immunity Flashcards

1
Q

immunity

A

protection from a disease

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2
Q

immune response

A

coordinated response of cells and molecules of the immune system

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3
Q

innate immunity

A

natural immunity, early rapid response developed by secretion of mediators
opsonins: tag microorganisms for more efficient recognition
cytokinin: regulate activity of other cells, amplify inflammation, initiation of the adaptive immune response
phagocytic lymphocytes: early response followed by macrophages
dendrites: from bone marrow, link innate and adaptive
nk cells: recognize infected and stressed cells respond by killing cells

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4
Q

adaptive immunity

A

specific or acquired immunity, less rapid but more effective
focused response to specific foreign agent
distinguishes between microbes and molecules to remember pathogens quickly and produces a heightened immune response on subsequent encounters with the same agent
composed of lymphocytes and their products
humoral and cell mediated immunity

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5
Q

macrophages

A

mature form of monocytes, located in most tissues, engulf and kill invading organisms, dispose of pathogens and infected cells, antigen-presenting cells for adaptive immunity (long lived)

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6
Q

granulocyte

A

short lived
neutrophils, basophils, eosinophils

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7
Q

lymphocytes

A

b lymphocytes produce antibodies, mediate humoral immunity
t cell lymphocytes cell mediated immunity
T helper cells: help b lymphocytes produce antibodies

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8
Q

central lymphoid tissue

A

bone marrow, thymus- immune cell production and maturation

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9
Q

peripheral lymphoid tissue

A

lymph nodes:
remove lymph, filter foreign material before it goes back to the blood, and center for proliferation and response of immune cells

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10
Q

spleen

A

left abdominal cavity, filters antigens from the blood, important in response to systemic infections

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11
Q

innate immune system consists of

A

epithelial layer: physical and chemical barriers between internal and external environments- epidermis, keratin, salty acidic environment, antibacterial proteins
phagocytic neutrophils
macrophages
dendritic cells

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12
Q

complement system

A

primary effector system for innate and adaptive systems
consists of protein activated microbed and promote inflammation and destruction of microbes

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13
Q

classical pathway of microbe recongition

A

adaptive immunity, recognizes antibody bound to surface of microbe or structure

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14
Q

lecitin pathway of microbe recognition

A

innate pathway uses plasma protein (mannose binding ligand) binds to residue

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15
Q

alternate pathway of microbe recognition

A

innate pathway, recognizes certain microbial molecules

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16
Q

lining of the respiratory, GU, and GI tracts

A

Mucus traps and washes away microorganisms
cillia: move microbes trapped in mucus to throat where it is coughed or sneezed out

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17
Q

antigens (adapative immunity)

A

aka immunogens stimulate an immune response
Ex: bacteria, fungi, virus, protozoa, parasites
Non microbial antigens: pollen, poison ivy, insect venom, transplanted organs
recognized by receptors on immune cells and cause antibodies to be formed

18
Q

t lymphocytes

A

Helper t cells: trigger immune response and are essential for differentiation of b cells into antibody producing cells
Regulatory T cells
Cytotoxic t cells

19
Q

antigen presenting cells

A

macrphages and dendritic cells that process and present antigen peptides to helper t cells

20
Q

cell surface major histocompatibility complex molecules (MHC)

A

key recognition molecules the immune system uses to distinguish self from nonself
Class one: present in all nucleated cells other than those of the immune system, interact with CD8+ T cells in the destruction of cells affected by intracellular pathogens or cancer
Class two: found on antigen presenting cells and b lymphocytes, aid in cell communication

21
Q

Humoral immunity (adaptive immunity)

A

protection from b lymphocytes: eliminates extracellular microbes and microbial toxins
primary tissue response: antigen first introduced into the body
latent period before detection of the antibody
activation takes one to two weeks but can be several weeks before it is detectable
secondary (memory response): occurs on second or subsequent exposure to antigen. rise in antibodies and occurs quicker due to memory cells. Ex: booster shots

22
Q

immunoglobulins

A

IgG: placenta
Ig A: breast milk
IgM
IgD
IgE: allergies

23
Q

passive immunity

A

immunity transferred through another source
Ex: crosses placenta in mother baby in utero or through breastmilk, transferred from other period or animals

24
Q

self regulation of the immune response

A

inadequate response can lead to immunodeficiency
excessive or inappropriate response can lead to allergic reactions or autoimmune disease
tolerance: inhibition of an immune response, non reactive to self antigens while producing immunity to foreign agents, can lead to inability to respond to infectious agents

25
newborns
protected by maternal antigens (IgG and IgA), a lot of IgG crosses in the last few weeks of pregnancy which makes preemie babies so immunodeficiency, HIV moms will pass HIV antibodies to baby, but may not transfer virus
26
aging
elderly have changes in immune response and are more susceptible to infections more autoimmune and immune complex disorders higher incidence of cancer and less response to vaccines
27
Hypersensitivity disorders
Disorders caused by immune response type one: immediate hypersensitivity disorders: IgE mediated, begin rapidly, allergic reactions, cytokinins secreted differentiate B cells into IgE which act as growth factors for mast cells and activate eosinophils Primary or immediate phase response, vasodilation, vascular leakage, smooth muscle contraction Secondary or late phase: intense infiltration of tissues with eosinophils and other acute or inflammatory cells, epithelial cell damage, leukotrienes, and prostaglandins produce response type two: antibody mediated disorders Type three: immune complex mediated disorders type four: cell mediated disorders
28
type one hypersensitivity: anaphylactic reaction
Life threatening- can occur within minutes of exposure Characterized by widespread edema, difficulty breathing, vascular shock secondary to vasodilation Results from antigen introduced by injection- insect sting, or absorption across skin, GI mucosa Level of severity depends on level of sensitization Treatment- airway, IV, epinephrine- relaxes bronchoconstriction, increases BP Pt should have epi-pen, family members should be trained, medi-alert bracelet
29
Type I Hypersensitivity: Local (Atopic) Reactions
Confined to specific site by exposure Atopic-genetically determined hypersensitivity to common allergens Mediated by igE- mast cell reaction Most common disorders- hives, allergic rhinitis (hayfever), atopic dermatitis, food allergies and some forms of asthma
30
Type I Hypersensitivity: Allergic Rhinitis
Characterized by sneezing, itching, and watery discharge from nose and eyes (rhinoconjunctivitis), can also be associated with sinusitis and bronchial asthma Severe attacks: general malaise, fatigue, muscle soreness, and HA Typical allergens: pollen from ragweed, grasses, tress and weeds, fungal spores, house dust and mites, animal dander and feather Diagnosis: skin ,serum or nasal smear (increase eosinophils) Treatment: antihistamines, topical and oral decongestants, desensitization
31
Type I Hypersensitivity: Food Allergies
Any food can trigger- most common are milk, eggs, peanuts, tree nuts, seafood, cooking food may change symptoms Acute response (hives and anaphylaxis), Chronic (asthma, atopic dermatitis and GI disorders) Can occur at any age, but usually childhood
32
Type II Hypersensitivity
Mediated by IgG or IgM antibodies directed against antigens on cell surfaces or connective tissue Antigens can be endogenous or exogenous (drug metabolites) 3 types of Type II Complement and antibody mediated destruction- mismatch blood transfusion rx, hemolytic dx of newborn due to ABO or rH incompatibility or drugs (HIT) Complement and antibody mediated inflammation-glomerulonephritis Antibody- mediated dysfunction- changes cell function Graves dx (TSH receptors), MG (ACE receptors)
33
Type III Immune complex-Mediated Disorders
Complement- and Antibody-Mediated Cell Destruction Involve formation and deposition of insoluble antigen-antibody complexes Responsible for vasculitis (SLE), systemic immune complex disease (serum sickness) and local immune complex disease
34
Type IV Cell- mediated Hypersensitivity
Direct cell cytotoxicity- sensitized CD8+T cells kill antigen-bearing target cells Delayed-type hypersensitivity reactions- presensitized CD4+T cells release cytokines that damage and kill antigen-containing cells- tuberculin skin test Allergic contact dermatitis- inflammatory response after sensitized- cosmetics, hair dyes, topical drugs- erythematous, popular and vesicular lesion, pruritus and weeping 12-24 hours post exposure, lasts days to weeks treatment with corticosteroid creams Hypersensitivity Pneumonitis- exposed to inhaled organic dusts or occupational antigens; labored breathing, dry cough, chills, fever, headache, chronic exposure may lead to chronic lung disease with little reversibility
35
Transplantation
Taking cells, tissues or organs (graft) from on individual (donor) to another (recipient) Rejection is a major barrier to transplantation- recipients immune system recognizes the graft as foreign and attacks it. Hyperacute rejection: occurs almost immediately after transplantation, caused by existing recipient antibodies and initiate type III Arthus- type sensitivity Acute rejection- occurs within first few weeks or months Chronic rejection occurs over prolonged period, caused by T-cell cytokines that damage BV causing ischemic damage to graft tissue
36
Graft versus Host Disease
Occurs most often in bone marrow transplants patients 3 things must occur: The transplant must have a functional cellular immune component The recipient tissue must bear antigens foreign to donor tissue Recipient immunity must be compromised to the point that cannot destroy transplanted cell Occurs most often in bone marrow
37
Autoimmune disease
Disruption in self-tolerance that results in damage to body tissues by immune system Self-tolerance is maintained through central and peripheral mechanisms that delete autoreactive B or T cells that suppress or inactivate immune responses that destroy host cells, defects in this mechanism predispose to autoimmune disease May be triggered by environmental stimuli, infections, genetic predisposition Treatment based on tissue involved, immunosuppressive drugs, steroids
38
Signs of immunodeficiency disorders
4 or more new ear infections in 1 year 2 or more serious infections in 1 year 2 or more months on antibiotics with little effect 2 or more PNA within 1 yearFailure of infant to gain weight or grow normally Recurrent deep skin or organ abscess Persistant thrush, fungal infections of skinNeed for IV ABX 2 or more deep seated infections including septicemia Family Hx
39
Acquired Immunodeficiency syndrome (AIDS)
Profound immunosuppression Transmitted blood or body fluids that contain the virus, sexual contact is the most frequent mode*Destroys CD4 cells 3 phases: Primary phase: shortly after infection- mono like symptoms Latency phase: may last for years Overt phase decrease in CD4 count Treatment involves drugs that interrupt replication of virus- no cure Treat opportunistic infections Diagnosis: ELISA- enzyme-linked immunosorbent assay Western blot if ELISA is +, the western blot can identify false-positive EIA results Home tests
40
Pregnancy and HIV
Women infected with HIV and transmit to offspring in utero, labor or breast milk HIV antibody can be present in babies from the mother, uninfected babies is usually disappears within 18 months