NURSING
Midterm Exam
Week 1
Chapter 9: Alterations in Immunity
Hypersensitive: know the difference between allergy, autoimmunity and alloimmunity
Hypersensitive: an altered immunologic response to an antigen that results in disease
Allergy: Immunity and hypersensitivity and is the deleterious effects of hypersensitivity to
environmental agents
Autoimmunity: a disturbance in the immunologic tolerance of self-antigens; a breakdown of
tolerance during which the body’s immune system begins to recognize self as antigens as
foreign. Examples sequestered antigens, infectious diseases with molecular mimicry,
neoantigens. Genetic factor: familial association.
Alloimmunity: occurs when the immune system of one individual produces an immunologic
reaction against tissue of another. Transplant rejection and transfusion reactions.
Know the types of hypersensitivity
Type I: (immunoglobulin E (IgE); most common)- mediated reaction mediated by antigen-
specific IgE and the products of tissue mast cells. IgE binds to crystalline fragment (Fc) receptors
on the surface of mast cells; cross linking causes the release of histamine from mast cell
degranulation. (H1 and H2 receptors and increases chemotactic activity. Cytotropic antibodies
bind to the cell surface and regains are antibodies that can bind to skin. Histamine enhances the
chemotaxis of eosinophils at site of Type I reaction. Most common allergy is pollen. Short life
span and can be beneficial to the host immune reactions to parasites. Symptoms of H1 bronchial
constriction, edema and vasodilation and H2 increase gastric secretions and decreases the release
of histamine from mast cells and basophils.
Type II: (Tissue specific hypersensitivity reactions; rare) specific cell or tissue being the target of
an immune response. Begins with antibody binding to tissue specific antigens. 1st the cell can be
destroyed by antibody and activation of the complement cascade through the classical pathway.
2nd antibody may cause cell destruction through phagocytosis. 3rd antibody complement cascade
results in release of C3a and C5a causes damage to the cell, neutrophils release granules. 4th
antibody dependent cell medicated cytotoxicity. (ADCC) antibody on the target cell is
recognized on NK cells and release toxic substances that destroy target cell. 5th does not destroy
target cells but causes it to malfunction
Ex: graves disease autoantibody binds to an activates receptors for TSH
Type III: (Immune complex Mediated Hypersensitivity Reactions; rare) case by antigen-antibody
complexes that are formed in the circulation and deposited later in vessel walls or extravascular
tissues. In type III the antibody binds to soluble antigen that was released into the blood or body
fluids and the complex is deposited in the tissues. This is not organ specific and symptoms have
little to do with the particular antigenic target of the antibody. Damage results from complement
activation and neutrophil lysosomal enzymes. Immune complex disease: dynamic as variations in
the ratio of antigen to antibody. Immune complex clearance Large: macrophages, small: renal
clearance, Intermediate: Deposited in tissues; cause problems. Periods of exacerbation and
remission. There are two types of Type III.
Serum Sickness: caused by the formation of immune complexes in the blood and their
subsequent generalized deposition in target tissues (ex medication administration)
, affected blood vessels joints and kidneys. Symptoms include fever, enlarge lymph nodes,
rash and pain at sites of inflammation. (Raynaud phenomenon)
Arthus Reaction: caused by repeated local exposure to an antigen that reacts with
performed antibody and forms immune complexes in the walls of the blood vessels.
Causes increased vascular permeability and an accumulation of neutrophils, edema,
hemorrhage, clotting and tissues damage. Symptoms begin within an hour and peak 6-12
hours later.
Type IV: (Cell Mediated Hypersensitive Reactions) Caused by T lymphocytes and do not involve
antibody. These are graft rejections and allergic reactions resulting from contact with substances
such as poison ivy or TB test, some autoimmune diseases. Induration: clear hard center.
Destruction of the tissue is usually caused by direct killing by toxins from cytotoxic T (Tc) cells.
Helper T (Th) 1 and Th 17 cells produce cytokines that recruit phagocytes, especially
macrophages.
Atopic Allergies: Inheritableness of allergies, one parent there is a 40% chance and both parents
there is an 80% chance. Produce more IgE and have more Fc receptors for IgE on their mast
cells.
Know the types of primary immunity
Primary immunity (congenital): most are a result of a single gene defect
5 Types
1.) B Lymphocyte deficiencies: defects in b cell response; lower levels of
circulating immunoglobulins and increases risk of infection.
Hypogammaglobulinemia or agammaglobulinemia. Bruton
agammaglobulinemia: Most severe. Mutation in IgM. X-linked hyper-IgM
syndrome: defective class switch. Prone to pneumonia, most common is
common variable immunodeficiency.
2.) T Lymphocyte deficiencies: partial or complete absence of T-cell immunity
from partial thymus (DiGeorge Syndrome) Chronic mucocutaneous
candidiasis- primary defect of T lymphocytes in response to a specific
infectious agent; the yeast Candida albicans.
3.) Combined T & B: defects that affect development of both, most severe SCID,
reticular dysgenesis: the most severe form of SCID. Adenosine deaminase
(ADA) deficiency results in excess purine. X linked SCID is due to defect in
the interleukin IL-2 receptor. Bare lymphocyte syndrome: cannot present
antigens. Major histocompatibility complex (MHC) class I and II deficiencies
Class II is more severe. Wiskott-Alrich syndrome (WAS) IgA and IgG levels
are usually normal but the IgM level is highly depressed. Deficiencies in DNA
repair (AT)= ataxia telangiectasia mutations of the ATM gene occur.
4.) Compliment deficiencies: often resemble antibody deficiencies with recurrent
infections. C3 deficiency is the most common form. Mannose-binding lectin
(MBL) deficiency: prone to yeast infections. Properdin deficiency prone to
meningococcal infections and it is X linked. Factor I and H deficiencies
(destroy C3) C5 and C9 deficiencies: C9 is the most common and all are
prone to Neisseria infections.
, 5.) Phagocytic deficiencies: (p.288) severe congenital neutropenia (cyclic
neutropenia is a mild form; prone to bacterial infections) Leukocyte adhesion
deficency (LAD) mutations occur in the adhesion molecules. C3 receptor
deficiency: those with this deficiency are prone to skin infections. Chediak-
higashi syndrome defect is in the lysosomal system therefore killing is
ineffective. Myeloperoxidase deficiency results in chronic granulomatous
disease. multistep process that involves initial adhesion between circulating
phagocytes and the endothelial cells lining the circulation.
Rh antigen
Primarily expressed on erythrocytes. Rh-positive: Express the D antigen on the RhD protein. Rh-
negative does not express the D antigen. 15% of North American white are Rh-negative. Rh-
negative individuals can make anti-D if exposed to Rh positive erythrocytes. Hemolytic disease
of the newborn when Rh-negative mother gives birth to an Rh positive to baby. WARM
autoimmune hemolytic anemia: IgG antibodies react with erythrocytes at normal body temp.
COLD autoimmune hemolytic anemia: IgM autoantibodies react with erythrocytes in the cooler
portions of the body.
immune deficiency
impaired function of components of the immune or inflammatory response, phagocytes or
complement. Failure of mechanisms of self-defense to function in their normal capacity. Primary
or secondary.
Symptoms
If patient has repeated severe infections recurrent with only short intervals of relative health and
has multiple infections at once. 8 or more ear infections, two or more serious sinus infections,
2+ pneumonia, recurrent abscess, infect unusual sites, persistent fungal infections within 1 year,
oral antibiotics ineffective, failure to thrive, chronic diarrhea. Most commonly fungal or virual.
Therapies
Immune deficiency usually treated by replacement therapy.
Gamma Globulin therapy IV or IM, FFP, transplant bone marrow, steroids, stem cells, individual
lacks a thymus is reconstitute a thymus, gene therapy.
Chapter 10: Infection
Know the process of infection
Colonization: vectors direct, mechanical, or biological after deposition in receptive environment
for microorganisms, adhere to tissue through specific surface receptors.
Invasion: invade surrounding tissue by evading the hosts defense mechanisms.
Multiplication: warm and nutrient-filled environment of human tissue cause most
microorganisms to multiply rapidly. (viral pathogens replicate within infected cells, some
bacteria are intracellular pathogens and replicate in macrophages and other cells.
Spread: may stay localized or enter the body areas; if the immune system is compromised,
spreading is quick.
Know what defines clinical disease
Incubation: is the period from initial exposure to the onset of the first symptoms, few hours to
years.
Prodromal: the occurrence of initial symptoms are often very mild with feelings of discomfort
and tiredness.
Invasion: invasion is farther and affects other body tissues.
, Convalescence: recovery occurs and symptoms decline or the disease is fatal or has a period of
latency.
Know the classes of microorganisms
Bacteria
True bacteria: divide by binary fission, cocci, bacilli, vibrios, sprilla, most disease caused by
bacteria in this category.
Filamentous bacteria: may have branching resembling fungi, mycobacteria, TB and leprosy.
Spirochetes: flexible spiral filaments that are motile, most anerobic, syphilis, lyme disease and
relapsing fever.
Mycoplasma: lack a rigid cell wall, small and pleomorphic of all bacteria smallest and simplest,
a typical pneumonia, PID and urethritis.
Rickettsia: intracellular parasites rod shaped spherical or pleomorphic, rocky mountain spotted
fever and typhus.
Chlamydia: intracellular parasites but more complex intracellular life cycles.
Fungi,
Eukaryotic microorganisms with thick rigid cell walls and the capacity to form a variety of
complex structures (mold yeast are dimorphic) resistant to bacterial cell wall inhibitors such as
PCN and cephalosporin, antifungal drugs are also toxic to human cells because composition is
similar. Systemic infection is usually from immunosuppression. Candida albicans is the most
common fungal infection.
Parasites and Protozoan
Establish symbiosis with another species unicellular protozoal to large worms. (helminths)
malaria, amoebae. Common cause of infection worldwide. Rarely transmitted human to human
are transmitted by vectors. Survive intracellularly, coat themselves, gene switch, antigenic
variation, degrade IgG and IgA, neutralize antibodies. Tissues damage from infestation and
toxins. Malaria is the most common infection worldwide.
viruses
Basic structure is virion (nucleic acid surrounded by the capsid) classified by the nucleic acid in
the virion (RNA and DNA whether single strand or double strand) and whether it uses the
enzyme transcriptase for replication. Most common affliction of humans common cold, cold
sores, HIV and several types of cancer. Viruses are intracellular parasites. Life cycle: completely
intracellular. Attaches and binds to host cell via protein receptors, penetrates the host cell,
releases genetic information into host cytoplasm. mRNA produces viral proteins, viral dna is
imbedded in the host cell and transmitted to daughter cells by mitosis. Antigenic shift is when
recombination of genes cause a new virus from two different species. Antigenic drift is mutation
of genes that express surface molecules.
Common micrroorganisms
Influenza
Know the definition of AIDS
Relies on both lab test and clinical symptoms for diagnosis. If individual is seropositive a
diagnosis of AIDS is made in association with various clinical symptoms. Decreased T cells,
Midterm Exam
Week 1
Chapter 9: Alterations in Immunity
Hypersensitive: know the difference between allergy, autoimmunity and alloimmunity
Hypersensitive: an altered immunologic response to an antigen that results in disease
Allergy: Immunity and hypersensitivity and is the deleterious effects of hypersensitivity to
environmental agents
Autoimmunity: a disturbance in the immunologic tolerance of self-antigens; a breakdown of
tolerance during which the body’s immune system begins to recognize self as antigens as
foreign. Examples sequestered antigens, infectious diseases with molecular mimicry,
neoantigens. Genetic factor: familial association.
Alloimmunity: occurs when the immune system of one individual produces an immunologic
reaction against tissue of another. Transplant rejection and transfusion reactions.
Know the types of hypersensitivity
Type I: (immunoglobulin E (IgE); most common)- mediated reaction mediated by antigen-
specific IgE and the products of tissue mast cells. IgE binds to crystalline fragment (Fc) receptors
on the surface of mast cells; cross linking causes the release of histamine from mast cell
degranulation. (H1 and H2 receptors and increases chemotactic activity. Cytotropic antibodies
bind to the cell surface and regains are antibodies that can bind to skin. Histamine enhances the
chemotaxis of eosinophils at site of Type I reaction. Most common allergy is pollen. Short life
span and can be beneficial to the host immune reactions to parasites. Symptoms of H1 bronchial
constriction, edema and vasodilation and H2 increase gastric secretions and decreases the release
of histamine from mast cells and basophils.
Type II: (Tissue specific hypersensitivity reactions; rare) specific cell or tissue being the target of
an immune response. Begins with antibody binding to tissue specific antigens. 1st the cell can be
destroyed by antibody and activation of the complement cascade through the classical pathway.
2nd antibody may cause cell destruction through phagocytosis. 3rd antibody complement cascade
results in release of C3a and C5a causes damage to the cell, neutrophils release granules. 4th
antibody dependent cell medicated cytotoxicity. (ADCC) antibody on the target cell is
recognized on NK cells and release toxic substances that destroy target cell. 5th does not destroy
target cells but causes it to malfunction
Ex: graves disease autoantibody binds to an activates receptors for TSH
Type III: (Immune complex Mediated Hypersensitivity Reactions; rare) case by antigen-antibody
complexes that are formed in the circulation and deposited later in vessel walls or extravascular
tissues. In type III the antibody binds to soluble antigen that was released into the blood or body
fluids and the complex is deposited in the tissues. This is not organ specific and symptoms have
little to do with the particular antigenic target of the antibody. Damage results from complement
activation and neutrophil lysosomal enzymes. Immune complex disease: dynamic as variations in
the ratio of antigen to antibody. Immune complex clearance Large: macrophages, small: renal
clearance, Intermediate: Deposited in tissues; cause problems. Periods of exacerbation and
remission. There are two types of Type III.
Serum Sickness: caused by the formation of immune complexes in the blood and their
subsequent generalized deposition in target tissues (ex medication administration)
, affected blood vessels joints and kidneys. Symptoms include fever, enlarge lymph nodes,
rash and pain at sites of inflammation. (Raynaud phenomenon)
Arthus Reaction: caused by repeated local exposure to an antigen that reacts with
performed antibody and forms immune complexes in the walls of the blood vessels.
Causes increased vascular permeability and an accumulation of neutrophils, edema,
hemorrhage, clotting and tissues damage. Symptoms begin within an hour and peak 6-12
hours later.
Type IV: (Cell Mediated Hypersensitive Reactions) Caused by T lymphocytes and do not involve
antibody. These are graft rejections and allergic reactions resulting from contact with substances
such as poison ivy or TB test, some autoimmune diseases. Induration: clear hard center.
Destruction of the tissue is usually caused by direct killing by toxins from cytotoxic T (Tc) cells.
Helper T (Th) 1 and Th 17 cells produce cytokines that recruit phagocytes, especially
macrophages.
Atopic Allergies: Inheritableness of allergies, one parent there is a 40% chance and both parents
there is an 80% chance. Produce more IgE and have more Fc receptors for IgE on their mast
cells.
Know the types of primary immunity
Primary immunity (congenital): most are a result of a single gene defect
5 Types
1.) B Lymphocyte deficiencies: defects in b cell response; lower levels of
circulating immunoglobulins and increases risk of infection.
Hypogammaglobulinemia or agammaglobulinemia. Bruton
agammaglobulinemia: Most severe. Mutation in IgM. X-linked hyper-IgM
syndrome: defective class switch. Prone to pneumonia, most common is
common variable immunodeficiency.
2.) T Lymphocyte deficiencies: partial or complete absence of T-cell immunity
from partial thymus (DiGeorge Syndrome) Chronic mucocutaneous
candidiasis- primary defect of T lymphocytes in response to a specific
infectious agent; the yeast Candida albicans.
3.) Combined T & B: defects that affect development of both, most severe SCID,
reticular dysgenesis: the most severe form of SCID. Adenosine deaminase
(ADA) deficiency results in excess purine. X linked SCID is due to defect in
the interleukin IL-2 receptor. Bare lymphocyte syndrome: cannot present
antigens. Major histocompatibility complex (MHC) class I and II deficiencies
Class II is more severe. Wiskott-Alrich syndrome (WAS) IgA and IgG levels
are usually normal but the IgM level is highly depressed. Deficiencies in DNA
repair (AT)= ataxia telangiectasia mutations of the ATM gene occur.
4.) Compliment deficiencies: often resemble antibody deficiencies with recurrent
infections. C3 deficiency is the most common form. Mannose-binding lectin
(MBL) deficiency: prone to yeast infections. Properdin deficiency prone to
meningococcal infections and it is X linked. Factor I and H deficiencies
(destroy C3) C5 and C9 deficiencies: C9 is the most common and all are
prone to Neisseria infections.
, 5.) Phagocytic deficiencies: (p.288) severe congenital neutropenia (cyclic
neutropenia is a mild form; prone to bacterial infections) Leukocyte adhesion
deficency (LAD) mutations occur in the adhesion molecules. C3 receptor
deficiency: those with this deficiency are prone to skin infections. Chediak-
higashi syndrome defect is in the lysosomal system therefore killing is
ineffective. Myeloperoxidase deficiency results in chronic granulomatous
disease. multistep process that involves initial adhesion between circulating
phagocytes and the endothelial cells lining the circulation.
Rh antigen
Primarily expressed on erythrocytes. Rh-positive: Express the D antigen on the RhD protein. Rh-
negative does not express the D antigen. 15% of North American white are Rh-negative. Rh-
negative individuals can make anti-D if exposed to Rh positive erythrocytes. Hemolytic disease
of the newborn when Rh-negative mother gives birth to an Rh positive to baby. WARM
autoimmune hemolytic anemia: IgG antibodies react with erythrocytes at normal body temp.
COLD autoimmune hemolytic anemia: IgM autoantibodies react with erythrocytes in the cooler
portions of the body.
immune deficiency
impaired function of components of the immune or inflammatory response, phagocytes or
complement. Failure of mechanisms of self-defense to function in their normal capacity. Primary
or secondary.
Symptoms
If patient has repeated severe infections recurrent with only short intervals of relative health and
has multiple infections at once. 8 or more ear infections, two or more serious sinus infections,
2+ pneumonia, recurrent abscess, infect unusual sites, persistent fungal infections within 1 year,
oral antibiotics ineffective, failure to thrive, chronic diarrhea. Most commonly fungal or virual.
Therapies
Immune deficiency usually treated by replacement therapy.
Gamma Globulin therapy IV or IM, FFP, transplant bone marrow, steroids, stem cells, individual
lacks a thymus is reconstitute a thymus, gene therapy.
Chapter 10: Infection
Know the process of infection
Colonization: vectors direct, mechanical, or biological after deposition in receptive environment
for microorganisms, adhere to tissue through specific surface receptors.
Invasion: invade surrounding tissue by evading the hosts defense mechanisms.
Multiplication: warm and nutrient-filled environment of human tissue cause most
microorganisms to multiply rapidly. (viral pathogens replicate within infected cells, some
bacteria are intracellular pathogens and replicate in macrophages and other cells.
Spread: may stay localized or enter the body areas; if the immune system is compromised,
spreading is quick.
Know what defines clinical disease
Incubation: is the period from initial exposure to the onset of the first symptoms, few hours to
years.
Prodromal: the occurrence of initial symptoms are often very mild with feelings of discomfort
and tiredness.
Invasion: invasion is farther and affects other body tissues.
, Convalescence: recovery occurs and symptoms decline or the disease is fatal or has a period of
latency.
Know the classes of microorganisms
Bacteria
True bacteria: divide by binary fission, cocci, bacilli, vibrios, sprilla, most disease caused by
bacteria in this category.
Filamentous bacteria: may have branching resembling fungi, mycobacteria, TB and leprosy.
Spirochetes: flexible spiral filaments that are motile, most anerobic, syphilis, lyme disease and
relapsing fever.
Mycoplasma: lack a rigid cell wall, small and pleomorphic of all bacteria smallest and simplest,
a typical pneumonia, PID and urethritis.
Rickettsia: intracellular parasites rod shaped spherical or pleomorphic, rocky mountain spotted
fever and typhus.
Chlamydia: intracellular parasites but more complex intracellular life cycles.
Fungi,
Eukaryotic microorganisms with thick rigid cell walls and the capacity to form a variety of
complex structures (mold yeast are dimorphic) resistant to bacterial cell wall inhibitors such as
PCN and cephalosporin, antifungal drugs are also toxic to human cells because composition is
similar. Systemic infection is usually from immunosuppression. Candida albicans is the most
common fungal infection.
Parasites and Protozoan
Establish symbiosis with another species unicellular protozoal to large worms. (helminths)
malaria, amoebae. Common cause of infection worldwide. Rarely transmitted human to human
are transmitted by vectors. Survive intracellularly, coat themselves, gene switch, antigenic
variation, degrade IgG and IgA, neutralize antibodies. Tissues damage from infestation and
toxins. Malaria is the most common infection worldwide.
viruses
Basic structure is virion (nucleic acid surrounded by the capsid) classified by the nucleic acid in
the virion (RNA and DNA whether single strand or double strand) and whether it uses the
enzyme transcriptase for replication. Most common affliction of humans common cold, cold
sores, HIV and several types of cancer. Viruses are intracellular parasites. Life cycle: completely
intracellular. Attaches and binds to host cell via protein receptors, penetrates the host cell,
releases genetic information into host cytoplasm. mRNA produces viral proteins, viral dna is
imbedded in the host cell and transmitted to daughter cells by mitosis. Antigenic shift is when
recombination of genes cause a new virus from two different species. Antigenic drift is mutation
of genes that express surface molecules.
Common micrroorganisms
Influenza
Know the definition of AIDS
Relies on both lab test and clinical symptoms for diagnosis. If individual is seropositive a
diagnosis of AIDS is made in association with various clinical symptoms. Decreased T cells,
