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Pathophysiology > Patho Unit 4 > Flashcards

Patho Unit 4 Flashcards

Understand: - Innate Immunity: Inflammation and Wound Healing (Ch 5) - Adaptive Immunity (Ch 6) - Infection and Defects in Mechanisms of Defense (Ch 7)

1
Q

Innate (natural) Immunity

A
  • Chemical and physical barriers
  • Non-specific mechanisms
  • Non-adaptive mechanisms
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2
Q

Adaptive (acquired) Immunity

A 
Specific
  - Responds to a unique pathogen
Adaptive
  - Variable response
2 Components
  - Cell-mediated and Antibody-mediated
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3
Q

First Line of Defense

A

Physical Barriers
- Skin, mucus membranes, vomiting, coughing, urination, defecation

Biochemical Barriers
- Mucus, perspiration, saliva, tears, cerumen, chemicals derived from normal flora, sebum

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4
Q

Second Line of Defense

A

Inflammation and Phagocytosis

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5
Q

Third Line of Defense

A

Adaptive, Specific immunity

- Cell mediated, Antibody mediated (humoral)

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6
Q

Inflammation

A
  • Immediate, non-specific, and non-adaptive
  • Universal response to injury
  • Mediated by chemicals found in circulation
  • Increases plasma and blood cells into tissues around the injury
  • Defends against infections
  • Promotes tissue repair and healing
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7
Q

Local Symptoms of Inflammation

microcirculation

A
  • Vasodilation
  • Increased capillary permeability
  • White cell migration from the capillaries to the site of inflammation
  • Inflammatory chemicals stimulate nociceptors
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8
Q

Local Symptoms of Inflammation

observable characteristics

A
  • Heat
  • Swelling
  • Redness
  • Pain
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9
Q

Vasodilation

A

Increased blood flow to decrease blood flow velocity

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10
Q

Exudation

A

Fluid and cells leak from blood vessels

  • Serous, fibrinous, purulent, hemorrhagic
  • Dilutes toxins
  • Brings in plasma proteins
  • Removes bacterial products and dead cells
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11
Q

Purpose and Benefits of Inflammation

A
  • Destroy injurious agents
  • Confine agents to limit their effects on the host
  • Stimulate components of the adaptive immune system
  • Promote regeneration and repair of tissue
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12
Q

Systemic Manifestations of Inflammation

A
  • Fever
  • Increased Pro-inflammitory and Anti-inflammitory plasma proteins by the liver
  • Leukocytosis (Neutrophils)
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13
Q

Events of Acute Inflammation

A

Activation of:

  • Complement System: direct or indirect destruction of cells (esp. bacteria)
  • Coagulation System: isolates infections by trapping pathogens and prevents hemorrhage
  • Kinin System: interacts with the coagulation system; pro-inflammatory
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14
Q

Complement System

A

A group of plasma proteins that participate at all levels of inflammation
- Enhances inflammation by opsonization of bacteria and degranulation of Mast cells
3 Pathways
- Classical
- Alternative
- Lectin

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15
Q

Classical Pathway of Compliment System

A

Activated by antigen-antibody complexes

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16
Q

Alternative and Lectin Pathways of Compliment System

A
  • Activated by biologic substances (bacteria, fungi, toxins)

- Non-antibody dependent

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17
Q

Coagulation System

A
  • Stops bleeding
  • Localizes microorganisms
  • Provides a meshwork for healing
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18
Q

Kinin System

A
  • Activated by the coagulation system (intrinsic pathway)
  • Primary kinin: bradykinin
  • Augments inflammation (pro-inflammatory): vascular permeability, vasodilation, smooth muscle contraction
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19
Q

Cytokines

A

Chemical signal from one cell that affects another

- Can be pro- or anti-inflammatory

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20
Q

Interleukins

A

Cytokines produced primarily by macrophages and lymphocytes in response to microorganisms and products of inflammation

  • Encourages cell adhesion
  • Chemotaxis
  • Proliferation and maturation of WBCs
  • Both pro- and anti-inflammatory
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21
Q

Interferons

A

Proteins produced to protect against viral infections and encourage the immune system

  • Defense against viral infections
  • Made by leukocytes to help other cells defend against viruses
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22
Q

Mast Cells

A

Large, granular cells in loose connective tissue, adjacent to blood vessels

  • Early initial activators of the inflammatory response
  • Degranulation
  • Synthesis of inflammatory mediators
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23
Q

Mast Cell Degranulation

A

Released from Granules:

  • Histamine
  • Mast cell protease = tryptase
  • Proteoglycans (increase endothelial cell permeability)
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24
Q

Effects of Histamine

A
  • Inflammation
  • Contracts smooth muscle in bronchi, GI tract, and uterus
  • Increases bronchial, intestinal, and salivary secretions
  • Dilation of cerebral blood vessels (headache)
  • Stimulates secretion of gastric juices
  • Stimulates nerve endings to cause pain and itching
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25
Q

Leukotrienes

A
  • Produce histamine like effect (slower, prolonged)
  • Play an important role in asthma
  • Inhibitors are used for more sever forms of asthma
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26
Q

Prostaglandins

A
  • Encourage vascular permeability, chemotaxis, and pain
  • Made by enzymes called Cyclo-oxygenases (COX)
  • Non-steroidal anti-inflammatory drugs are COX inhibitors
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27
Q

Phagocytosis and Phagocyte Migration

A
  • Rolling
  • Margination
  • Diapedesis
  • Exudation
  • Phagocytosis
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28
Q

Phagocyte Rolling

A

Cells slowed by interaction with endothelium

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29
Q

Margination

A

Increased stickiness by producing adhesion proteins on the cell

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30
Q

Diapedesis

A

Emigration of phagocytes through the retracted endothelial junctions and basement membrane

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31
Q

Neutrophils

A
  • 70% of WBCs, live 5 days on average
  • “Dive into pus and die”
  • Phagocytose invaders, the drop chemical bombs on them to kill them
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32
Q

Macrophages

A
  • Migrate into tissues
  • Enter the site after 24 hours to help replace Neutrophils
  • Survive longer than Neutrophils
  • Professional Antigen-Presenting Cells (APCs)
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33
Q

Chronic Inflammation

A

Lasts longer than 2 weeks
- Occurs when the body fails to remove the cause of the inflammation (weak pathogens, large, resistant or persistent pathogens, or weak immune system)

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34
Q

Granuloma

A

Formed by Macrophages which join together like bricks in a wall to encircle the offender

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35
Q

Regeneration of Tissue

A

Results in the restoration of the structure, therefore function
- The goal of healing in inflammation

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36
Q

Repairing Tissue

A

The replacement of destroyed tissue with scar tissue

- Scar tissue restores strength, but not function

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37
Q

Wound Healing

A
  1. Clean up wound by phagocytizing particulate matter (debridement)
  2. Healing continues by:
    - Filling in the wound
    - Covering and sealing the wound
    - Shrinking the wound
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38
Q

Simple Wounds

A

Regenerated and healed by primary intention

  • Minimal tissue loss
  • Examples: paper cut, incised wounds, sutured laceration
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39
Q

Open Wound

A

Requires more tissue replacement and healing occurs through secondary intention
- Examples: pressure sore, non-sutured laceration, burns

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40
Q

Regeneration and Repair Stages

A
  1. Inflammation
    - Coagulation and infiltration of cells to facilitate healing
    - Debridement and angiogenesis
  2. Proliferation of New Tissue
    - Fibroblast proliferation, collagen synthesis, and epithelialization
  3. Remodeling and Maturation
    - Cellular differentiation, scar tissue remodeling, capillaries removed from scar tissue
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41
Q

Dysfunctional Wound Healing

during inflammatory phase

A
  • Hemorrhage
  • Infection
  • Chronic inflammation (excess granuloma formation)

Affected by:
- Diabetes, hypoxia, nutritional deficiency, reactivation of inflammatory responses, and anti-inflammatory medications

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42
Q

Dysfunctional Wound Healing

impaired collagen synthesis

A

From nutritional deficiency

- Lack of vitamin C (scurvy), iron, calcium, and copper

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43
Q

Dysfunctional Wound Healing

excessive collagen synthesis

A

Adhesions, hypertropic and keloid scars

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44
Q

Dysfunctional Wound Healing

wound disruption

A

Reopening (dehiscence) due to collagen disruption

- Wound healing by primary intention is now healing by secondary intention

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45
Q

Dysfunctional Wound Healing

excessive wound contraction

A

Vasoconstriction

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46
Q

Lymphocytes

A
  • The most important cells of the adaptive immune response
  • Originate in bone marrow and mature in either the bone marrow or in the lymph system
  • Precursor cells differentiate into T cells (in the thymus) and B cells (in the bone marrow)
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47
Q

Antibody-Mediated (humoral) Immunity

A

B lymphocytes

  • When stimulated develop into plasma cells
  • The proteins released from plasma cells are antibodies
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48
Q

Cell-Mediated Immunity

A

T lymphocytes

  • Recognize specific antigens
  • Can directly attack abnormal cells
  • Mediate adaptive immune responses
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49
Q

Immunogen

A

A molecule that will induce an immune response

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50
Q

Antigen

A

Molecule or fragment that binds with products of the immune system (antibodies, T cells, and B cells)

  • IDs the cell as self or non-self
  • IDs the type of cell
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51
Q

What makes an Antigen more immunogenic/antigenic?

A
  • Large in size
  • Organic
  • Complex in structure
  • Foreign (or at least recognized that way)
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52
Q

Natural Immunity

A

Not gained through modern medicine

  • Active: body is exposed to disease and makes antibodies
  • Passive: a baby receives antibodies from its mother through the placenta or breast milk
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53
Q

Artificial Immunity

A

Gained through artificial means

  • Active: a person receives an injection of an attenuated of an attenuated (changed/weakened) pathogen that stimulates to body to form an antibody
  • Passive: Injection of prepared antibody
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54
Q

Active Immunity

A

Long term immunity

- The body responds to a pathogen (antigen) to make antibodies

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55
Q

Passive Immunity

A

Short term immunity

- The body receives antibodies with no effort of its own

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56
Q

Immunoglobulins

A

Antibodies, distinguished by structure, location, and function

Classes: IgM, IgG, IgA, IgE, and IgD

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57
Q

IgM

A
  • Very effective activator of the Complement System (1st responders)
  • Pentamer
  • 10% of total plasma antibody
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58
Q

IgG

A
  • Actively transported across the placenta
  • Monomer
  • 75% of plasma antibody
  • Longest half-life of the immunoglobulins (long-term immunity)
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59
Q

IgA

A
  • Located in the plasma and body secretions
  • Lacrimal glands, salivary glands, and lymphoid tissues in the breasts, bronchi, intestines, and GI tract
  • Protects against pathogens that are inhaled, swallowed, or come in contact with external surfaces
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60
Q

IgE

A
  • Low plasma concentration
  • Bound to Eosinophils, Basophils, and Mast cells
  • Triggers release of histamine from Mast cells
61
Q

IgD

A

?

62
Q

Secretory Immune System

A

IgA secreted in gut by MALT

  • M cells found in Peyer’s Patches within gut wall pass antigens from the lumen to the MALT beneath
  • There, B cells are stimulated to make IgAs
63
Q

MALT

A

Mucosal-Associated Lymphoid Tissue

- Similar to lymph nodes, but protrude into gut lumen

64
Q

Primary vs Secondary Immune Response

A
  • When stimulated initially, plasma cells begin to make large amounts of anitbody
    1. IgMs first
    2. IgGs later
  • Memory B cells stay in a resting state until there is a secondary exposure
  • The process of presentation is made faster because the immune system has developed memory
65
Q

Fetal and Neonatal Immunity

A

Innate immunity is functioning (at a reduced capacity) at birth

66
Q

Erythema Toxicum Neonatorium

A

Rash present in about 1/2 of newborns

- Caused by normal flora colonizing the skin, causing inflammation

67
Q

Fetal and Neonatal Immunity

IgG

A

Crosses the blood-placental barrier

  • At birth, baby’s IgG levels are in equilibrium with mother’s so baby has a natural passive immunity
  • Baby produces no IgG of his/her own at birth
68
Q

Fetal and Neonatal Immunity

IgM

A

Does not cross the blood-placental barrier

  • Must be made by newborn
  • Newborn levels are 20% or those of adults, and it takes about 2 years to reach adult levels
69
Q

Fetal and Neonatal Immunity

IgA

A

Levels very low at birth

  • Adult values of salivary IgA reached at about 2 months
  • Mother’s breast milk provides passive natural immunity via secreted IgA
70
Q

Major Histocompatibility Complex

A

A group of genes on chromosome 6 that code for MHC proteins

  • Proteins are grouped in classes I, II and III
  • Because of their role in tissue transplants, the MHC molecules are also referred to as Human Leukocyte Antigens (HLA)
71
Q

MHC Molecules

A

“Flags” that identify cells (who they belong to and what organ/tissue)
- Also play a role in the immune response by providing information about what the cell has encountered (what the APC ate/whether the cell is infected with a virus)

72
Q

MCH/HLA Class I

A

Molecules are located on all nucleated cells

- Present ENDOGENOUS antigens (self)

73
Q

MCH/HLA Class II

A

Molecules are located on “Professional” Antigen Presenting Cells

  • Macrophages, dendritic cells and some B Lymphocytes
  • Present EXOGENOUS antigens (foreign)
74
Q

Clusters of Differentiation

CD

A

Another protocol for identification of cell surface markers

  • Not on a particular chromosome
  • Over 300 have been identified
75
Q

Links between Innate and Adaptive Immunity

A

Antigen Presenting Cells

  • Macrophages
  • Dendritic cells
  • Some B cells
76
Q

T Lymphocytes

A

Cell-Mediated Immunity

  • Recognize specific antigens
  • Can directly attack abnormal cells
77
Q

T helper (CD4+) Cells

A
  • Recruited by the “advertising” of antigens displayed by MHC II markers on the surface of APCs
  • Release cytokines and stimulate division by autocrine activation
  • Divide to form T memory cells, T helper1 (activate T cytotoxic cells/cell-mediated immunity), and T helper2 (activate B cells/antibody-mediated immunity)
78
Q

T cytotoxic (CD8+) Cells

A
  • Activated by T helpers
  • When activated, release compounds that kill cancerous or virally infected cells
  • Apoptosis is preferred for virally infected cells
  • Perforin used to trigger cytolysis
79
Q

T regulator (supressor) Cells

A
  • No CD marker makes them hard to study
  • Seem to down regulate immune responses to save normal cells from destruction
  • Overactivity can lead to cancer
  • Under-activity can lead to autoimmune disease
80
Q

Mutualism

A

Both the host and the microorganism benefit

- E. coli that lives in the large intestine

81
Q

Commensalism

A

One organism benefits, the other is neutral

- Skin bacteria

82
Q

Parasitism

A

One organism benefits, the other is harmed

- Tapeworm and Round worms

83
Q

Pathogenicity

A

The ability of a pathogen to cause disease

- Presence of enzymes, toxins, number, capsules, intracellular invasion

84
Q

Virulence

A

The ability of a pathogen to cause sever disease

  • Cause cellular injury because they circumvent defensive barriers
  • Directly damage cells, interfere with metabolism, and limit the functionality of the cell
85
Q

Communicability

A

The ability to spread from one individual to another and cause disease

86
Q

Infectivity

A

The ability of a microorganism to invade and colonize within the host and produce infection

87
Q

Toxigenicity

A

The ability to produce toxins and influence virulence

88
Q

Bacteria

A
  • Unicellular
  • Aerobic or anaerobic
  • Can live as opportunists, commensals, and intra/extracellular barasies
  • Produce toxins: hemolysins, leukocidins, coagulases
89
Q

Bacterial Shapes

A
  • Cocci
  • Bacilli
  • Spirillia
  • Spirochetes
  • Pleomorphic
90
Q

Cocci

A

Spherical, non-motile bacteria

  • Diplo- (pair)
  • Strepto- (chain)
  • Staphylo- (irregular chain)
91
Q

Bacilli

A

Rod-shaped bacteria

92
Q

Spirillia

A

Rod-shaped, rigid, spiral organisms

93
Q

Spirochetes

A

Non-rigid, spiral rods

94
Q

Pleomorphic

A

Cells that do not fit in any of the other categories/ have no defined shape

95
Q

Bacterial Cell Wall

A
  • Composed of Peptidoglycan (a large molecular network of glucose and amino acids)
  • Cell wall characteristics determine if a bacteria is classified as Gram + or Gram -
96
Q

Spherical bacteria in clusters with a thick cell wall

A

Gram-positive staphylococci

97
Q

Spherical bacteria in pairs with a thin cell wall

A

Gram-negative diplococci

98
Q

Spherical bacteria in chains with thick cell wall

A

Gram-positive streptococci

99
Q

“Kinda” spherical and “kinda” rod-shaped bacteria with a thin cell wall

A

Gram-negative coccobacilli

100
Q

Gram-Positive Bacteria

A
  • THICK cell wall
  • Produce EXOTOXINS
  • Stain purple
101
Q

Exotoxins

A
  • Released during the cell’s LIFE cycle
  • Cause SPECIFIC symptoms
  • Examples: botulism, tetanus, staph food poisoning, toxic shock syndrome
102
Q

Gram-Negative Bacteria

A
  • THIN cell wall
  • Produce ENDOTOXINS
  • Stain red
103
Q

Endotoxins

A
  • Released during cell DEATH
  • Produce GENERALIZED symptoms
  • Example: salmonella food poisoning
104
Q

Sporulation

A

The formation of endospores

  • Produced when conditions are unfavorable
  • Help the chromosomal contents of the bacteria survive extreme temperatures, radiation and harsh chemicals
  • Once optimum conditions return, the spores will germinate
105
Q

Viruses

A
  • Not technically living
  • Obligate intracellular parasite
  • Provides the RNA and DNA to replicate, and the host cells provide the energy and resources
  • Components include nucleic acid, capsid, and an optional envelope
106
Q

Viral replication depends on…

A
  • Absorption
  • Penetration
  • Uncoating
  • Replication
  • Assembly
  • Release new virions
107
Q

Fungi

A
  • Important for decomposition and recycling of organic material
  • Divided into YEASTS and MOLDS
  • Release MYCOTOXINS and enzymes that damage connective tissue
  • Can cause superficial and deep infections
  • Some are part of the normal body flora and act as opportunists
108
Q

Mycoses

A

Diseases caused by fungi

109
Q

Immunodeficiencies

A

Usually manifested by the tendency to develop unusual or recurrent infections

  • Occur because of the impairment of one or more components of the immune or inflammatory response
  • Can be unsafe to administer vaccines because the person could get sick
110
Q 
Primary Immunodeficiencies 
(congenital)
A
  • Occurs during leukocyte development in the fetus or embryo
  • Can affect one or more white cell lines
  • The number of cells affected dictates the degree of the deficiency
  • If the T and B lines are affected, the patient will have a normal number of the other leukocytes, but low lymphocytes and diminished antibodies
111
Q

Di George Syndrome

A

Partial or complete lack of the thymus

  • PRIMARY Immunodeficiency
  • Patient demonstrates lymphopenia and decreased T cell function
112
Q

Burton’s Agammaglobulinemia

A

Failure of early B cells to become mature B cells

- PRIMARY Immunodeficiency

113
Q

Wiskott-Aldrich Syndrome

A

IgM production is depressed

- X-linked recessive disorder

114
Q

Selective IgA Deficiency

A
  • Produce other types of antibody but not IgA
  • Can cause chronic intestinal candidiasis
  • Increased allergen uptake and more severe allergic responses (allergens aren’t stopped coming in)
115
Q 
Secondary Immunodeficiencies 
(acquired)
A
  • Nutritional deficits
  • Chemotherapeutic agents
  • Corticosteroids
  • Burn victims
  • Emotional stress
  • Others: pregnancy, infancy, infections, malignancies, aging, diabetes, anemia
116
Q

Graft-Verses-Host Disease

GVHD

A

Immunodeficiencies can put a patient at risk

- Immunologically active transfusions can attack an immunocompromised recipients’s cells

117
Q

Human Immunodeficiency Virus

HIV

A
  • Retrovirus
  • Spread primarily through contact with blood or body fluids
  • It is speculated that lesions from other STDs provide opportunities for the virus to enter the host
  • Concentrations are high in blood and semen and low in vaginal fluid, tears, sweat and breast milk
  • Has been transmitted through infected tissue transplants
118
Q

Retrovirus

A
  1. Binds to the cell surface
  2. Inserts its RNA
  3. Uses Reverse Transcriptase to convert RNA to DNA
  4. Inserts its viral genetic material into the target cell DNA, which can begin replicating immediately or remain latent for a period of time
119
Q

AIDS Pathophysiology

A
  • Virus’s gp120 protein binds to the CD4 receptor
  • Therefore, HIV infects mainly CD4+ (T helper) cells
  • The number of CD4+ cells continues to diminish until the patient is prone to opportunistic infections
120
Q

Testing for HIV

A
  • Window period: lag time between infection and detection (currently about 7 days)
  • Antigen and Antibody tests for screening and confirmation (err on the side of false positive)
  • Count CD4+
121
Q

Treatment for HIV

A

Highly Active Antiretroviral Therapy (HAART)
- 3 synergistic drugs
Drugs can be:
- Entry inhibitors
- Reverse Transcriptase Inhibitors (NNRTI)
- Integrase inhibitors
HIV vaccine doesn’t control mutations

122
Q

Hypersensitivity

A

An inappropriate immune response that damages the host

- 4 types, though almost all will overlap to some degree

123
Q

Allergy

A

Hypersensitivity to an antigen from the environment

124
Q

Autoimmunity

A

Hypersensitivity to antigen from self

125
Q

Alloimmunity

A

Hypersensitivity to an antigen from donated tissue

126
Q

Type I Hypersensitivity

A

Immediate, IgE Mediated

  • IgE antibody reacts with antigen and stimulates mast cell degranulation
  • Can be an inherited tendency to respond to allergens with continual production of IgE

Symptoms: allergic rhinitis, asthma, urticaria (hives), anaphylactic shock, diarrhea, and/or vomiting

127
Q

Type II Hypersensitivity

A

Tissue-Specific

- Free antibody (IgG/M) reacts with cell-surface antigens and activates phagocytosis and compliment

128
Q

Desensitization of Type I Hypersensitivity

A
  • Denatured allergen injected under skin

- IgGs intercept the allergen preventing it from binding to IgEs

129
Q

Type III Hypersensitivity

A

Immune Complex-Mediated

  • Antibodies react with free, soluble antigen to form complexes that precipitate in the tissues
  • When soluble antigen combines with antibody, complexes precipitate out of plasma and deposit in tissues, bind/activate complement and cause tissue damage
130
Q

Type IV Hypersensitivity

A

Delayed (48-72 hours), T cell-Mediated

  • The only one that isn’t antibody dependent
  • Sensitized cytotoxic T cells to attack tissues
  • Sensitized helper T cells release lymphokines that recruit macrophages
131
Q

Examples of Type II Hypersensitivity

A
  • Transfusion Reactions
  • Hemolytic Disease of the Newborn
  • Autoimmune Thyroditis
  • Autoimmune Glomerulonephritis
132
Q

Examples of Type III Hypersensitivity

A
  • Autoimmune diseases (Lupus, Rheumatoid arthritis)
  • “Farmers Lung” (hypersensitivity to inhaled allergens in dairy farmers)
  • Glomerulonephritis
133
Q

Examples of Type IV Hypersensitivity

A
  • Poison Ivy/Oak
  • Topical drugs
  • Soaps
  • Perfumes… (really any chemical substance)
  • TB skin test
  • Acute transplant rejection
134
Q

Self/Non-Self Recognition

Immune Tolerance

A

Deletion of Lymphocytes that have receptors for the body’s own tissues

  • T cells are tested in the Thymus
  • B cells are tested in the Bone Marrow
135
Q

Autoimmunity

detailed

A

The breakdown of tolerance in which the body’s immune system begins to recognize self-antigens as foreign

  • Result from a genetic predisposition and a hypersensitivity to an environmental stimulus
  • There is a strong correlation with some MHC allele and autoimmune diseases
136
Q

Systemic Lupus Erythematosus

SLE

A
  • Chronic, systemic inflammatory disease
  • Production of a variety of autoantibodies
  • Positive Anti-Nuclear Antibody (ANA) test
  • Circulating immune complexes deposit in tissue, especially Glomerular membrane
  • “Lupus” (wolf-like), photo-sensitive “red” facial rash
  • Other symptoms include Anemia and Lymphocytopenia
137
Q

Clinical Manifestations of SLE

A
  • Arthritis 90%
  • Vasculitis and rash 70-80%
  • Renal disease 40-50%
  • Anemia 50%
  • Cardiovascular disease 30-50%
138
Q

Graft Rejection

A
  • Transplants are complicated by an alloimmune response to donor HLA antigens
    • Classified as hyperacute, acute, or chronic depending on activation time
139
Q

Graft Rejection

hyperacute

A
  • Patient has preexisting IgG or IgM antibody to the tissue
  • Antibody binds to the tissue and activates an inflammatory response (Type II hypersensitivity)
  • This results in the cessation of blood flow to the graft - “white graft”
  • Pre-transplant tests minimize this risk
140
Q

Graft Rejection

acute

A
  • Cell-mediated rejection that occurs ~ 2 weeks after the transplant (Type IV hypersensitivity)
  • Immunosuppressive drugs try to minimize this response
141
Q

Graft Rejection

chronic

A
  • Can occur after months or years of normal function
  • Reaction to MINOR HLA antigens
  • No matter how much the immune response is suppressed, the tissue is still foreign
  • Symptoms: slow, progressive organ failure and damage to endothelial cells of the blood vessels
142
Q

Haptens

A

Antigens that are too small to be immunogens alone, but become one after combining with larger carrier molecules
- Ex: Poison Ivy initiates an allergic reaction after binding to large-molecular-weight skin proteins

143
Q

Epitope

A

The part of an antigen recognized by antibody

144
Q

Neutralization

A

Inactivating or blocking the binding of antigens to receptors

145
Q

Agglutination

A

Clumping insoluble particles

146
Q

Precipitation

A

Making soluble antigen into insoluble precipitate

147
Q

Opsonization

A

Flagging cells for distruction

- Tightens affinity of adherence between the phagocyte and target cell

148
Q

Chemotaxis

A

Attraction of microorganisms or phagocytes to substances released in the environment/tissues

Pathophysiology (11 decks)

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