiation

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51
Q

Common Variable Immunodeficiency cause

A

idiopathic, mutations BAFF or ICOS

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52
Q

Common Variable Immunodeficiency path

A

Decreased plasma cells and immunoglobulins

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53
Q

Common Variable Immunodeficiency RF

A

FH

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54
Q

Common Variable Immunodeficiency comp

A

Increased risk for AI disease, bronchiectasis, lymphoma, sinopulmonary infections, granulomatous infiltration

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55
Q

Common Variable Immunodeficiency clinical

A

recurrent infections

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56
Q

Chronic Mucocutaneous Candidiasis def

A

T-cell dysfunction

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57
Q

Chronic Mucocutaneous Candidiasis clinical

A

persistent and noninvasive Candida labicans infx of skin and mucous membrane

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58
Q

Severe Combined Immunodeficiency def

A

combined defects in T, B lymphocyte development, function

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59
Q

Severe Combined Immunodeficiency cause

A

SCID, cytokine receptor defects, adenosine deaminase deficiency, mutation y-chain subunit of IL receptors, RAG mutation

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60
Q

Severe Combined Immunodeficiency path

A

X-linked recessive

combined defects in T,B lymphocytes development or function

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61
Q

Severe Combined Immunodeficiency RF

A

male

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62
Q

Severe Combined Immunodeficiency clinical

A

recurrent infx, oral candidiasis (thrush), chronic diarrhea, failure the thrive, morbilliform rash

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63
Q

Spleen function

A

Filtration
Iron metabolism
Prevention of infection
Red blood cell and platelet storage

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64
Q

Bone marrow function

A

Immune cell production (origin of stem cells)
Production of cytokines in BM serves as necessary signals to B cells to differentiate by up-regulating B cell markers
B cell maturation

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65
Q

Bone marrow Microscopic Anatomy

A

red: hematopoietic island widely distributed throughout loose connective tissue network, large thin walled sinusoids, granulocytes, monocytes, megakaryocytes, lymphocytes,
yellow: connective tissue, adipocytes, dormant hematopoietic clusters,
reticulin: type III collagen, macrophages,

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66
Q

Bone marrow embryo

A

mesodermal cells in yolk sac

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67
Q

Tonsils Microscopic Anatomy

A

stratified squamous epithelium
antigen presenting cells
lymphoid follicles surrounded by connective tissue w/ tonsillar crypts
center contains lymphocytes

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68
Q

Tonsils Function

A

Filtration of macrophages, circulation of B and T cells, immune response activation

Waldeyer ring consists of lingual, palatine, pharyngeal, and tubal tonsils

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69
Q

Palatine tonsil

A

between the palatoglossal arch anteriorly and the palatopharyngeal arch posteriorly
stratified squamous epithelium w/ 15-20 crypts
lymphocytes, bacteria and desquamated epithelial cells

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70
Q

Lingual tonsil

A

small round elevations that sit on the most posterior part of the tongue base
stratified squamous epithelium one crypt

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71
Q

Tubal tonsils

A

posterior to the opening of the Eustachian tube (the torus tubaris) in the nasopharynx.

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72
Q

Pharyngeal tonsil

A

nasopharynx
attached to periosteum of sphenoid bone
ciliated pseudostratified columnar epithelium, goblet cells

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73
Q

Lymph node function

A

Place where T and B cells hang out
ECF excess with antigens percolates through LNs and memory T and B cells can activate against any antigen previously seem

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74
Q

Mediastinal Lymph node

A

trachea, esophagus

path: lung CA, TB, sarcoidosis, granulomatous dz

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75
Q

Submandibular, submental LN

A

D: oral cavity, ant. tongue, lower lip
P: oral cavity cancer

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76
Q

Hilar LN

A

D: lungs
P: lung CA, TB, sarcoidosis, granulomatous dz

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77
Q

Axillary LN

A

D: upper limb, breast, skin above umbilics
P: mastitis, breast ca

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78
Q

Periumbilical LN

A

D: abdomen, pelvis
P: gastric ca

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79
Q

Celiac LN

A

D: liver, stomach, spleen, pancreas, upper duodenum
p: mesenteric lymphadenitis, IBD, celiac dz

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80
Q

Superior mesenteric LN

A

lower duodenum, jejunum, ileum, colon (splenic flexure)

p: mesenteric lymphadenitis, IBD, celiac dz

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81
Q

Inferior mesenteric LN

A

colon (splenic flexure to upper rectum)

mesenteric lymphadenitis, IBD, celiac dz

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82
Q

Para-aortic LN

A

testes, ovaries, kidneys, fallopian tubes, uterus

metastasis

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83
Q

External iliac LN

A

cervix, vagina (upper third), superior bladder, body of uterus

STI, medial foot/leg cellulitis

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84
Q

Internal iliac LN

A

lower rectum to anal canal, bladder, middle 1/3 vagina, cervix, prostate

STI, medial foot/leg cellulitis

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85
Q

Superficial inguinal LN

A

anal canal, skin below umbilicus, scrotum, vulva, vagina lower 1/3

STI, medial foot/leg cellulitis

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86
Q

Popliteal LN

A

dorsolateral foot, posterior calf

lateral foot/leg cellulitis

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87
Q

Interferon-gamma

A

Th1, secreted by NK cells and T cells in response to Ag or Il-12 from macrophages, stimulates macrophages to kill phagocytosed pathogens, inhibits differentiation of Th2, induces IgG class switch

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88
Q

IL-4

A

induces differentiation of T cells into Th2 cells, promotes growth of B cells, enhances class switching to IgE and IgG

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89
Q

IL-5

A

promotes growth and differentiation of b cells, enhances class switching to IgA, stimulates growth and differentiation of eosinophils, Th2

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90
Q

IL-10

A

TGF-B and IL-10 both attenuate the immune response, decreases expression of MHC class II and Th1 cytokines, inhabits activated macrophages and dendritic cells, secreted by reg T cells, Th2

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91
Q

IL-13

A

promotes IgE production by B cells, induces alternative macrophage activation, Th2

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92
Q

INF y

A

secreted by NK cells and T cells in response to antigen or IL-12 from macrophages, stimulates macrophages to kill pathogens; inhibit differentiation of Th2 cells, induces IgG

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93
Q

HLA A3

A

Hemochromatosis

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94
Q

HLA B8

A

Addison disease, Myasthenia gravis, Graves

Don’t Be late(8), Dr. Addison, or else you’ll send my patient to the grave

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95
Q

HLA B27

A

Psoriatic arthritis, Ankylosing spondylitis, IBD-associated arthritis, Reactive arthritis

PAIR

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96
Q

HLA C

A

Psoriasis

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97
Q

DQ2/DQ8

A 
Celiac disease
I ate(8) (2) much gluten at Dairy Queen
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98
Q

DR2

A

Multiple sclerosis, hay fever, SLE, Goodpasture syndrome

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99
Q

DR3

A

Rheumatoid arthritis, DM1, Addison disease

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100
Q

DR5

A

Hashimoto thyroiditis

Hashimoto is an odd Dr (DR3, DR5)

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101
Q

IL-1

A

acute inflammation, (Macrophages and Monocytes) Fever, T-cell prolif

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102
Q

IL-2

A

(CD4 cells) Stimulates T cells, NK cells, CD4 and CD8

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103
Q

IL-3

A

Stimulates bone marrow

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104
Q

IL-6

A

Stimulates acute phase protein production and fever

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105
Q

IL-11

A

(Fibroblast) Megakaryocyte potentiator, stimulates IgG

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106
Q

TNF-alpha

A

activates endothelium, WCB recruitment, vascular leak

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107
Q

IL-8

A

chemotactic factor for neutrophils

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108
Q

IL-12

A

differentiation of T cell into Th1 cells, activate NK cells

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109
Q

INF-a

A

leukocytes) Inhibits tumor proliferation, enhances NK growth

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110
Q

INF-B

A

(fibroblasts)

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111
Q

Response to foreign body

A

albumin and fibrinogen attach to surface -> over time small proteins get replaced w/ larger proteins -> neutrophils migrate to area and adhere to protein layer -> release ROS and proteolytic enzymes -> increase vascular permeability -> monocytes turn into macrophages -> proliferation and recruitment and replace neutrophils -> release TNF alpha, IL-1b, IL-6, and IL-8 -> macrophage cover exposed surface of implant via integrins -> macrophage undergo cytoskeletal remodeling they flatten over the surface of the implant in an attempt to engulf and phagocytose it -> continue to recruit macrophages -> release degrading enzymes and ROS to break down implant -> break it down -> stops -> if don’t break down -> encapsulation of implant w/ fibrous tissue

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112
Q

Structure of Complement

A

plasma proteins

C1: C1s, C1r, 6C1q bind to Fc portion of antibody, require Ca

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113
Q

Function of Complement

A

destroy gram negative bacteria
C3b - Opsonization, allow for phagocytosis (C3b binds to lipopolysaccharides on bacteria)
C3a, C4a, C5a - Anaphylaxis, mast cells and basophils
C5a and C3a - Neutrophil, eosinophils, monocytes, and macrophage chemotaxis
C5b-9 (MAC) - Cytolysis, kills infected cells or pathogen

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114
Q

Pathway of Classic Complement

A

2 or more C1q bind to antibodies bound to antigen -> C1 twists exposes C1r and C1s allowing C1r to cleave C1s -> C1 cleaves C4 into C4b and C4a -> C4b binds to surface of pathogen -> C1 cleaves C2 into C2a and C2b -> C2b bind to C4b on pathogen -> C3 convertase cleaves tons of C3 into C3b and C3a -> C3b binds to C3 convertase turning it into a C5 convertase (C4b2b3b) -> cleaves C5 into C5a and C5b-> C5b binds to C6, C7, C8 bind to cell membrane and penetrate through it -> multiple C9 join and create a channel straight through pathogen membrane

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115
Q

Lectin binding pathway

A

mannose binding lectin protein binds to mannose on cell surface -> cleaves C4 and C2 -> C3 convertase -> C3 convertase cleaves tons of C3 into C3b and C3a -> C3b binds to C3 convertase turning it into a C5 convertase (C4b2b3b) -> cleaves C5 into C5a and C5b-> C5b binds to C6, C7, C8 bind to cell membrane and penetrate through it -> multiple C9 join and create a channel straight through pathogen membrane

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116
Q

Alternative Complement Pathway

A

at slow rate of cleavage of C3 into C3b and C3a-> C3b binds to cell membrane -> factor B will bind to C3b and that will allow factor B to be cleaved by factor D into Bb and Ba -> Bb will stay bound to C3b -> acts as a C3 convertase -> C3b binds to C3 convertase turning it into a C5 convertase (C4b2b3b) -> cleaves C5 into C5a and C5b-> C5b binds to C6, C7, C8 bind to cell membrane and penetrate through it -> multiple C9 join and create a channel straight through pathogen membrane

C1 inhibitor and factor I stops this

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117
Q

Control of thymus

A

insulin, insulin-like growth factor

118
Q

Control of bone marrow

A

Stim: loss of blood, lack of iron, exercise, infection
Inhibit: immunosuppression

119
Q

Mucous Membranes/

MALT Anatomy

A

Enteroendocrine cells, local gut immunity
Peyer’s patch - Encapsulated lymphoid tissue in ileal submucosa, where they can detect large antigens that accidentally diffused across intestinal epithelium

120
Q

Lymphatic fluid composition

A

albumin, oxygen, glucose, animo acids, hormones, lipids, dendritic cells and fluid

121
Q

Lymphatic fluid function

A

return fluid to heart, helps large molecules like hormones and lipids enter blood, and immune surveillance

122
Q

Lymphatic fluid transport

A

fluid enters capillaries -> vessels -> trunks (lumbar, Bronchomediastinal, subclavian, jugular, intestinal) -> ducts (right lymphatic or thoracic) -> veins (jugular and subclavian)

smooth muscle reacts to arterial pulse and skeletal muscle squeezing keep lymph moving

collect interstitial fluid and return it to heart

123
Q

Synthesis of Lymphatic Fluid

A

when pressure in the interstitial space is higher than the lymphatic capillary mini valves open up allowing lymph to enter

124
Q

Degradation of Lymphatic Fluids

A

lymph nodes remove foreign materials, enters back into heart via subclavian vein

125
Q

Activation of Innate immune response

A

macrophage recognizes pathogen by bind its pattern recognition receptor on a pathogen with a certain pathogen associated molecular patterns

NK cells

126
Q

Activation of Adaptive immune response

A

antigen presenting cells engulf antigen and present on MCH

127
Q

What are the antibodies associated w/ Myasthenia Gravis?

A

anti-postsynaptic ACh receptor

128
Q

What are the antibodies associated w/ SLE

A

Antinuclear, anticardiolipin, lupus anticoagulant, Anti-dsDNA, anti-smith, anti-histone

129
Q

What are the antibodies associated w/ Sjogern syndrome?

A

anti-Ro/SSA, anti-La/SSB

130
Q

What are the antibodies associated w/ RA?

A

Rheumatoid factor, Anti-cyclic citrullinated peptide

131
Q

What are the antibodies associated w/ scleroderma?

A

anti-Scl-70 (anti-DNA topoisomerase I

132
Q

What are the antibodies associated w/ limited scleroderm (CREST syndrome)?

A

anticentromere

133
Q

What are the antibodies associated w/ polymyositis?

A

anti-synthetase, anti-SRP, anti-helicase

134
Q

What are the antibodies associated w/ autoimmune hepatitis?

A

anti-smooth muscle, anti-liver/kidney microsomal-1

135
Q

What are the antibodies associated w/ Goodpasture syndrome?

A

Anti-glomerular basement membrane

136
Q

DiGeorge Syndrome cause

A

Microdeletion of chromo 22q11.2, TBx1

137
Q

DiGeorge Syndrome path

A

mutation in TBx1 -> pouch 3 and 4 of pharyngeal pouches -> lack of thymus and parathyroid gland -> deficiency in mature T cells and hypocalcemia

138
Q

DiGeorge Syndrome RF

A

FH

139
Q

DiGeorge Syndrome comp

A

Heart murmur

Frequent infections

140
Q

DiGeorge Syndrome clinical

A

truncus arteriosus, tetralogy of Fallot, poor immune system function, cleft palate, long face, small teeth, broad nose, low Ca2+, delayed development with behavioral and emotional problems

141
Q

Drug-Induced Immunodeficiencies def

A

impaired immune system function due to medications used in the treatment of systemic diseases

142
Q

Drug-Induced Immunodeficiencies cause

A

Methyldopa, minocycline, hydralazine, isoniazid, phenytoin, sulfa drugs, etanercept, procainamide, Azathioprine, Ciclosporin, Mycophenolate mofetil, Cyclophosphamide, prednisone, omalizumab, dupilumab, secukinumab, ixekizumab, brodalumab,

143
Q

Drug-Induced Immunodeficiencies path

A

drugs that suppress immune system -> infections

144
Q

Drug-Induced Immunodeficiencies comp

A

life-threatening infections

145
Q

Drug-Induced Immunodeficiencies clinical

A

Manifests as recurrent, severe, opportunistic infections

146
Q

Human Immunodeficiency Virus (HIV)/Acquired Immune Deficiency Syndrome def

A

virus that targets cells in the immune system

147
Q

Human Immunodeficiency Virus/Acquired Immune Deficiency Syndrome cause

A

HIV 1 or HIV 2 (rare)

sexual intercourse, M to M, IV drug, mother to child

148
Q

Human Immunodeficiency Virus/Acquired Immune Deficiency Syndrome path

A

HIV targets CD4+ cells (macrophage, dendritic cells, T helper cells) attaches via gp120 -> another gp120 attaches to CXCR4/CCR5 receptors on cell -> virus enters the cell -> injects single stranded RNA into cell -> reverse transcriptase transcribe into a double stranded proviral DNA -> enter nucleus and attaches to DNA -> anytime immune proteins are made so is viral proteins -> during this process they will mutate and created different strains and can infect other immune cells-> leading to high levels of HIV in blood -> immune system counterattacks and controls replication (12 weeks) -> viral replication slowly increases while T cells decrease (chronic 2-10 y)

149
Q

Human Immunodeficiency Virus/Acquired Immune Deficiency Syndrome RF

A

unprotected sex, multiple partners, sharing needles, unsafe injection, unsterile cutting or piercing, needle stick injuries, having sex with someone w/ STI

150
Q

Human Immunodeficiency Virus/Acquired Immune Deficiency Syndrome comp

A

x4 strain destruction to T cells

151
Q

Human Immunodeficiency Virus/Acquired Immune Deficiency Syndrome clinical

A

swollen lymph nodes, hairy leukoplakia (white patch on tongue), oral candidiasis

AIDS: <200 T cells, persistent fever, fatigue, weight loss, diarrhea, recurrent bacterial pneumonia, pneumocystis pneumonia, candidiasis of esophagus, Kaposi sarcoma, primary lymphoma

152
Q

Anaphylaxis def

A

severe allergic reaction

153
Q

Anaphylaxis cause

A

peanut, shellfish, antibiotics, insect bites, blood products (IgG)

154
Q

Anaphylaxis path

A

first exposure -> antigen presenting cell pick up antigen -> presents to T cell -> activates produce cytokines -> B cell switch to IgE antibodies -> mast cells and basophils -> second exposure -> mast cells and basophils release proinflammatory molecules -> leak into blood system due to histamine, tryptase -> bronchoconstriction, blood vessel dilation, break down proteins ->

155
Q

Anaphylaxis RF

A

atopy, asthma

156
Q

Anaphylaxis comp

A

hypotension, MI, anaphylactic shock, LOC

157
Q

Anaphylaxis clinical

A

angioedema, SOB, coughing, wheezing, abdominal cramps, vomiting, diarrhea

158
Q

Autoimmune Hemolytic Anemia def

A

increased RBC breakdown due antibodies to RBC

159
Q

Autoimmune Hemolytic Anemia cause

A

Warm: idiopathic, penicillin, cephalosporins, children (viral, SLE, lymphomas, leukemia)

Cold: leukemia, lymphoma, viral pneumonia, mycoplasma, infectious mononucleosis

160
Q

Autoimmune Hemolytic Anemia path

A

warm >37 IgG on Rh antigen in spleen-> macrophage, neutrophils, NK cells, and T cells bind to Fc portion of antibody -> superoxide granules or phagocytosis cause conformational change induced hemolysis of RBC

cold 0-10 IgM on L, I, P antigen in liver via complement system

161
Q

Autoimmune Hemolytic Anemia RF

A

immune deficiencies, malignancies, certain drugs, measles, varicella, mycoplasma, H. influenza, lymphoproliferative disorders, autoimmune disorders, exposure to cold

162
Q

Autoimmune Hemolytic Anemia comp

A

gallstones, kidney damage, multiorgan failure

163
Q

Autoimmune Hemolytic Anemia clinical

A

hematuria, jaundice, hemoglobinuria, bounding heart rate, SOB, fatigue, pallor, hepatosplenomegaly

164
Q

Goodpasture Syndrome def

A

autoimmune disease that affects lungs and kidneys

165
Q

Goodpasture Syndrome cause

A

autoimmune

166
Q

Goodpasture Syndrome path

A

autoantibodies IgG to alpha 3 chain of type 4 collagen bind -> activate complement system -> ROS are released in area, MAC is formed -> damage to BM

167
Q

Goodpasture Syndrome RF

A

HLA-DR15, infection, smoking, oxidative stress, hydrocarbon-based solvents

168
Q

Goodpasture Syndrome comp

A

chronic kidney disease

169
Q

Goodpasture Syndrome clinical

A

cough, hemoptysis, restrictive lung disease

hematuria, proteinuria, edema, HTN

170
Q

Myasthenia Gravis def

A

muscle weakness due to antibodies

171
Q

Myasthenia Gravis cause

A

autoimmune disease, bronchogenic carcinoma, thymic neoplasm

172
Q

Myasthenia Gravis path

A

antibodies that bind to nicotinic acetylcholine receptors on muscle cell membrane-> don’t respond to contract signal and activate classical complement pathway -> inflammation, muscle cell destruction

muscle specific receptor tyrosine kinase antibodies -> target proteins in muscle cell

173
Q

Myasthenia Gravis RF

A

women 20-30

male 60-70

174
Q

Myasthenia Gravis comp

A

myasthenic crisis (breathing muscles)

175
Q

SLE (Lupus) def

A

a disease that systemic affect multiple organs and causing redness of skin

176
Q

SLE (Lupus) cause

A

autoimmune disease, genetics,

177
Q

SLE (Lupus) path

A

environmental triggers -> damaged cells release contents into cell and genetic factors cause them not to be cleared effectively -> b cell make antibodies -> antinuclear antibodies bind to antigen -> get into blood -> deposit in kidney, skin, joints, heart -> complement system -> cell to die ->

178
Q

SLE (Lupus) path

A

environmental triggers -> damaged cells release contents into cell and genetic factors cause them not to be able to clear them effectively -> b cell make antibodies -> antinuclear antibodies bind to antigen -> get into blood -> deposit kidney, skin, joints, heart -> complement system -> cell to die

179
Q

SLE (Lupus) comp

A

Skin scarring, Joint deformities, Kidney failure, Stroke, Heart attack, Pregnancy complications, Hip destruction (also called avascular necrosis), Cataracts

180
Q

SLE (Lupus) comp

A

Kidney failure, Stroke, Heart attack, Pregnancy complications, avascular necrosis, Cataracts, DVT, hepatic vein thrombosis,

181
Q

SLE (Lupus) clinical

A

relapsing and remittance
fever, joint pain, rash, weight loss, malar rash after sun exposure, discoid rash, photosensitivity of skin, ulcers of mouth or nose, serositis (pleuritis, pericarditis), myocarditis, endocarditis (vegetations form around mitral valve), arthritis, proteinuria, diffuse proliferative glomerulonephritis, seizures, psychosis, anemia, thrombocytopenia, leukopenia

182
Q

Polyarteritis nodosa def

A

widespread inflammation, weakening, and damage to small and medium-sized arteries

183
Q

Polyarteritis nodosa cause

A

hepatitis B, hepatitis C, hairy cell leukemia

184
Q

Polyarteritis nodosa path

A

necrotizing vasculitis of the renal, coronary, and mesenteric arteries

immune complexes lead to medium vessel inflammation

185
Q

Polyarteritis nodosa RF

A

men

186
Q

Polyarteritis nodosa comp

A

renal failure, MI

187
Q

Polyarteritis nodosa clinical

A

secondary HTN, hematuria, abdominal pain, bloody stools, livedo reticularis, palpable purpura

188
Q

Poststreptococcal

glomerulonephritis def

A

kidney glomeruli become inflamed after streptococcal infection

189
Q

poststreptococcal

glomerulonephritis cause

A

Group A beta-hemolytic Streptococci

190
Q

poststreptococcal

glomerulonephritis path

A

Group A beta-hemolytic Streptococci -> immune complexes of IgG or IgM and antigen get deposited GBM sub epithelial -> C3 complement, cytokines, oxidants, proteases -> damage podocytes -> RBC and proteins can filter through

191
Q

poststreptococcal

glomerulonephritis RF

A

children, recent impetigo or pharyngitis infx

192
Q

poststreptococcal

glomerulonephritis clinical

A

oliguria, proteinuria, hematuria, peripheral and periorbital edema

stary sky, anti-DNase B

193
Q

granulomatous inflammation def

A

type of inflammation when chronic inflammation can’t get rid of offending agent, development of nodules

194
Q

granulomatous inflammation cause

A

tuberculosis or foreign body, sarcoidosis, leprosy, crohn’s disease, cat starch disease, fungal infection, autosomal recessive and x-linked recessive for NADPH oxidase

Natural forests contain lions, tigers, frogs, snakes, and cats

195
Q

granulomatous inflammation path

A

unable to kill pathogen -> macrophages turn into epithelioid cells -> epithelioid cells plus lymphocytes, multinucleated giant cell, and fibroblast come together -> cause more tissue destruction

196
Q

granulomatous inflammation RF

A

FH

197
Q

granulomatous inflammation comp

A

obstruction

198
Q

granulomatous inflammation clinical

A

recurrent infections, bacteremia, fungemia

199
Q

transplant rejection def

A

when transplanted tissue is attacked by new host immune system

200
Q

transplant rejection cause

A

blood group, major histocompatibility antigen, minor blood group antigens,

201
Q

transplant rejection path

A

innate immunity -> attraction, activation of phagocytes-> humoral immunity -> activation of B cells -> antibody secretion -> adaptive response -> cellular immunity -> killer T cells induce apoptosis

202
Q

transplant rejection RF

A

HLA, inadequately immunosuppressed

203
Q

transplant rejection comp

A

organ failure

204
Q

transplant rejection clinical

A

fever, chills, dizziness, nausea, malaise, night sweats,

205
Q

progressive systemic sclerosis (scleroderma) def

A

normal tissue is replaced with dense connective tissue

206
Q

progressive systemic sclerosis (scleroderma) cause

A

autoimmune, anti-SCL 70, anti-RNA polymerase III, anti-centromere

207
Q

progressive systemic sclerosis (scleroderma) path

A

injury to endothelial cells of small arteries -> express adhesion molecules -> T cell attach and migrate out side blood vessels -> release TGF-beta causing inflammation and damage -> release fibroblasts that produce collagen -> excessive firbosis -> reduce blood flow -> ischemia

208
Q

progressive systemic sclerosis (scleroderma) RF

A

women, genetics, cytomegalovirus, parvovirus B19, silica dust, organic solvents, vinyl chloride, cocaine, 35-50, drugs

209
Q

progressive systemic sclerosis (scleroderma) comp

A

painful ulcers, disfigurement, disability, renal, cardiac failure pulmonary insufficiency, interictal absorption

210
Q

progressive systemic sclerosis (scleroderma) clinical

A

start in finger and move up across arm swollen doughty -> tight shiny, stiff, sclerodactyly, calcinosis
microstomia, beaked nose, Raynaud phenomena, GERD, malabsorption, cough, difficulty breathing,

211
Q

rheumatic fever def

A

inflammatory condition of heart

212
Q

rheumatic fever cause

A

Streptococcus pyogenes, group A beta-hemolytic

213
Q

rheumatic fever path

A

antibodies are produced against M protein on Streptococcus -> cross react with body cells -> activate immune cells and release cytokines -> damage to heart

214
Q

rheumatic fever RF

A

children, poverty, crowding

215
Q

rheumatic fever comp

A

mitral stenosis, death to myocarditis, chronic rheumatic heart disease, infective endocarditis

216
Q

rheumatic fever clinical

A

migratory polyarthritis, pancarditis, myocarditis, friction rub, subcutaneous nodules, erythema marginatum, Sydenham chorea, fever,

217
Q

Sjögren syndrome def

A

autoimmune destruction of exocrine glands (lacrimal and salivary)

218
Q

Sjögren syndrome cause

A

autoimmune to exocrine glands, HLA DRW52, HLA DQA1, HLA DQB1, infection

219
Q

Sjögren syndrome path

A

damage to salivary glands -> parts of salivary gland get picked up by antigen presenting cells -> present antigen on MHC in lymph node -> binds to T cell -> activate B cell via cytokines -> make antibodies anti-SS-A and anti-SS-B -> enter blood T cell and antibodies -> exocrine gland -> T cell secrete cytokines, promote more immune cells to area, fibroblasts -> decreased exocrine glands

220
Q

Sjögren syndrome RF

A

women, 40-60YO

221
Q

Sjögren syndrome comp

A

Dental caries

MALT lymphoma

222
Q

Sjögren syndrome clinical

A

Dry, itching, redness, burning, and blurring of vision
xerostomia, difficulty tasting, swallowing, cracks and fissures
ulceration, perforation, crusting, and bleeding of nose and respiratory passages
difficulty speaking
Joint pain
Bilateral parotid enlargement
dry skin and vagina, swelling of glands, recurrent infx

223
Q

primary amyloidosis def

A

deposits of proteins w/ abnormal shape that stick together and settle in tissues that cause damage to tissue

224
Q

primary amyloidosis cause

A

multiple myeloma

225
Q

primary amyloidosis path

A

abnormal proteins begin to build up -> clump together and can’t be destroyed by proteases -> go out of cell and from b-sheets that deposit in extracellular space -> cause damage
immunoglobulin light chain gets misfolded and deposited

226
Q

primary amyloidosis RF

A

men, 60-70, FH, kidney dialysis

227
Q

primary amyloidosis comp

A

CHF, CHD

228
Q

primary amyloidosis clinical

A

proteinuria, hypoalbuminemia, edema, hyperlipidemia, restrictive cardiomyopathy, arrhythmia, malabsorption, enlargement of liver, spleen, or tongue, reduced sensory, motor, digestion, or blood pressure

229
Q

secondary amyloidosis def

A

build up of misfolded proteins in tissues

230
Q

secondary amyloidosis cause

A

serum amyloid A

231
Q

secondary amyloidosis path

A

serum amyloid A builds up in blood -> some misfolded into AA amyloids -> accumulate into tissue

232
Q

secondary amyloidosis RF

A

Rheumatoid arthritis, IBD, cancers, familial Mediterranean fever

233
Q

secondary amyloidosis comp

A

CHF, CKD

234
Q

secondary amyloidosis clinical

A

proteinuria, hypoalbuminemia, edema, hyperlipidemia, restrictive cardiomyopathy, arrhythmia, malabsorption, enlargement of liver, spleen, or tongue, reduced sensory, motor, digestion, or blood pressure

235
Q

erythema infectiosum (fifth disease) def

A

infection by Parvovirus B19

236
Q

erythema infectiosum (fifth disease) cause

A

Parvovirus B19, respiratory droplets, infected blood transfusion, placenta

237
Q

erythema infectiosum (fifth disease) path

A

respiratory tract -> travels through blood to bone marrow -> uses receptor-mediated endocytosis via p-antigen and enters erythroid progenitor cells -> replicates and produces non-structural protein 1 toxic to human cells -> RBC apoptosis -> copies of virus end up in blood -> IgG and IgM are produced -> form immune complexes (10-14) ->

238
Q

erythema infectiosum (fifth disease) RF

A

children, immune-compromised

239
Q

erythema infectiosum (fifth disease) comp

A

aplastic crisis, anemia, hydrops fetalis, fetal loss, pure red blood cell aplasia,

240
Q

erythema infectiosum (fifth disease) clinical

A

mild fever, headache, aching muscles -> rash, joint pain (hands, wrist, knee, feet bilaterally), lace-like rash

241
Q

Haemophilus influenzae type b def

A

encapsulated, gram negative, coccobacillus, non-motile, facultative anaerobic, catalase and oxidase positive

242
Q

Haemophilus influenzae type b cause

A

Haemophilus influenzae via respiratory droplets

243
Q

Haemophilus influenzae type b path

A

Haemophilus influenzae -> colonizes the nasopharynx, and may penetrate the epithelium and capillary endothelium
has capsule w/ pili, adhesion protiens, IgA protease, LOS

244
Q

Haemophilus influenzae type b RF

A

children, splenectomy, sickle cell, cancer, congenital deficiency of complement components, acute viral infection (influenza)

245
Q

Haemophilus influenzae type b comp

A

meningitis,

246
Q

Haemophilus influenzae type b clinical

A

fever, sore throat, dyspnea, warm tender area of erythema on cheek or periorbital area, chills, hypotension, tachycardia, vomiting, sore neck, altered mental status, bone pain, weakness, pain swelling and tenderness of joint

H. influenzae hates your throat, lungs, head, and bones

247
Q

influenza types

A

type A: 8 RNA segments, 8 hemagglutinin and neuraminidase, H3N2, H1N1
Type b: 8 RNA segments, less common,
type c: 7 RNA segment, least common, hemagglutinin-esterase-fusion

248
Q

influenza cause

A

type A influenza

249
Q

influenza path

A

respiratory droplets -> get in mouth, nose, lungs or touching surface -> uses hemagglutinin to bind to sialic acid sugar on epithelial cells -> endocytosis -> RNA gets worked on by RNA polymerase -> translated into proteins and new virus -> buds out of cell via neuraminidase cleaving sialic acid sugars
1-4 days

250
Q

influenza RF

A

younger than 6 mon, >65, close contact w/ sick person, immunosuppression, pregnancy,

251
Q

influenza comp

A

acute otitis media, bronchiolitis, croup, sinusitis, pneumonia, reye syndrome, febrile seizures,

252
Q

measles cause

A

measles virus

253
Q

measles path

A

airborne live up 2 hours in air or surface -> infect epithelial cells in trachea/bronchi -> hemagglutinin binds to CD46, SLAM, or Nectin-4 and fusion protein lets it get into cell -> RNA get transcribed by RNA polymerase -> translated into viral proteins -> wrapped in lipid envelope and sent out of cell -> picked up by dendritic cell and alveolar macrophage -> lymph node where it spread -> blood to more lung, intestine, brain (10-14 day)

254
Q

measles RF

A

< 5 years, pregnant women, immunocompromised, unvaccinated

255
Q

measles comp

A

death, pneumonia, diarrhea, encephalitis, otitis media, subacute sclerosing panecephalitis

256
Q

measles clinical

A

high fever, cough, conjunctivitis, coryza -> days after rash on mucus membrane -> red, blotchy, maculopapular rash cephalocaudal progression -> after 4 day rash fades and cough remains

257
Q

Mononucleosis def

A

enveloped, linear, double-stranded DNA

258
Q

Mononucleosis cause

A

Epstein-Barr virus

259
Q

Mononucleosis path

A

saliva or respiratory secretion -> epithelial cells it replicates viral DNA and form new proteins -> lysis of epithelial cells -> viruses travel to tonsils and attach to B cells via CD21 receptor -> virus enters latent phase and carries virus to other B cells (liver, spleen, lymph nodes) -> B cell make antibodies and CD8 t cells kill B cells

260
Q

Mononucleosis RF

A

15-24, kissing, sharing drinks or food

261
Q

Mononucleosis comp

A

splenic rupture, B cell lymphoma, Burkitt’s lymphoma, nasopharyngeal carcinoma

262
Q

Mononucleosis clinical

A

fever, pharyngitis, lymphadenopathy (posterior cervical), fatigue, tonsillitis, palatal petechiae, hepatosplenomegaly, rash (faint, non-itchy, pink macules or patches on trunk and arms)

263
Q

Mumps def

A

viral polymerase enzyme, single stranded RNA, phospholipid bilayer, hemagglutinin, neuraminidase, fusion protein

264
Q

Mumps cause

A

mumps virus -> enters cell RNA gets transcribed by viral polymerase -> translated -> viral proteins -> HN and F proteins bind other epithelial cells together

265
Q

Mumps path

A

respiratory droplets -> mumps virus -> enters cell RNA gets transcribed by viral polymerase -> translated -> viral proteins -> HN and F proteins bind other epithelial cells together -> damage to nasopharynx

266
Q

Mumps RF

A

children

267
Q

Mumps comp

A

testicular atrophy, decrease in sperm count and motility

268
Q

Mumps clinical

A

swelling of parotid salivary gland, ear ache, trismus, meningitis, encephalitis, headache, neck stiffness, hearing loss, difficulty w/ balance, orchitis, epididymitis, glomerulonephritis, arthritis, myocarditis, pancreatitis

269
Q

Roseola Infantum def

A

double stranded linear DNA, icosahedral capsid, tegument, viral glycoproteins

270
Q

Roseola Infantum cause

A

Human Herpes Virus 6

271
Q

Roseola Infantum path

A

respiratory droplets -> virus attaches to dendritic cells -> travel to lymph nodes -> CD4 T cells bind and virus infects them -> DNA gets transcribed and translated in CD4 T cells -> viral proteins are made -> packaged and leave cell destroyed -> can infect monocytes, macrophages, NK cells, astrocytes, megakaryocytes, glial cells -> goes into latent state in monocytes
incubation 1-2 week

272
Q

Roseola Infantum RF

A

children 6 month -2 years

273
Q

Roseola Infantum comp

A

encephalitis

274
Q

Roseola Infantum clinical

A

high fever, periorbital edema, acute otitis media, rhinorrhea, cough, vomiting, diarrhea, bulging fontanelle, cervical, occipital or postauricular lymphadenopathy, Nagayama spots -> maculopapular rash

275
Q

Rubella def

A

single-stranded RNA, icosahedral capsid, spherical outer lipid envelope, mRNA

276
Q

Rubella cause

A

rubella virus

277
Q

Rubella path

A

respiratory droplets -> virus binds to receptor on endothelial cells in nasopharynx -> enters the cell -> virus gets surrounded by cell creating an endosome -> viral RNA is uncoated and nucleus, ER, and Golgi apparatus are moved close to it -> virus replicated and make proteins -> surrounded by membrane and exocytose -> spreads to lymphatic and blood vessels -> lymph nodes replicates -> enters urine, CSF, synovial fluid -> infected cells get apoptosis

pregnant female -> through placenta -> congenital rubella syndrome

278
Q

Rubella RF

A

unvaccinated, coming in contact w/ someone

279
Q

Rubella comp

A

congenital rubella syndrome (sensorineural hearing loss, cataracts, retinopathy, damage to retina, patent ductus arteriosus, dermal extramedullary hematopoiesis, intellectual disability, behavioral disorders, skin lesions, DM< enlarged liver and spleen)

280
Q

Rubella clinical

A

asymptomatic
14 after incubation: children have fever, swelling of lymph nodes, pink macules rash spread to trunk and extremities
teen and adult: arthralgia, arthritis,

281
Q

Scarlet Fever def

A

infection leading to bright red skin rash

282
Q

Scarlet Fever cause

A

streptococcus pyogenes

283
Q

Scarlet Fever path

A

erythrogenic toxin -> a consequence of local production of inflammatory mediators and alteration of the cutaneous cytokine and dilatation of blood vessels, intrapapillary hemolysis

284
Q

Scarlet Fever RF

A

close contact with another person with scarlet fever, >3

285
Q

Scarlet Fever comp

A 
ear infection
throat abscess
sinusitis
pneumonia
meningitis
rheumatic fever
286
Q

Scarlet Fever clinical

A

exudative pharyngitis, fever, and bright-red exanthem

287
Q

Toxoplasmosis cause

A

toxoplasma gondii

288
Q

Toxoplasmosis path

A

ingestion of oocytes -> oocyst wall dissolved by proteolytic enzymes in stomach/SM I -> frees sporozoites from w/in oocyst -. parasites invade intestinal epithelium surrounding cells -> differentiation into tachyzoites -> replicate inside vacuoles until host cell rupture -> release tachyzoite to tissues -> host immune response-> tachyzoite turn into bradyzoites (semi-dormant) inside host cells

289
Q

Toxoplasmosis RF

A

consumption of raw/undercooked meat, ingestion of contaminated water, soil, vegs, previvor’s blood transfusion, organ transplant, transplacental transmission

290
Q

Toxoplasmosis def

A

a disease that results from infection with the Toxoplasma gondii parasite

291
Q

Toxoplasmosis clinical

A

initial: swollen lymph nodes, headache, fever, fatigue, muscle aches, pains
chronic/latent: asymptomatic
immunocompromised: headache, confusion, poor coordination, seizures, cough, dyspnea,

NPLEX I (2022) (20 decks)

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