Chapter 1, 4, 10 - Pathophysiology 1 Exam 1

Metaplasia

Conversion of one cell type to another

Tissues that are the most vulnerable (ones that cannot regenerate effectively)

• CNS

• Kidney

• Cardiac Tissue

• Skeletal Tissue

Menopause

Average age of 50 years old

Dyspareunia

Painful sexual intercourse

Aging does what to vaginal pH

Increases it and makes it predisposed to recurrent vaginal infection

Changes in the Skin as you age mucosa

Dermis thins, Sweat gland and receptors decline, Skin is dry and wrinkled, Hair greys and thins

Cardiovascular changes as you age

Size and number of cardiac muscle fibers decrease, Fatty tissue and collagen fibers accumulate, Reduced strength of contraction

Arteriosclerosis

Stiffness of wall of arteries

Atherosclerosis

Build up of plaque in arteries

Osteoporosis

Loss of calcium and bone mass allowing fractures of spine pelvis and limbs to be more common

Risk factors of osteoporosis

Hereditary predisposition, Decreased estrogen levels, Sedentary, Decreased intake of calcium, C, and D, Decreased intestinal calcium absorption

Risk reduction of osteoporosis

Adequate calcium and D intake, Weight-bearing exercises, Drugs and hormone therapy

Osteoarthritis

Degeneration of cartilage in joints, Associated with trauma or sports injury, Articular cartilage thins

Musculoskeletal changes with age

Skeletal muscle mass declines, Strength of muscle contractions decrease, Flexibility reduced, Stiffness, Coordination and balance reduced

Respiratory changes with age

Ventilation (expiration and inspiration) is limited, Vascular changes

Neurologic changes with age

Reduction in neurons, Lipid accumulations in neurons, Loss of myelin, Decreased response to neurotransmitters, Slower response time

Changes in vision with age

Lenses become less flexible and can yellow, resulting in cataracts

Sensation changes with age

Hearing loss, Sense of taste loss, Smell loss, Diminished thirst sensation

Gastrointestinal changes with age

Muscle weakness and fatigue, Atrophy of mucosa and glands, Constipation in older adults

The urinary system changes with age

Kidney function is reduced and weakened urinary sphincter and bladder

Disorders common in older populations

Osteoarthritis, obesity, diabetes type 2

What is the issue with having multiple disorders as you age

Large number of medications

Cause is unknown?

Idiopathic

Subsequent pathologic condition resulting from an illness

Sequela

Example of age differences

Heart rate in infants vs. elderly

The levels of prevention

Primary, secondary, tertiary

Example of secondary prevention

Screening (mammogram)

Precipitating factor

A condition that triggers an acute episode

M-phase

Mitosis + cytokinesis and is eukaryotic nuclear and cell division

What is an excessive immune response

Over or high-functioning

What is a deficient immune response

Inadequate functioning

Two categories of inappropriate immune response

Excessive immune response, Deficient immune response

Two types of excessive immune responses

Autoimmunity and hypersensitivity

What is autoimmunity

Where the immune system attacks own tissues

What is hypersensitivity

May or may not involve autoimmunity and has exaggerated immunologic responses occurring in response to an antigen or allergen

True or false: Autoimmune disorders range from organ-specific diseases to organ-nonspecific diseases

True

Examples of organ-nonspecific

System lupus erythematosus

Examples of organ-specific

Multiple sclerosis and type 1 diabetes mellitus

With autoimmunity what does an individual's immune system recognize

Its own cells as foreign and mounts an immune response that injures self tissues

What is autoimmunity also known as

The breakdown of self intolerance

Do either the polygenic or multifactorial theory explain self-tolerance of autoimmune diseases

No

What genetic factors/triggers are involved in autoimmunity

Different cytokine profiles can be associated with autoimmunity, MHC (major histocompatibility) genes (HLA), Gender

Is gender an issue where females are at a high risk of developing autoimmune diseases than males?

Yes

lupus statistic

7:1; Female:male

MHC genes (HLA)

Genetic factors associated with certain autoimmune disorders like HLA-B@& and ankylosing spondylitis, increasing the risk of autoimmune disorders.

environmental triggers for autoimmune diseases

Chronic or multiple viral or bacterial infections, environmental and/or occupational stress, especially in genetically susceptible individuals.

basic mechanism of hypersensitivity

Specific antigen-antibody reaction or specific antigen-lymphocyte interaction.

hypersensitivity first exposure

No, hypersensitivity does not occur on the first exposure.

how many types of hypersensitivity

Four types.

hypersensitivity normal immune response

Yes, it is just inappropriately triggered, excessive, or produces undesirable effects on the body.

hypersensitivity mediated by antibodies

Types I, II, and III.

hypersensitivity mediated by T cells

Type IV.

immediate hypersensitivity reaction timing

About 15-30 mins after exposure to antigen/allergen.

Type I hypersensitivity

Known as immediate hypersensitivity.

etiology of immediate hypersensitivity

Typical allergens include proteins from plant pollen, dust mites, animal dander, foods, and medications (like penicillin).

pathogenesis of type 1 hypersensitivity

IgE is the principal mediating antibody; mast cells and basophils are principal effector cells, releasing mediators causing an inflammatory response.

hypersensitivity 1 receptors

There are H1-H4 receptors, and they cause different responses.

clinical manifestations of Type 1 hypersensitivity

Mild: hives, seasonal allergic rhinitis, eczema; More problematic: throat constriction, localized edema, wheezing, tachycardia, anaphylaxis.

Type II hypersensitivity

Also known as tissue-specific IgG/IgM mediated hypersensitivity.

Type 1 hypersensitivity treatments

Antihistamines, beta-adrenergic, corticosteroids, anticholinergics, anti-IgE therapy, desensitization therapy.

pathogenesis of tissue-specific IgG-IgM-mediated hypersensitivity

IgG or IgM are the principal mediating antibodies; all reactions occur after the binding of the antibody to a specific antigen located on a cell surface.

Type II hypersensitivity timing

Often it is immediate but can occur over time.

example of Type II hypersensitivity

Transfusion reaction, hemolytic disease of the newborn, myasthenia gravis, Graves' disease and lymphocytic thyroiditis, hyperacute graft rejection.

transfusion reaction

Individual receives blood from someone with a different blood group type; recipient antibodies attach to the donor's RBC antigens.

hemolytic disease of the newborn

Mother's IgG Rh-positive antibodies cross the placental barrier and attack the fetus's RBCs; monitored with RHoGAM if Rh-negative.

myasthenia gravis

Affects the neuromuscular junction: primarily the AChR; causes muscular weakness, ptosis, diplopia.

Graves' disease and lymphocytic thyroiditis

Immune attack on the thyroid gland; antibodies attack thyroid-stimulating hormone receptors, leading to excess thyroid hormones T3 and T4.

hyperacute graft rejection

Transplanted donor tissue has an antigen to which the recipient has performed antibodies; can occur quickly with revascularization.

Type III hypersensitivity

Also known as immune complex-mediated hypersensitivity.

Is Type III hypersensitivity tissue specific

No

Mechanism of injury of Type III hypersensitivity

Activation of complement and other proinflammatory mediators in response to the antigen-antibody complex

More info on Type III hypersensitivity

Tissue injury is caused by an inflammatory reaction to the antibody-antigen complex; Complement is the mediator; Phagocytic cells get attracted to tissue and cause tissue damage

Pathogenesis of type III hypersensitivity

Involves antigens forming antigen-antibody complexes that precipitate out of the blood or body fluid and are then deposited into tissues

Type IV hypersensitivity Is a rapid or delayed response?

Delayed

• Tissue damage resulting from a delayed cellular reaction to an antigen

Type III Hypersensitivity examples

immune complex glomerulonephritis, Systemic lupus erythematosus

IVa

contact hypersensitivity

IVb

Persistent Asthma

IVc

Stevens-Johnson syndrome

IVd

Pustular psoriasis

Persistent asthma

is an example of which type IV hypersensitivity: IVb

Contact hypersensitivity

is an example of which subclass of Type IV: IVa

Stevens-Johnsons syndrome

is an example of which subclass of Type IV: IVc

Pustular psoriasis

is apart of which Type IV: IVd

most familiar subcategory of Type IV

Iva - contact hypersensitivity

two types of deficient immune responses

Primary and secondary disorders

Primary disorders

B cell disorders, T cell disorders, combined B and T, Congenital (IgA deficiency), Acquired (HIV/AIDS)

Secondary disorders

Non immune system disorders, Malnutrition, Hyperlipidemia, Defective endocrine response, Treatments that secondarily affect immune function, Chemotherapy

IgA deficiency is an example of T cell disorder

False

true or false: IgA deficiency is an example of B cell disorder

True

deficient immune responses result from

Functional decrease in one or more components of immune system

Selective IgA deficiency

Congenital, Example of B cell disorder

Etiology and pathogenesis of selective IgA Deficiency

The most common B cell primary immunodeficiency disorder, 1 in 600 (Caucasian) and 1 in 2600 (Asian), Characterized by apoptosis of B cells or failure of IgA bearing B cells to become plasma cells

Congenital primary immunodeficiency disorders examples

Selective IgA Deficiency, DiGeorge Syndrome, Severe combined immunodeficiency disorders, Wiskott-Aldrich syndrome

example of a T cell disorder

DiGeorge syndrome

Clinical manifestations of selective IgA deficiency

People may exhibit no symptoms, May be prone to respiratory, gastrointestinal and urinary tract infections, Tend to have autoantibodies (including anti-IgA-antibodies), High incidence of allergic, vascular, and endocrine autoimmune diseases

Etiology and pathogenesis of DiGeorge syndrome

Deletion of a section of chromosome 22 (22q11), Autosomal dominant developmental T cell disorder, An abnormal chromosome is usually inherited from the mother, Defective fetal development

Clinical manifestations of DiGeorge syndrome

Defective fetal organ development, Cardiac and vessel abnormalities, Susceptible to recurrent infections

Wiskott-Aldrich syndrome

X-linked immunodeficiency disorder that affects both T and B cells, Only occurs in males, Increased susceptibility to infections and malignancy, Low platelets, Bleeding, hemorrhage in the brain, Treatment: bone marrow transplant, antibody replacement therapy, and antibiotics,

congenital primary immunodeficiency disorders affect both B and T cells

SCID, Wiskott-Aldrich syndrome

Severe combined immunodeficiency disorders (SCID)

inherited (variety of genetic factors), Absence or dysfunctional T cells (T-B+) or both T and B cells (T-B-), Characterized by severe immune system dysfunction and a variety of clinical features, Untreated infants are severely ill with high rate of early mortality (< 1 year), Treatment: Stem cell transplantation