NURM-102 - Infection and Inflammation Exam Review

Incubation

Time from exposure to first symptoms when pathogens multiply

Prodromal

Feeling not good but being unsure
Developing specific signs and symptoms

Convalescence

Start to feel better

Older adult considerations

• Less coughing —> Secretion stasis

• UTI due to immobility or incontinence

• Skin is less elastic and takes longer to heal

General Immunity

Natural immunity, inflammation response

• Present at birth

Specific immunity

Acquired immunity, either through antibody-mediated or cell-mediated

Inflammatory response phases

1. Vascular changes

2. Cellular changes

3. Tissue repairs

Vascular changes

• Vasoconstriction —> Increased capillary permeability —> Vasodilation

• Hyperemia - Excess fluid seeps out of vessels —> Swelling

Cellular changes

• Clotting cascade —> Fibrin production = Mesh-like network keeping swelling localized

• Neutrophils and monocytes eat and leave crumbs (exudate)

Healing by PRIMARY intention

Well-approximated edges with minimal tissue loss

Healing by SECONDARY intention

Deep wound healing from bottom up

• Wound heals by contraction

Phases of wound healing

1. Hemostasis

2. Inflammatory

3. Proliferation

4. Maturation

Hemostasis

Vasodilation —> Stop bleeding

Inflammatory phase

Fibroblasts release collagen and growth factor to clean out wound bed

Proliferation phase of WOUND HEALING

Clean wound —> Granulation tissue (pink)

• Continued collagen production to heal

Maturation

Granulation tissue reaches surface + collagen —> Scar tissue

How does MACERATION affect wound healing?

Excess moisture softens skin layers and separates them

Important nutrients for wound healing

• Protein

• Vitamins A and C

• Zinc

Natural Passive Immunity

Antibodies from mother/breastmilk

Artificial passive immunity

Antibodies from another person, eventually destroyed because they’re not our own

Natural Active Immunity

Antibodies developed after surviving a specific microorganism

Artificial Active Immunity

Immunizations with small amounts of attenuated/dead microorganisms or portions of their antigen protein

Phases of specific immunity

1. Recognition

2. Proliferation

3. Response

4. Effector

Recognition phase

Lymphocytes patrol looking for microorganisms and alert lymph nodes when they spot something

Proliferation phase of SPECIFIC IMMUNITY

• Circulating lymphocytes with antigens go back to lymph nodes

• Antigens stimulate dormant T and B cells

Response phase

• B-cells make antibodies for antigens

• T-cells kill non-self cells

Antibody-mediated immunity

Brought on by B cells

• Lock and key antigen/antibody response

• Liver produces complement protein that causes cell lysis

Cellular-mediated immunity

Brought on by T-cells

• T cell recognizes antigen as foreign and stimulates other killer T cells to end non-self cells

Local signs of infection

Redness, swelling, pain and tenderness

Normal WBC count

5,000-10,000

Neutrophils

Increase in pus infection

Basophils

Increases in parasitic infection

Eosinophils

Increases in allergic reactions

Lymphocytes

Increases in bacterial and viral infections

Monocytes

Increases in severe infections