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Summary NR 507 – Week 3 Edapt Notes: Obstructive & Restrictive Lung Diseases – Pathophysiology Study Notes

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This document covers Week 3 Edapt notes for NR 507, focusing on the pathophysiology of obstructive and restrictive lung diseases. It explains disease mechanisms, functional changes in the respiratory system, and key differences between obstructive and restrictive pulmonary disorders, making it useful for exam preparation and concept review.

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NR 507 – Week 3 Edapt Notes: Obstructive &
Restrictive Lung Diseases – Pathophysiology Study
Notes


Grave's disease (hyperthyroidism) - example of altering thyroid function, but does not
destroy thyroid tissue

Incompatible blood type- example of cell/tissue damage that occurs; severe transfusion
reaction occurs and the transfused erythrocytes are destroyed by agglutination or
complement-mediated lysis.

Type 1 Hypersensitivity VS. Type 2 Hypersensitivity - Type 1 Hypersensitivity
Organ Specific
Antibody binds to the antigen on the cell surface

Type 2 Hypersensitivity
Not Organ Specific
Antibody binds to the soluble antigen outside the cell surface that was released into the
blood or body fluids, and the complex is then deposited in the 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

Hypersensitivity: Type 4 - Delayed response

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 = anaphylactic reaction
systemic response of hypotension, severe bronchoconstriction
Main treatment: epinephrine reverses the effects

Hypersensitivity: Type 2 - Type 2: Cytotoxic reaction; tissue specific (ex: thyroid tissue)

Macrophages are the primary effectors cells involved

,Can cause tissue damage or alter function


Does not involve antigen/antibody complexes like Types 1, 2 and 3

Is T-cell mediated

Differentiating Between the Rash of a Type 1 vs. Type 4 Reaction: - Type 1: Immediate
hypersensitivity reactions, termed atopic dermatitis, are usually characterized by widely
distributed lesions

Type 4: Contact dermatitis (delayed hypersensitivity) consists of lesions only at the site
of contact with the allergen

The key determinant is the timing of the rash:
-Type 1 = Immediate
-Type 4 = Delayed: Several days following contact, ex would be poison ivy

Treatment of Type 4 Rash - A non-severe case of contact dermatitis would be treated
with topical corticosteroid.

Why not epinephrine or antihistamines?
-Epinephrine is for emergent Type 1 anaphylactic reactions. Antihistamines act on the
H1 receptors. Type 4 does not involve mast cells and H1 receptors.

Antibiotics not appropriate since not an infection

Autoimmunity - Autoimmune disease can be familial, Affected family members may not
all develop the same disease, but several members may have different disorders
characterized by a variety of hypersensitivity reactions, These include autoimmune and
allergic reactions
Associations with particular autoimmune diseases have been identified for a variety of
major histocompatibility complex (MHC) alleles or non-MHC genes

Alloimmunity - General term used to describe when an individual's immune system
reacts against antigens on the tissues of other members of the same species.

Examples: Neonatal disease where the maternal immune system becomes sensitized
against antigens expressed by the fetus, Transplant rejection, Transfusion reaction

Primary Immunodeficiency - Most primary immune deficiencies are result of single gene
defects
Something is lacking with the immune system itself.

Example: B-lymphocyte deficiency - one of the most severe forms of a primary
immunodeficiency

, Secondary Immunodeficiency - Complication of some other physiological
condition/disease, Malnutrition one of most common causes worldwide. Example: Pt.
with HIV gets pneumocystis carinii

Hematology - Anemias, Involve RBCs, Most of body's iron stores come from the
recycling of iron from old RBCs

Iron Deficiency Anemia - Microcytic/Hypochromic Anemia, Caused by disorders of
hemoglobin synthesis, particularly iron deficiency, Ferritin is an important measurement
that reflects the body's total iron stores, The NP will order a ferritin level to get an idea of
the body's total iron stores, Low ferritin reflects anemia

Major Lab Marker for Anemia - Increased RBC distribution width (RDW) is one of the
earliest lab markers in developing microcytic or macrocytic anemia

Folate Deficiency - Can cause megaloblastic anemia, Alcoholics can easily get folate
deficiency

Ferritin level normal
Hgb low
Hct low

Vitamin B-12 Deficiency - Fatigue, Dyspnea, Peripheral Neuropathy in BLE (numbness
and tingling)

Risk Factors: Older adults, H-pylori infection

Affects Vitamin B-12 absorption

Hemolytic Anemia - Who is at risk?

RBCs destroyed, Mismatched blood types destroy RBCs.
Autoimmune hemolytic anemia due to autoantibodies against erythrocytes that the
immune system perceives as an antigen and then attacks it. Allergic reaction to a drug
causes drug-induced hemolytic anemia

Acute Blood Loss Anemia - Trauma victims who are losing blood, GI bleed (Acute)

Aplastic Anemia - Diagnosis made by blood tests and bone marrow biopsy.

AA is suspected if levels of circulating erythrocytes, leukocytes and platelets diminished:
-Granulocyte count less than 500/ uL
-Platelet count less than 20,000/ uL
-Absolute reticulocyte count less than or equal to 40 x 109/ L

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