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Hypersensitivity Reactions, Autoimmunity, and Hematology: A Comprehensive Overview, Exams of Nursing

A comprehensive overview of hypersensitivity reactions, autoimmunity, and hematology, covering key concepts, examples, and clinical implications. It delves into the different types of hypersensitivity reactions, their mechanisms, and associated diseases. The document also explores autoimmunity, alloimmunity, and primary and secondary immunodeficiency. In the hematology section, it focuses on anemia, discussing various types, causes, and diagnostic markers. The document concludes with an overview of cardiac blood flow, stroke volume, cardiac output, and heart failure.

Typology: Exams

2024/2025

Available from 03/03/2025

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NR 507 ACTUAL MIDTERM EXAM NEWEST
TESTBANK WITH 200 QUESTIONS AND
VERIFIED ANSWERS ASSURED SUCCESS
Hypersensitivity Type 1
Type 1: Allergic Reaction
Mediated by IgE
Inflammation due to mast cell degranulation
local symptoms: Itching, rash
Systemic symptoms: wheezing
Most dangerous form: anaphylactic reaction-systemic hypotension, severe bronchoconstriction
Main treatment: epinephrine
Hypersensitivity Type 2
Type 2: Cytotoxic, tissue-specific (thyroid tissue)
Primary effector cells: Macrophages
Can cause tissue damage or alter the function
Example: Graves disease (alters thyroid function but does not alter tissue)
Example: Incompatible blood type (cell/tissue damage)- Severe transfusion reaction occurs and the
transfused erythrocytes are destroyed by agglutination or complement-mediated lysis
Hypersensitivity Type 2 and 3 difference
Type 2: Organ-specific, the antibody binds to an antigen on the cell surface
Type 3: Not organ-specific, the antibody binds to soluble antigen outside the cell surface that was
released into the blood or body fluids and then the complex is distributed into tissues
Hypersensitivity Type 3 Examples
Rheumatoid Arthritis: antigen/antibodies are deposited in the joints
Systemic Lupus Erythematosus (SLE)- very closely related to autoimmunity-antigen/antibodies deposit in
organs that cause tissue damage
Scope of damage of SLE- Type 3 Hypersensitivity- autoimmune response
rash confined to cheeks (malar rash)
discoid rash (raised, patchy, scaly)
photosensitivity
oral/nasopharyngeal ulcers
hematologic disorders
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NR 507 ACTUAL MIDTERM EXAM NEWEST

TESTBANK WITH 200 QUESTIONS AND

VERIFIED ANSWERS ASSURED SUCCESS

Hypersensitivity Type 1 Type 1: Allergic Reaction Mediated by IgE Inflammation due to mast cell degranulation local symptoms: Itching, rash Systemic symptoms: wheezing Most dangerous form: anaphylactic reaction-systemic hypotension, severe bronchoconstriction Main treatment: epinephrine Hypersensitivity Type 2 Type 2: Cytotoxic, tissue-specific (thyroid tissue) Primary effector cells: Macrophages Can cause tissue damage or alter the function Example: Graves disease (alters thyroid function but does not alter tissue) Example: Incompatible blood type (cell/tissue damage)- Severe transfusion reaction occurs and the transfused erythrocytes are destroyed by agglutination or complement-mediated lysis Hypersensitivity Type 2 and 3 difference Type 2: Organ-specific, the antibody binds to an antigen on the cell surface Type 3: Not organ-specific, the antibody binds to soluble antigen outside the cell surface that was released into the blood or body fluids and then the complex is distributed into tissues Hypersensitivity Type 3 Examples Rheumatoid Arthritis: antigen/antibodies are deposited in the joints Systemic Lupus Erythematosus (SLE)- very closely related to autoimmunity-antigen/antibodies deposit in organs that cause tissue damage Scope of damage of SLE- Type 3 Hypersensitivity- autoimmune response rash confined to cheeks (malar rash) discoid rash (raised, patchy, scaly) photosensitivity oral/nasopharyngeal ulcers hematologic disorders

immunologic disorders non-erosive arthritis serositis renal disorder (proteinuria) neurologic disorders (seizures) antinuclear antibody (ANA) Autoimmunity Familial Affected family members may not have same dz, but several members may have other disorders characterized by a variety of hypersensitivity reactions that include autoimmune or allergic reactions Associations with particular autoimmune diseases have been identified for a variety of major histocompatibility complex (MHC) alleles or non-MHC genes Alloimmunity When an individual's immune system reacts against antigens on the tissues of other members of the same species Examples: neonatal dz where the maternal immune system becomes sensitized against antigens expressed by the fetus, transplant rejection, transfusion reaction Hypersensitivity Type 4 delayed response does not involve antigen/antibody complexes like Type 1 T-cell mediated Relationship between Type 2 and type 4 Hypersensisivity Organ rejection involves cytotoxicity (type 2) T-cells play a major role in organ rejection (Type 4- T-cell mediated) Antigens from target cells stimulate T-cells to differentiate into cytotoxic (type 2) T-cells These T-cells have direct cytotoxic activity along with help T-cells involved in delayed hypersensitivity (type 4) Difference between Type 1 and Type 4 Rash Type 1: Immediate hypersensitivity reactions, termed atopic dermatitis are characterized by widely distributed lesions Type 4: contact dermatitis (delayed hypersensitivity) consists of lesions only at the site of contact with the allergen Key determinant is timing of rash: Type 1- immediate Type 4: delayed-several days following contact (poison ivy) Treatment of Type 4 Hypersensitivity Rash

Serum Ferritin: N/I RBC: I Serum Iron: N/I Total iron-binding capacity: N Transferrin: N/I Mean Corpuscular Hemoglobin Concentration (MCHC) Measure of the average concentration inside a single RBC Examples of Anemias with normal MCHC Aplastic anemia Post-hemorrhagic anemia hemolytic anemia Examples of Anemias with low MCHC Iron deficiency anemia Siderblastic anemia Thalassemia Examples of Anemias with high MCHC Hereditary Spherocytosis- a result of mild cellular dehydration, MVC is low bc of membrane loss and cell Dehydration Liver disease Hyperthyroidism Sickle Cell Iron Deficiency anemia Is a microcytic/hypochromic anemia Caused by disorders of hemoglobin synthesis, particularly iron deficiency Ferritin is an important measure that reflects the body's total iron stores The NP will order ferritin level to get an idea of body's iron stores Low ferritin reflects anemia, but does not tell you what type Major Lab Markers for Anemia Increased RBC distribution width (RDW) is one of the earliest lab markers in developing microcytic and macrocytic anemia Folate Deficiency Can cause megaloblastic anemia Alcoholics can easily get folate deficiency Vitamin B-12 Deficiency Fatigue Dyspnea

***Peripheral neuropathy in BLE Risk factors: older adults, H-pylori infection, affects Vitamin B-12 absorption Hemolytic Anemia Who is at risk? RBCs are destroyed Mismatched blood types- destroy RBCs (cytotoxic type 2) Autoimmune hemolytic anemia due to autoantibodies against erythrocytes that the immune system perceives as an antigen and then attacks it Allergic Reaction to drug causes drug induced hemolytic anemia Acute Blood Loss Trauma victims who are losing blood Aplastic Anemia Dx is made by blood test and bone marrow biopsy AA is suspected if levels of circulating erythrocytes, leukocytes, and platelets are diminished A granulocyte count less that 500/uL A platelet count less than 20,000/uL Absolute reticulocyte count less than or equal to 40 x 109/L Sickle Cell Anemia Sickle cell trait Inherited a normal Hb gene from one parent and an abnormal Hb gene from the other parent Thalassemia Inherited blood disorder that causes decreased circulating hemoglobin Many genetic mutations Cardiac blood flow Inferior/ superior vena cava, right atrium, right ventricle, pulmonary artery to lungs, back through pulmonary veins, left atrium, right ventricle, aorta, systemic circulation Stroke Volume, Cardiac Output, Heart Sounds Cardiac output: the volume of blood pumped from each ventricle per minute CO = SV x HR Preload Diastolic filling with venous blood (stretching) Contractility Systolic ejection Afterload Resistance to systolic ejection (pressure) HTN, Vascular Stenosis reduces afterload Situations that impact hearts effectiveness

Sustained, laterally displaced apical pulse Mid-systolic crescendo-decrescendo murmur heart loudest at the base and radiating to the neck S4 gallop present Aortic Regurgitation SOB that progressively worsens High pitched early diastolic murmur heard loudest at the left lower sternal border Diastolic rumbling sound at the hearts apex Systolic crescendo-decrescendo murmur heard at the left upper sternal border CXR pulmonary edema and cardiomegaly Mitral Stenosis As mitral stenosis progresses, symptoms of decreased cardiac output occur, especially during exertion SOB with activity Pounding, racing heart Associated with history of rheumatic heart dz a low-pitched murmur heard best at the hearts apex JVD and bilateral crackles in the lungs an ECG- afib and ventricular hypertrophy Mitral Regurgitation SOB JVD Crackles in bases Blowing pansystolic murmur heard best at the hearts apex and radiates to the back and axilla Obstructive Pulmonary Disease Decreased FEV1 indicates airway obstruction along with a low FEVV1/FVC ratio 56% Restrictive Pulmonary Disease FEV1/FVC ratio above 70% Asthma Airways are constricted Intrinsic: triggered by something internal such as anxiety Extrinsic: Triggered by something in outside/environmental- pet dander, mites ***in the mildest form of asthma (intermittent), short-acting beta 2 agonist inhalers are used ***Mild-persistent asthma will have night symptoms 3-4 days a month COPD Dx based on symptoms, physical examination, chest imaging, pulmonary function tests and blood gas analyses. Pulmonary function testing reveals airway obstruction (decreased FEV1) that is progressive and unresponsive to bronchodilators

Emphysema Chronic Bronchitis COPD Staging GOLD 1: Mild- FEV1 greater/equal to 80% GOLD 2: Moderate- FEV1 greater/equal to 50%, but less than 80% GOLD 3: Severe- FEV1 greater/equal to 30%, but less than 50% GOLD 4: Very severe- FEV less than 30% Emphysema The damage occurs in alveoli Impairs gas exchange Issue is in expiration- can breathe air in but cant get it out Air trapping Pursed lip breathing Increased A&P diameter Barrel chest Xray- Lateral view, flattened diaphragm, increased AP diameter Chronic Bronchitis Productive cough with copious amounts of sputum Dyspnea Wheezing Rhonchi cyanosis of skin and mucus membranes Damage occurs in the airway- not alveoli