Confined patho exam 1

Atrophy

decrease in cell size

Physiologic atrophy

thymus in childhood development, ovaries in post-menopausal women, and brain cells in aging

Pathologic Atrophy

Disuuse atrophy, malnutrition, and ischemia

Hypertrophy

increase in cell size

Physiologic hypertrophy

runner’s heart and muscular growth due to increase in demand

Pathologic hypertrophy

Chronic hemodynamic overload due to heart pumping against increased resistance (hypertension)

Hyperplasia

increased in cell number

Compensatory hyperplasia

enables cells to regenerate (liver removal leads to 70% regeneration by week 2)

Pathologic hyperplasia

Excessive hormonal stimulation and growth factors lead to thyroid enlargement by TSH, thickening of uterine endometrium due to imbalance of estrogen and progesterone, and benign prostatic hyperplasia (enlargement of prostate gland)

Dysplasia

abnormal change in cells size, shape, or organization

Where is dysplasia common?

Cervix and GI tract

Another name for Dysplasia?

Atypical hyperplasia

Metaplasia

Reversible replacement of one mature cell type with another

Physiologic metaplasia

Tissue repair and regeneration

Pathologic metaplasia

Smoking causes ciliated columnar epithelium to be replaced with stratified squamous epithelium

Hypoxic Injury

Lack of O2 to cells caused by ischemia, lack of O2 in the air, and decreased RBC production

What is the most common type of cell injury?

Hypoxic Injury

Apoptosis

Genetically programmed cell death

Physiologic Apoptosis

Fetal shaping, tissue remodeling, and aging cells

Pathologic Apoptosis

Increased apoptosis leads to neurological disorders and ischemic injury and decreased apoptosis leads to cancer

Necrosis

Violent inflammatory unregulated cell death by rapid loss of plasma membrane, excessive organelle swelling, and complete mitochondrial dysfunction

Fatty Necrosis

Destruction of fat tissue (pancreatitis)

Caseous Necrosis

Associated with TB (cheese-like)

Liquefactive

Tissue turns to liquid (seen in abscesses and brain tissue)

Coagulative

caused by ischemia or infarction of organs like heart and kidneys

Grangenous Necrosis

Due to prolonged ischemia, infarction, or necrosis; clostridium perfringens emit gas gangrene during destruction

These cells arrive early and in great numbers at site of inflammation

Neutrophils

Explain the cellular response in inflammation

WBCs adhere to inner walls of vessels and migrate through the walls into tissues

1st responder in innate immunity

Neutrophils

Arrive early and in great numbers at site of inflammation and kill pathogens by oxidative burst

Neutrophils

Released from bone marrow to circulate in blood and then migrate to tissue to mature into macrophags

Monocytes

Engulf and digest microbes to clear damaged area

Macrophages

Present antigens to T cells and release cytokines to attract other cells and initiate adaptive immunity

Dendritic Cells

Part of lymph system and found where pathogens enter the body (epithelial tissue)

Dendritic Cells

Phagocytic Cells involved in inflammation

1. Neutrophils

2. Monocytes

3. Macrophages

4. Dendritic Cells

These cells release histamine and are involved in allergic and hypersensitivity reactions

Eosinophils and basophils

Involved in pro-inflammatory response, allergic reactions, and hypersensitivity

Mast Cells

Non-phagocytic cells involved in inflammation

Eosinophils, basophils, and mast cells

5 Cardinal Signs of localized inflammation

1. Redness: vasodilation and increased blood flow

2. Heat: vasodilation and increased blood flow

3. Swelling: increased permeability and fluid leakage

4. Pain: due to edema and inflammatory mediators

   1. Loss of function: pain + edema

3 Plasma Protein Systems

1. Complement

2. Clotting

3. Kinin

Complement System

30+ proteins in blood activated by cascade system; function by O: opsonization (tagging pathogen for destruction) I: inflammation and L: lysis (MACs poke holes in membrane)

Clotting System

group of plasma proteins that when activated form a blood clot of platelets and fibrin strands; activated by substances released from tissue damage

Kinin System

stimulates the clotting system and has histamine like effects such as increased permeability, vasodilation, and stimulates nerve endings in pain

Physical barriers in 1st line of defense

Skin, mucous membranes, cilia in lungs, normal flora

Chemical Barriers in 1st line of defense

Enzymes in secretions like sweat and saliva

How is washing part of 1st line of defense?

Handwashing, urine flushes urinary tract, and saliva cleanses oral cavity

2nd line of defense?

Part of innate immunity and involves inflammation response, phagocytic and NK cells, and antimicrobial proteins

Characteristics of innate immunity

Non specific, present at birth, no memory, and immediate response

3rd line of defense?

Adaptive immunity (B Cells + antibodies in blood and T Cells in tissues)

Characteristics of adaptive immunity

Acquired, has memory, specific against pathogens and damaged tissues, and delayed response

Why does wound disruption occur?

Occurs due to ischemia, malnutrition, increased bleeding, increased fibrin deposition, diabetes, and infection

Keloid

Raised area that grows outside of original wound due to excessive collagen production during healing process

Hypertrophic scar

Raised area within original boundary of wound due to excessive collagen production during healing process

Dehiscence

wound pulls apart at suture line increasing risk for infection

Contracture

excessive wound contraction results in anatomic deformity

Evisceration

disembowelment: surgical wound opens up and tissue or organs come out

Mature into plasma cells that produce antibodies for humoral immunity

B Cells

Bone marrow derived and involved in fighting extracellular pathogens

B cells

Provide cell mediated immunity against intracellular pathogens

T Cells

T Killer Cells

bind to surface of invading cells and disrupt membrane (Cytotoxic T cells)

T Helper Cell

Stimulate B Cells to mature into plasma cells (CD4)

T regulator cells

reduce humoral response to keep balance

Antigens

glycoprotein found on cell wall of microbes, infected cells, or abnormal tissue; target of antibodies

Antibodies

bind to antigens of pathogens and agglutinate bacteria together so phagocytic cells can destroy pathogen

APCs

Antigen Presenting Cells; load antigen to present to T Cell

Examples of APCs

Dendritic Cells, macrophages and monocytes

Natural Killer Cells

targets infected/cancer cells by phospholipid apoptosis

Major Histocompatibility Complex (MHC)

on the surface of APCs and important in recognizing self vs. non-self; only T Cells whose antigen receptors fit antigen will respond to it

Name the cells of adaptive immunity

1. B Lymphocytes

2. T Lymphocytes

3. Antigens

4. Antibodies

5. APCs

6. Natural Killer Cells

7. Major Histocompatibility Complex

Active Acquired Immunity

Exposure to antigen by illness or vaccine in which immune system is activated and body has to MAKE antibodies; long-term and memory cells are produced

Passive Acquired Immunity

Premade antibodies in which there is an immediate response but no memory cells are produced (short-term); involved antibodies in breast milk and HepB immunoglobulins

Antibody Classes: gives long-term immunity and immunologic memory

G

Antibody Classes: crosses the placenta to provide passive immunity

g

Antibody Classes: clinical significance is raised after infections and measured to determine immunity status

g

Antibody Classes: prevents mucosal membranes from infection

a

Antibody Classes: passive immunity in breast milk

A

Antibody Classes: prevents attachment to epithelial cells

A

Antibody Classes: clinical significance is 1st line of defense in mucosal immunity and deficiency is common

A

Antibody Classes: 1st antibody in immune response

M

Antibody Classes: agglutinates pathogens due to large size

M

Antibody Classes: activates the complement system efffectively

M

Antibody Classes: clinical significance is raised in infection and diagnostic serology

M

Antibody Classes: involved in allergic and hypersensitivity reactions

E

Antibody Classes: release of histamine

E

Antibody Classes: clinical significance is raised in parasitic infection, asthma, allergic rhinitis, and eczema

E

Antibody Classes: B-cell receptor

Mostly D but also sometimes M

Antibody Classes: Involved in B cell maturation and activation

D

Antibody Classes: clinical significance is not well known and is very low in serum concentrations

D

B cells mature into these cells that will go on to produce antibodies to a specific antigen

Plasma cells

Multiple myeloma patients lack these cells leaving them at risk for infection

Plasma cells

Antibody Classes: dominant antibody in bodily secretions such as tears and saliva

A

This mechanism of hypersensitivity reaction is responsible for contact dermatitis caused by poison ivy

Type 4: Cytotoxic T cells and macrophages cause inflammation without antibody involvement

Receiving a vaccine so the body develops antibodies without having to become sick with the disease is an example of this type of immunity

Active Acquired

This type of hypersensitivity reaction is responsible for systemic lupus erythematosus?

Autoimmune (type 3)

This disease is a hypersensitivity reaction resulting from antibody production and immune complex deposition, leading to chronic inflammation and tissue damage in kidneys, joints, and skin

SLE

Most common primary immunodeficiencies in infants

Severe Combined Immunodeficiency (SCID)

Congenital disorder resulting from abnormal development or maturation of immune cells leading to significant defects in both cellular and humoral immunity

SCID

Hypersensitivity reaction responsible for transplant rejection of organ

Alloimmune

These reactions occur when the immune system recognizes transplanted tissue as foreign and attacks it

Alloimmune reactions