N339 Exam 2 Flashcards
With healing, ______ are stimulated by a variety of growth factors. Healing begins 3-4 days after insult; mediated by __________ (type of cytokine), that are released by platelets and immune cells. GFs communicate with fibroblasts and _______ cells. Fibroblasts lay down collagen fibers that help rebuild the tissue. Providing the _____ ______ FRAMEWORK FOR HEALING. Endothelial cells grow into the new connective tissue to make _______.
fibroblasts growth factors endothelial CONNECTIVE TISSUE capillaries
fever, neutrophilia, lethargy, and muscle catabolism are all systematic manifestations of _______.
inflammation
Most systemic manifestations are elicited by ______ (three cytokines) and released by ______ and inflamed tissues.
IL-1, IL-6, and TNF-α
macrophages
The 3 cytokines CAUSE LIVER TO MGR ACUTE PHASE PROTEINS (______ and ______) WHICH CAUSE AN INCREASE IN ______ PRODUCTION.
BRADYKININ AND COMPLEMENT
FIBRINOGEN
ACUTE PHASE PROTEINS AREN’T “acute inflammation”. They are phase related only and present they always indicate _______ INFLAMMATION.
SYSTEMIC
Acute phase proteins from the liver cause an increase in the level of ______ in the blood. Fibrinogen coats the RBCs and causes them to ______ more readily. This change in RBCs causes an increase in the _______ _____ ______, which is indicative of the presence of inflammation
fibrinogen
aggregate
Erythrocyte Sedimentation Rate (ESR)
Previous exposure to ______ antigens is not required for the activation of innate immune defenses. ______ is an important aspect of innate immunity that involves localization of harmful agents and the bringing of _______ cells to the area. Classic manifestations of inflammation are redness, swelling, heat, pain, and loss of ____.
foreign
Inflammation
phagocytic
function
Inflammatory chemicals such as histamine, prostaglandins, and leukotrienes are released from injured tissues, ______, macrophages, and neutrophils. These chemicals increase vascular _______ , vasodilate, and attract immune cells to the area (______).
mast cells
permeability
chemotaxis
______ migrate to the inflamed area, collect at the side of the vessel, and squeeze through into the tissue. Neutrophils arrive in large numbers in acute _______ infection and begin active phagocytosis. Neutrophils and macrophages produce_____ ______ agents to destroy and digest antigens.
Phagocytes
bacterial
proteolytic enzymes and oxidizing
With _____ inflammation, macrophages and lymphocytes predominate
chronic
Healing is mediated by ___________ released from platelets and immune cells that stimulate ______ to divide and manufacture extracellular matrix proteins. Endothelial cells respond to ______ growth factors by forming capillary networks.
growth factors
fibroblasts
angiogenic
Inflammatory exudate functions to transport immune cells, antibodies, and nutrients to the tissue and dilute the offending substances. ______ exudate is watery and low in protein; _____ exudate is thick, sticky, and high in protein; _______ exudate contains infective organisms, leukocytes, and cellular debris; and _______ exudate contains red blood cells.
Serous
fibrinous
purulent
hemorrhagic
______ manifestations of inflammation include fever, neutrophilia, lethargy, muscle ______, increased ________ proteins (CRP), and increased ____. These responses are attributable to the___, ____ and ____ released from macrophages and inflamed tissues.
Systemic catabolism acute phase ESR IL-1, IL-6, and TNF-α
_________: immune system recognizes parts of our body as being foreign b/c of mutation on cells (identifies self tissue as foreign tissue due to some change).
Autoimmunity
What are the 4 types of hypersensitivity?
Type I (Immediate, Atopic, Anaphylactic) Type II (Cytotoxic, Cytolytic) Type III (Immune Complex) Type IV (Delayed Hypersensitivity)
Deficient Immune ______ leaves us open to disease.
Primary Immunodeficiency Disorders
Secondary Immunodeficiency Disorders
Responses
Autoimmune diseases occur when ____ _____ is lost and reactions between self antigens and the immune system occur.
self tolerance
True or False:
Exact mechanism of autoimmune diseases is unknown
True
What are 3 Factors involved in autoimmunity?
Gender
Genetic Factors
Environmental Factors
Discuss Gender with regard to autoimmunity.
certain diseases are more dominant ex. SLE systemic lupus erythematosus
-estrogen may play role in autoimmune response.
Provide an example of a genetic factor to autoimmunity.
Ex. familial clustering with RA
What environmental factors influence autoimmunity?
extrinsic factors viruses, bacteria, antibiotics may trigger B-Cells to mfr autoantibodies.
________: pathogen w/ receptors that are almost identical to normal tissue ; can evade or trigger immune response.
ANTIGENIC OR MOLECULAR MIMICRY
____ _____: antigens that are hidden. Ex. Vasectomy triggers immune response. During embryological and fetal dvlpt, testes devlp separately, so sperm antigens aren’t available for tolerance, w/ vasectomy, have bleeding, antigens send msg to attack tissue.
SEQUESTERED ANTIGENS
___________: shut down immune response after offending antigen has been neutralized (by phago or binding up of pathogen). Triggers release of Antibodies from B-Cells. antibodies. If we have too few suppressor cells, then not enough to shut down immune response.
SUPPRESSOR T-CELLS
________ disorders occur when the immune system erroneously reacts with “self” tissues. These disorders are thought to be polygenic and ______; however, the exact etiologic process is unknown.
Autoimmune
multifactorial
The theory involving release of ____ _____ suggests that self antigens that do not come in direct contact with lymphocytes during fetal development may cause autoimmune reactions if they are subsequently released from sequestration.
sequestered antigens
Abnormal production of subclasses of T lymphocytes, particularly____ ______, has been proposed as a reason for the development of autoimmunity, as well as the development of abnormal ______ that do not respond to suppressor T cell signals.
suppressor T cells
B cells
A genetic component is probable, inasmuch as certain autoimmune disorders are more commonly associated with particular _____ and female _____.
MHC types
gender
______ may also be causative in the development of autoimmune disorders. Viruses may alter ____ cells, thus precipitating an immune attack. Formed antibodies may then ______ with similar but uninfected cells.
Viruses
self
cross-react
What’s a type I hypersensitivity response called?
-Anaphylactic
What is the mechanism for Type I hypersensistivity?
IgE mediated- mast cell degranulation
With type II hypersenitivity (cytotoxic) which mechanism is classic?
IgG and IgM antibody formation
Type IV hypersensitivity is cell mediated (delayed). What type of mechanism is responsible for the response?
sensitized T-lymphocytes release cytokines and produce T-cell mediated cytotoxicity (ie not antibody mediated)
Type I hypersensitivity is an immediate allergic or ____type of reaction mediated primarily by sensitized ___cells. The reaction is initiated when __ antibodies located on the mast cell membrane are bound by antigen, with subsequent cross-linking of IgE receptors. Mast cell ____ releases chemicals that mediate the signs and symptoms of anaphylaxis. Released histamine, kinin, prostaglandins, interleukins, and leukotrienes cause increased vascular permeability, vasodilation, hypotension, urticaria, and bronchoconstriction. Examples of type I reactions include drug reactions, bee sting reactions, and asthma.
anaphylactic
mast
IgE
degranulation
In a type I hypersensitivity reaction, Released
1.
2.
3.
4.
5.
cause increased vascular permeability, vasodilation, hypotension, urticaria, and bronchoconstriction.
- histamine,
- kinin,
3, prostaglandins, - interleukins,
- leukotrienes
Type II hypersensitivity occurs when _____are formed against antigens on cell surfaces, usually resulting in ____of target cells. Cell lysis may be mediated by activated ______ (membrane attack complex) or by phagocytic cells that are attracted to target cells by the attached antibodies. Examples include transfusion reactions, erythroblastosis fetalis, myasthenia gravis, and hyperacute graft rejection.
antibodies
lysis
complement fragments
Type III hypersensitivity reactions occur when antigen-antibody complexes are deposited in tissues and result in the activation of ______ and subsequent tissue inflammation and destruction. Antigen-antibody complexes activate the complement cascade and subsequently attract phagocytic cells to the tissue. Persistent low-grade infections, inhalation of antigens into alveoli, and autoimmune production of antibodies may result in chronic production of antigen-antibody complexes. Examples include glomerulonephritis and SLE.
complement
Type IV hypersensitivity reactions are ______and do not require antibody production, in contrast to type I, II, and III reactions. Sensitized T cells react with altered or foreign cells and initiate ______. Contact dermatitis, tuberculin reactions, transplant rejection, and graft-versus-host disease are examples.
T-cell mediated
inflammation
What are 3 possible causes of human anaphylaxis?
Medications
Biological Agents
Food
Name two types of medications that cause anaphylaxis?
Penicillin and Radiation contrast media
Name 3 types of Biological Agents that cause anapylaxis?
Insulin
vaccines
insect stings
Name 3 types of Foods that cause anaphylaxis?
nuts
shellfish
Citrus fruits
What type of hypersensitivity is observed with the wrong type of blood transfused?
Type II antibody mediated (cytotoxic)
When complement induces or enhances recruitment and phagocytosis it is referred to as ______.
OPSONIZATION
Type II hypersensitivity: with antibody mediated cell destruction: cell _____ is changed so that cell destructs, membrane proteins fall apart. ALSO activates _____: which causes direct cell lysis, “recruitment and phagocytosis” (opsonization)
metabolism
complement
Rh sensitivity is an example of what kind of hypersensitivity?
Type II antibody mediated.
Myasthenia Gravis is an example of what type of hypersensitivity?
Type II Ab mediated.
With Myasthenia Gravis, individual develops Ab to motor end plate _____, those Ab form receptor complexes w/ motor end plate receptors blocking receptor from normal _____and also cause receptor _____. results in poor or no muscle _____.
receptors
neurotransmitter
destruction
contraction
