Unit 4

Stroke Volume is determined by 3 variables

Stroke Volume is determined by 3 variables

end-diastolic volume, total peripheral resistance, contractility

Cardiac output formula

CO=SV(HR)

Total blood volume

5.5

Average SV

70-80 ml/beat

Without neuronal influence, what beats

SAwha node

what does norepinephrine do to the heart

depolarize

what does ACh do to the heart

hyperpolarize

EDV

volume of blood in ventricles at the end of diastoleTP

TPR

resistance blood flow in arteries (e.g. cholesterol)

what happens when edv increases

myocardium contraction increases

if actin is overlapping

actin-myosin reduce and contraction is weak

when actin is separated

contraction is harder/greater

medulla secretes

adrenaline, increasing heart contraction (adrenal gland receives signal)

parasympathetic increases or decreases HR

decrease

sympathetic increases what

cardiac rate and contraction strength

veins bring blood….. heart

to the heart

how long does it take for blood to circulate

1 min

what happens to veins when losing blood

vasoconstriction

vasocontriction is caused by sympathetic or parasympathetic

symp

is SV increases what happens to CO

it increases too

inhalation does what to pressure

decreases

do veins have a lot of pressure

no

what type of walls do veins have

thin walls, to accommodate more blood w/o increase in pressure and have valves

where are veins placed

near skeletal muscles, so everytime you move, the blood is being pumped

veins mm Hg prssure

0-10 mm Hg

2/3 of body h2o is where

inside cells, intracellular

1/3 of body h2o is where

extracellular, outside cell. 80% interstitial, 20% blood plasma

Innate immunity

non-specific

first line of defense

innate immunity

which immunity is inherited

innate

first line of dense: epithelial membranes, stomach acidity, cells that can engulf/kill pathogens, interferons, fever

innate

learned defense

adaptive

from exposure to specfic pathogens fx of lymphocytes

adaptive

which immunity is specific

adaptive

external structures

skin, digestive tract, respiratory, genitourinary

internal structures

phagocytic, interferons, complement proteins, endogenous, natural killer, mast cells

includes internal and external defenses

innate

inhibit replication of viruses

interferons (internal, innate immunity)

secreted by leukocytes and other cells; produces fever

endogenous (internal, innate immunity)

destroy cells innfected with viruses, tumor cells, and mismatched transplanted tissue cells

natural killer cells (intenral, innate)

release histamine and other mediators of inflmmation, and cytokines that promote adaptive immunity

Mast cells (innate, internal)

ACtivaton of innate

cells identify “self” from “non self”

use PAMPs (molecular patterns unique to pathogens)

immune cells= “toll-like” receptors bind to PAMPs to their surface

-LPS (gram -) and Peptidoglycan (gram +)

10 toll-like receptors ID’d

cells respond by secretion og chemokines to recruit immune cells or activate specific

____ proteins promote phagocytoses, lysis of target cells and inflammation

complement

Immune system exposes to DAMPs, danger associated molecular patterns, stimmulate innate and inflammation, tissue damage that causes nercrosis

local inflammation

three phagocytic cells

1. neutrophils

2. mononuclear: monocytes in blood and macrophages and dendritic cells in tissues) arrive later

3. organ specific, luver, spleen, lymph nodes, lungs, brain, some called “fixed” phagocytes

location: blood and all tissues

neutrophils (phagocyte)

kupffer cells location

liver (phagocyte)

microglia location

CNS (phagocyte)

phagocytosis process in tissues

Neutrophils and monocytes squeeze through gaps in post-capillary venule walls to enter tissue in a process called extravasation, or diapedesis. 2) Attracted to site by a process called chemotaxis by cytokines called chemokines 3) The pathogen becomes engulfed by pseudopods. 4) The vacuole containing the pathogen fuses with a lysosome. 5) The pathogen is digested

what portion of the body regulates fevers

hypothalamus

what do cytokines produce

fevers, including sleepiness and a fall in plasm iron concentration (limits bacterial activity)

T/F DAMPs stimulates inflammation

true

phagocyte eats microbe

phagocyte “eats” the microbe (similar to the way an amoeba eats) by engulfing it with cytoplasm, so that the microbe is internalized. The microbe thereby becomes surrounded by a membrane derived from the plasma membrane (fig. 15.2) and is contained within a vacuole. This vacuole then fuses with a lysosome, which contains digestive enzymes. However, the lysosomal enzymes may be released before the fusion is complete, killing the cell and contributing to the inflammation of the infected area

apoptosis process

signal macrophages to attack by displaying on their surface a phospholipid molecule (phosphatidylserine) that normally is found only on the inner layer of the plasma membrane. The phosphatidylserine provides an “eat me” signal to macrophages. However, unlike the activation of phagocytes in response to foreign pathogens, other inflammatory processes are suppressed when macrophages eat apoptotic body cells. This limits the “collateral damage” that would otherwise occur as a result of the inflammation.

component of the nonspecific defense system.

fever

Fever is thereby produced as a response of

the body to infection, rather than produced directly by the invading bacteria or viruses

The cell wall of gram-negative bacteria contains

endotoxin, a lipopolysaccharide that stimulates monocytes and macrophages to release various cytokines. These cytokines, including interleukin-1, interleukin-6, and tumor necrosis factor, act to produce fever, increased sleepiness, and a fall in the plasma iron concentration.

produced a nonspecific, short-acting resistance to viral infection

interferons

—— interferon is produced predominantly by hematopoietic cells) in response to microbial infections

alpha

is produced only by particular lymphocytes and a related type of cell called a natural killer cell.

gamma interferon

cells is part of the immunological defense against infection and cancer.

gamma interferons

specific in their actions

antibodies

proteins produced by a particular type of lymphocyte.

antibodies

molecules that stimulate the production of specific antibodies (or

other specific immune response)

antigens

foreign to the blood and other body fluids.

antigens

Many small organic molecules are not antigenic by themselves but can become antigens if they bind to

proteins

Leukocytes, erythrocytes, and blood platelets are all ultimately derived from

(“stem from”) unspecialized cells in the bone marrow.

The lymphocytes that seed the thymus become

T lymphocytes, or T cells (the letter T stands for thymus-dependent)

T lymphocytes, therefore, either come from or had an ancestor that came from

the thymus.

Most of the lymphocytes that are not T lymphocytes are called

B lymphocytes, or B cells.

marrow produces—-lymphocytes

B

bone marrow and thymus are considered the

primary lymphoid organs.

combat bacterial infections, as well as some viral infections, by secreting antibodies into the blood and lymph.

B lymphocytes

provide humoral immunity, although the term antibody-mediated immunity

B lymphocytes

attack host cells that have become infected with viruses or fungi, transplanted human cells, and cancerous cells.

T lymphocytes

do not secrete antibodies; they must come in close proximity to the victim cell, or have actual physical contact with the cell, in order to destroy it.

T lymphocytes

provide cell-mediated immunity

t-lymphocytes

occurs more slowly in adulthood, and appears to be accomplished mostly by production of—— in the secondary lymphoid organs rather than in the thymus.

T lymphocytes

Lymphocytes move from the

primary lymphoid organs (bone marrow and thymus) to the blood, and exit

the

blood through specialized postcapillary venules in lymph nodes to travel in the

lymph from lymphoid organ to lymphoid organ.

events that occur when bacteria enter a break in the skin and produce

local inflammation

local inflammation; Macrophages and mast cells (discussed shortly), which are resident in the tissue, release a number of cytokines and chemokines that attract phagocytic neutrophils and promote

the innate immune responses of phagocytosis and complement activation

found in most tissues, but are especially concentrated in the skin, bronchioles (airways of the lungs),

Mast cells

best known for their production of histamine, a molecule that produces many of the symptoms of allergy

mast cells

mast cells secrete —— vasoactive molecules, pro- inflammatory cytokines, and other molecules that have a variety of effects.

serotonin,

cause the endothelial cells of capillaries and postcapillary venules to contract away from each other, creating gaps between the cells of the endothelium.

mast cell molecules

Histamine and heparin, together with protease enzymes important in inflammation, are stored in

granules within the mast cells.

do lymphcytes die i the course of the infection

lymphocytes can travel through the lymphatic system and re-enter the circulation.

immobilize the bacteria, facilitate their phagocytosis, and may also kill them directly by means of antimicrobial enzymes.

NETs

what releases NETs

neutrophils

produces a viscous, protein-rich fluid that, together with dead neutrophils, forms

pus

ingest microorganisms and fragments of the extracellular matrix by phagocytosis.

Macrophages

which aids in the destruction of bacteria

NO

redness and warmth (due to histamine-stimulated vasodilation); swelling (edema) and pus; and pain

local inflammation:

secrete antibodies that bind to specific antigens.

B lymphocytes

protein factories that produce 2k antibody proteins per sec

plasma cells

are stimulated to become plasma cells and memory cells

B lympho

Antibodies bind to antigens on

bacteria