Physiology Exam 3

recognition of what is self and what is not self. Defense against foreign invaders

Immunity

1. Cells and organs
2. Cytokines
3. Complement
4. Antibodies

Components of the immune system

white blood cells

Leukocytes

neutrophils, basophils, eosinophils

Polymorphonuclear granulocytes (innate immunity)

B cells, T cells, NK cells

Lymphocytes (adaptive immunity)

Produced in bone marrow
Phagocyte
Releases chemicals involved in inflammation

Neutrophil

Produced in bone marrow
Release factors involved in inflammation

Basophil

Produced in bone marrow
Destroy multicellular parasites
Participate in immediate hypersensitivity reactions

Eosinophil

NK, B, and T cells
NK and B mature in bone marrow
T cells mature in thymus
Serve as essential recognition cells in specific/adaptive immune responses

Lymphocyte

Produced in bone marrow
In tissues, differentiates into macrophages
Phagocyte

Monocyte

derivatives of B cells, make antibody

Plasma cells

derivatives of monotyes, in tissues, phagocyte

Macrophages

antigen presenting cell (APC), present antigen to T cells

Dendritic cells

found in connective tissues- skin granulocytes, important in wound healing + inflammatory response

Mast cells

proteins capable of killing bacteria and viruses

Complement proteins

Messengers of the immune system, chemicals released by immune cells

Cytokines

Too few WBCs (AIDS)

Leukopenia

Too many WBCs (infection)

Leukocytosis

Bacterial infection

High neutrophils

Viral infection

High lymphocytes

Proteins released by immune cells to perform a specific function
Allow immune cells to communicate with each other

Cytokines

General defense. Attack invader based on general properties.
Involves phagocytes + complement
Cells recognize lipids or carbs on invader cell

Innate responses

Body produces antibodies to specific antigen.
Involves lymphocytes
Cells and antibodies recognize proteins on invader cell

Adaptive responses

Hyperemia, chemotaxis, diapedesis, colony, phagocytosis, complement, attack complex, tissue repair

Steps of inflammation

Mast cells (tissue basophils) and damaged tissue cells release histamine (vasodilator) and other factors
Increased capillary permeability: fluid and plasma proteins leak into tissue
Area becomes red, swollen, warm

Hyperemia

Injured tissues release chemicals that draw phagocytes to area.
Macrophages become more active, Collectively these form "pus"

Chemotaxis

neutrophils and phagocytes squeeze through endothelial cells to reach site of infection

Diapedesis

Stimulating factors released by damaged endothelial cells and macrophages to produce more WBCs

Colony

Substances called opsonins bind to proteins on microbe and adheres phagocyte to microbe
Engulfs by endocytosis

Phagocytosis

Plasma proteins circulating in blood, activated by carbs on microbial membranes; undergo cascade reactions to become activated (30 proteins)

Complement

MAC, forms pores in microbial membrane
Some cause vasodilation, inc. vessel permeability to protein, and chemotaxis
C3b: complement proteins that acts as an opsonin (bind to antigens and mark them)

Attack complex

Fibroblasts divide and secrete collagen, angiogenesis occurs
May be imperfect->scarring

Tissue repair

Antiviral cytokines
Cell is infected by virus->secretes IFN

Interferons (IFNs)

Developing lymphocytes insert 1 type of receptor that will bind to a specific antigen into plasma membrane. Progeny called clones

Adaptive immune response stage 1

Binding of antigen causes lymphocyte activation/proliferation. Clonal expansion. Some carry out attack, some become memory cells.

Adaptive immune response stage 2

Effector lymphocytes carry out attack. Extra lymphocytes after attack is carried out die of apoptosis.

Adaptive immune response stage 3

Produce lymphocyte precursors/early stages
Bone marrow and thymus

1st degree lymphoid tissues

Where immune cells and antigens meet. Where antigens activate the receptors on the lymphocytes.
Lymph nodes, spleen, tonsils

2nd degree lymphoid tissues

Occur in clusters throughout body
Channels (macrophages) and nodules (lymphocytes, antigens)

Lymph nodes

Like lymph nodes, but for circulating blood. large collections of lymphocytes, macrophages, and dendritic cells.

Spleen

In pharynx. Filled with lymphocytes, macrophages, and dendritic cells -> crypts open to pharynx.

Tonsils and adenoids

Cancer of lymph nodes

Lymphoma

When activated, differentiate into plasma cells -> secrete antibodies- travel all over body, bind to specific antigens and guide attack, act as opsonins

B cells

A protein that acts against a specific antigen, mediated responses: humoral responses

Antibody

General term for lymphocytes that are responsible for immunological memory and protective immunity, some plasma cells differentiate into memory cells

Memory cells

attack cells -> bk activated, enter blood, seek out targets

CD8+ T cells

helper cells, activated, secrete cytokines that help B and CD8 cells function (neither cells can function without CD4)

CD4+ T cells

B cell receptors

Immunoglobulins

Provide specific responses for bacteria

IgG and IgM

participate in allergic responses

IgE

in gastrointestinal, respiratory, and genitourinary tracts. Act locally. Antibodies in milk.

IgA

functions unclear.

IgD

Does not recognize "free" antigen. Must be "presented" by proteins on other cells

TCR

found on surface of all of body's cells, except RBCs.
TCR of CD8+ T cells binds to MHC class I

MHC class I

only present on antigen presenting cells (APCs)
TCR of CD4+ T cells binds to MHC class II

MHC class II

macrophages, B cells, and dendritic cells

APCs

Created in: 2nd lymphoid organs after cells meet antigen
B cells live in body for decades
T cells live 8-15 years
Allows faster response, basis for vaccines

Memory B and T cells

Bind to opsonized (by Abs) viruses and cancer cells via Fc receptor
Can recognize virally infected cells
Forms an immune synapse

NK cells

Released by NK cell, pokes holes in target cell membrane

Perforin

Derived through the holes that kill the target cell.

Granzymes

infects and kills CD4+ T cells
Causes AIDS

HIV

CD4+ T cells bind to the HIV virus via:CD4+ protein itself and a coreceptor
HIV kills CD4+ T cells and causes apoptosis of uninfected CD4+ T cells, no effective cure
No CD4+ T cells: B cells and CD8+ T cells can not function -> patient dies from infections + cancer

AIDS

rapidly replicating virus kills large numbers of CD4+T cells but they are replaced and numbers remain constant. No symptoms.

1-5 years HIV

Balance is lost, # of CD4+ T cells goes down. Remain asymptomatic until T cell numbers get very low

Next 5 years HIV

Immune response causes inflammation and damage to body itself.
Antigens that cause allergy: Allergens (ragweed, pollen, poison ivy)

Allergy (hypersensitivity)

Themselves are harmless, inappropriate immune response causes damage

Allergens

No antibodies involved
Pronounced secretion of cytokines by helper T cells activated by antigen
Cytokines act as: Inflammatory mediators, takes several days to develop
ex. Tuberculosis skin test

delayed hypersensitivity

Initial exposure leads to: IgE synthesis, some memory cells
Re-exposure: antigen elicits a more powerful antibody response

immediate hypersensitivity

Composed of: Small quantities of living or dead microbes
Memory cells are produced after exposure to antigen—creates rapid, effective response to future infection.

Vaccines

a substance that is combined with the antigen (killed or inactivated virus or microbe) to enhance immune response against it

Adjuvant

Body's own proteins act as antigens and immune system attacks them

Autoimmune disease

Cardiac Muscle

Intercalated discs, desmosomes, gap junctions, arranged in layers and surround hollow cavities, squeezing

Sympathetic innervation of heart

throughout heart, release primarily norepinephrine

Parasympathetic innervation of heart

mainly in atria, release ACh

Blood supply to heart

Coronary arteries—supply myocardium with nutrients

Conducting cells

in contact with cardiac muscle cells via gap junctions, these cells initiate the heartbeat and spread the AP through the heart

Parasympathetic heart rate

Slows rate
R vagus nerve -> SA node: slows firing
L vagus nerve -> AV node
Act to lengthen time to threshold

Sympathetic heart rate

Speeds rate
Branches of thoracic spinal nerves go to SA & AV nodes & to ventricles

Systole

ventricular contraction and blood ejection

Diastole

ventricular relaxation and blood filling

Isovolumetric ventricular contraction

AV valves, aortic and pulmonary valves are closed. Tension is building in the ventricles

Ventricular ejection

blood flows out of ventricle, pulmonary and aortic valves open

Stroke volume

Volume of blood ejected

Isovolumentric ventricular relaxation

all valves are closed, ventricle is relaxing. Atria are filling. Pressure builds in the atria

Ventricular filling

AV valves open and blood flows in, SL closed. 80% of blood flows into ventricle before the atria contract

Lub-Whistle-Dup

Stenotic, SL

Lub-Gurgle-Dup

Insufficient, AV

Lup-Dup-Whistle

Stenotic, AV

Lup-Dup-Gurgle

Insufficient, SL

Cardiac Output (CO)

The volume of blood each ventricle pumps multiplied by the # of beats/min

Beta-blockers

Slow down HR by blocking beta adrenergic receptors- norepinephrine can’t bind

Frank-Starling mechanism

ventricle contracts more forcefully when more blood enters during diastole
Ventricle walls stretch when more fluid enters: More stretch=more forceful contraction