Etiology

Pathogenesis

Clinical Manifestations

Diagnosis

Incidence

sign- an objective finding (temperature, blood work results)

symptom- subjective data (nausea, headache)

It is to decrease the probability of disease before the disease occurs 

ex//: flu shot and prenatal care

direct screening and public education (to make sure you don't have a disease)

ex//: screening for an STD

restoration of optimal health during/after having a disease

ex//: hospital care and rehabilitation

What is evidence based practice?

the purposeful maintenance of a stable internal environment. 

*it is constant*

Helps put the body back into balance like a heater in a house. What a change is detected in homeostasis, effector system returns the sensed function to set point range

ex//:  when the body is too cold, body shivers to get to correct temperature. When it reaches the correct temperature, it shuts off the need to shiver. 

Previous experience

Physiologic reserve

Time

Genetics

Age

Health status

Nutrition

Sleep/wake Cycle

Psychosocial factors

Sympathetic vs. Parasympathetic. A whole body neuroendocrine response. 

Stages:

1. Alarm

2. stage of resistance

3. stage of exhaustion

Hypertrophy of the adrenal glands (overuse, dumps too many hormones into the body)

Atrophy of the thymus gland (since immune system is based out of the thymus gland, immune system decreases)

GI Ulcers

What are the functions of cortisol in the General Adaption Syndrome and the effects it may have on the body?

Stays ready for whatever stressor the body may encounter. In the exhaustion stage, cortisol increases in the body and makes new formation of glucose, stimulates breakdown of stored energy, reduces inflammation and immune functions, reduces WBC accumulation at sites of injury/infection, and stimulates gastric acid secretion

*stress triad*

Altered physiological function (cardiovascular, GI)

altered psychological factors (depression, accidents, drugs)

1. Free radical injury

2. hypoxic cell injury

3. physical cell injury

4. Radiation injury

5. Chemical injury

6. Biologic Agent cell injury

7. Nutritional imbalances cell injury

Occurs when a chemical species with one or more unpaired electrons are in the outer orbit which react since they are unstable. When they react with cellular membranes and nucleic acids it causes cell damage 

A lack of oxygen which effects aerobic metabolism and ATP generation. It makes the cell run on anaerobic respiration which causes a decrease in pH, decrease in ATP production, inhibition of Na/K pump, and cellular edema

Is reversible with the return of oxygen

(x-rays) directly injures/kills cells by breaking cell bonds

*energy above visible UV light*

*energy below visible light*

affects cells by causing rotation and vibration of molecules (UV light - sun)

(viruses and bacteria)

They are able to replicate self and change cells

excess: causes obesity, too much vitamins and minerals and no where to store them. 

deficiencies: starvation- leads to lack in essential nutrition (fats and proteins) making body not be able to run properly.

Hypoxic (lack of oxygen) --> decreased pH --> reduced ATP production --> inhibition Na-K pump-->

edema in cells

ATP maintains your K and Na pump. If you don't produce enough ATP, pump doe not work so cellular edema occurs. Ca also influxes into the cell and this is a death sentence. 

Because viruses or bacteria replicate and change the DNA within own cells.

*gram (-) is worse because it puts out toxins*

An increase in cell size and functional capacity.

Can be caused by increased work load, pathologic reasons (adaptive hypertension in the heart/ compensatory in organs)

An increase in the number of cells in an organ or tissue (only in mitotic division)

Causes: pregnancy (hormonal) or regeneration of liver (compensatory)

Deranged cell growth of tissue that results in cell size, shape, and appearance.

*ABNORMAL* PRECANCEROUS*

Cellular Edema (Na-K pump), and intracellular accumulations (normal cellular consitutants errors in metabolism), accumulation of pigments.

endogenous examples: melanin, jaundice

exogenous: coal dust 

cells die but catalytic enzymes not destroyed enzymes are not broken down (looks like mush)

ex//: stroke; what it does to the brain

Development of acidosis and subsequent denaturing of the cells enzymatic and structural proteins. 

ex//: necrosis of myocardium, cant function- heart- MI

death of adipose tissue from trauma and release of destruction enzymes

ex//: pancreas 

associated with TB lesions. Immune mechanisms wall of dead cells/ middle becomes white/soft/fragile

ex//: TB lesions

Coagulation necrosis in extremities due to decreased blood flow. Skin wrinkles, shrinks, and turns black.

ARTERIAL PROBLEM

Liquefaction necrosis due to interference of venous blood return. Area turns cold, swollen, black, fowl odor. Occurs in extremities and internal organs. 

ex//: VENOUS PROBLEM

Shrinkage of cell and wrinkling of cell membrane. The cell death makes room for new cells to grow. Cell suicide eliminates worn out cells.

PATHOLOGIC (for disease) PHYSIOLOGIC (for normal body function)

Regeneration

Repair

Intention

Inflammatory Phase

Proliferative Phase

Remodeling Phase

Time of injury

Preparation for healing

Blood clotting

clean debris

growth of blood vessels

Occurs 2-3 days after initial injury

Fibroblasts make collagen 

3 weeks after initial injury

Continues collagen synthesis and increases strength of wound 

High protein diet for wound healing

nutrition

oxygenation

immune response

infection

age helps with nitrogen levels

Separation of wound edges after suturing (about 5-12 days after closing) 

Obese patients are more at risk

New Growth. 

Abnormality of cellular growth

Men: Prostage

Women: Breast

Men/Women Mortality: Lung/Bronchus

G0- A resting phase where the cell has left the cycle and stopped dividing

G1- Cells increase in size. Ensures everything is ready for DNA synthesis

S- DNA replication

G2- Gap btw DNA synthesis and mitosis, cell grows. Ensures everything ready to enter M

M- Growth stops. Energy focused on division of 2 daughter cells. Middle of mitosis ensures cell ready to complete cell division

• Slow division - most time spent in G0
• Specific shape for an organ/tissue
• Cytoplasm > nucleus
• Performs specific differentiated function
• Tightly adherent : DOESN'T MIGRATE
• Contact inhibition: WON'T divide if something is next to them
• Growth is orderly and well regulated

• Rapid division- no time in G0
• Anaplastic morphology- cant identify type or shape of cell
• Nucleus > Cytoplasm
• Lose some or all differentiated functions
• loosely adherent: ability to migrate
• Loss of contact inhibition: outgrows boundaries(invasion)
• Poorly regulated growth- cells wont die to make room for new ones. IMMORTALITY 

Normal cells in the wrong place at the wrong time at the wrong rate. Show continuous growth. Maintain morphology and differentiation. They are nonmigratory and adhere tightly. They have orderly growth

*wont harm the body. Just need to be removed

Initiation

Promotion

Progression

(the on-switch)

Code for components of the cellular growth activating pathways. When activated, they become oncogene and promotes cancer 

There are 2 major genes involved in suppressing cancer. 

Rb gene and P53

Off switch

Inhibit cellular proliferation. Cancers arise when function is lost

A mutation; an irreversible event. Must occur in cell that is able to divide. Requires a promoter (carcinogen) 

Hyperactivity vs. Inactivity

Chemical carcinogens

Physical

Viral

Dietary

Pharmaceutical

Some retroviruses are carcinogenic. Microbes invade self cells, insert own genetic material into human DNA and mutation actives oncogene. Occurs with both DNA and RNA. 

ex//: Hep B/C, Herpes II, Epsien- Bar

Diethylstilbestrol- increased cervical risk in children in womb

Estrogen- endometrial and breast

Environmental factors that play a part in cancer.

80% of cancers in USA result from extrinsic carcinogens

Internal factors

Immunocompetence, age and genetics

To grade the levels of differentiation and number of mitoses. 

Staging classifies tumors according to clinical spread of the disease

Tumor original, if metastases, will most likely spread to a specific area depending on the type of cancer

ex//: Prostate cancer will most likely metastasize in the bone

Grading: how differentiated a cell is (want it to be differentiated) 

Staging: metastasis is bad, worst! If progresses, migrates to distant area. 

T= primary tumor

N= regional lymph nodes

M= distant metastasis

Substances produced by the tumor or released by normal cells in response to the presence of a tumor. 

Can be caused by normal cells that were over exposed to carcinogens or cells developed in fetal development that reappear later as cancer

C- changes in BM or bladder

A- a sore that won't heal

U- unusual bleeding

T- thickening or lump

I- indigestion/ difficulty swallowing

O- obvious change in wart or mole

N- nagging cough

To neutralize, eliminate or destroy microbes that invade the body.

TO recognize and eliminate cancer cells

The immune system only responds against non self cells, therefore not attacking healthy self cells.

*self tolerance: ability to recognize self vs non self cells

Inflammation

antibody-mediated immunity (humoral)

cell-mediated immunity

Skin and mucous membranes

mononuclear phagocyte system

lymphoid system

bone marrow

Part of the Lymphoid group

Major cells of antibodies (mediated immunity). ability to produce antibodies, and require help from helper T cells to respond to infection/disease

Part of Lymphoid group

Major cells of cell-mediated immunity

Helper-T cells interact with antigens and secrete cytokines that stimulate B-cell proliferation and antibody production

Part of Lymphoid group

(Natural Killer cells) Look for cells that don't belong in the body. Innate  immune cells. Can kill tumor cells and virally infected cells with out previous exposure.

(Natural/ nonspecific immunity)

Red Blood Cells

Monocytes

Granulocytes

Part of Myeloid group

They are immature macrophages. 5% of total WBC count. They circulate in the blood stream for 3 days prior to entering tissue and maturing

Part of Myeloid group

Also known as neutraphils. 

First responders to infection. No energy reserve (6 hour lifespan). Only mature cells are capable of phagocytosis. Produce potent chemical mediators that enable non self cells to destroy microbes. 

20 plasma proteins that interact in a cascade fashion to produce important mediators or inflammation and immunity is activated by microbial agents or by antigen/antibody complexes. 

System, clotting

one activates one thing which activates another- everything is connected in the immune system and is important in inflammation and immunity 

Increase in vascular permeability

Recruitment/emigration of leukeocytes

Phagocytosis of antigens and debris

Innate (natural) immunity

cellular and biochemical defenses that are in place before encounter with infectious agent. 

Epithelial cells (blocks entry)

Phagocytic neutraphils/macrophages (digest microbes)

NK cells (kill intracellular microbes/ foreign agents)

Complement system (amplifies the inflammatory response)

IgG (most common)- activates complement + crosses placenta

IgM0 activates complement + responsible for ABO incompatability

IgA - Secretory antibody found in mucous, saliva, tears, and b. milk

IgD - stimulates the B cells to multiply and mature

IgE -helps clear parasites and prevent respiratory infections ; mediates many of the hypersensitivity reactions

B cells - bone marrow and lymph tissue

T cells- in thymus

Major Histocompatibility Complex. 

Cluster of genes on chromosome 6 (also known as human leukocyte antigen HLA)

Proteins by these genes re displayed on the surface of body cells and mark them as self cells (bar scanner) 

T-Cells

They recognize foreign antigens displayed on the surface of cells through specialized receptors called T cell receptors

They stimulate and organize response of total immune system

HELPER T CELLS- activation results in secretion of CYTOKINS necessary for colonal expansion of B and T lymphocytes

CYOTOXIC T CELLS- locate and kill abnormal cells through actions of perforins (toxin to kill bad cells)

B CELLS

MEMORY B CELLS- contain antigen receptors and function in manner similar to memory T. When exposed to same antigen, memory cells respond more rapidly

PLASMA CELLS- Short lived antibody producing factories. Have receptors on their surfaces to bind to antigens. Each B cell binds only on particular antigen. Long lasting immunity is possible

Antibodies are proteins that bind to a specific antigen.

Antibodies precipitate

agglutination (antibodis binds to antigen forming large insoluable comples that precipitates out body fluids)

neutralizes (neutralizes toxin before reaches cells Opsonization (detecting antigen easily), complement activation

Innate: defenses in place before encounter with antigen. Provides rapid protection against infection. Able to distinguish btw self and non self but not specific agents

Adaptive: acquired through exposure of antigens. Not only able to distinguish btw self and non self but to recognize and destroy specific foreign agents based on their distinct antigenic properties

Active: from having disease

Passive: temporary type that is transferred from another source (in utero from mother to infant)

Normal immune response that is inappropriately triggered or excessive or produces undesirable effects on the body

Four types I-IV

Problem with B and/or T cells. 

No immune system (lack of B and T), severe infections, cant live ouside of sterile environment

Aids- no T cells, immune response never called on

Leukemia

a deficient immune response

I,II,III: mediated by antibodies produced by B cells

IV: mediated by T Cells

Atopic (local) or Anaphylactic (systemic)

IgE hypersensitivity (strong genetic linkage)

Sign and symptoms of allergic reaction after contact with antigen

IgE and mast cells for complex and on subsequent exposure to allergen, mast cell is degranulated

The release of mediators cause an inflammatory response

It is tissue specific - cytotoxic

Antibody mediated by IgG or IgM

Antibodies are formed against antigens on cell surface usually resulting in lysis of target cells. 

may be activated by complement or by Phagocytic cells that are attracted to target cells by attached antibodies (ex//: transfusion reactions, graft vs host)

Antigen antibodies complexes are deposited in tissues and result in the activation of complement and inlammation/destruction

Persistent low grade infections, inhalation of antigens into alveoli, and autoimmune production of antibodies may result in chronic production of antigen-antibody complexes

ex//: glomerulonephritis and SLE

Delayed hypersensitivity, cell mediated, does not require antibody production.

Sensitized T cells react with altered/foreign cells and initiate inflammation. Slow onset 24 hours post exposure

ex//: contact dermatitis, tuberculin rxn

Primary Immunodeficiencies congenital disorder

Affects 1 in 400 people

Failure of IgA bearing lympocytes to become plasma cells

Constant respiratory, GI, and GU infections

Prevent infections/ treat with antibiotics

Primary Immunodeficiencies Cogenital Disease

Have immature B cells and unable to produce antibodies

No apparent problems until 4-5 months of age due to passive maternal IgG protection

A Primary Immunodeficiencies Congenital Disease

Developmental T cell disorder with total or partial loss of the thymus gland function

associated with other congenital problems such as cardiac

B cell levels are normal; may have abnormal antibody response due to decreased T cells

No immune system - lack of B and T cells

characterized by severe infections and or neoplasms

cant live out of steril environment

treatment: bone marrow transplant or gene therapy

Human Immunodeficiency Virus

Defective cell mediated immunity and a decrease in CD4+ cells or helper T cells

caused by retrovirus: has only RNA as genetic material