final Flashcards
primary reproductive organs
ovaries
accessory reproductive organs
uterine tubes, uterus, vagina, external genitalia, mammary glands
gametes are made using
mitotic division
what is the site of oocyte production
ovarian follicles
what is the site of sex hormone release
ovarian follicles (estrogen and progesterone)
mature follicle forms from
secondary follicle
mature follicle components
- secondary oocyte surrounded by zona pellucida
- then corona radiata
- antrum
when ovulation occurs corona radiata goes
with the egg as it goes into uterine tube so in order to fertilize the egg it has to make it through both of these layers (corona radiata, zona pellucida) to reach the egg
what cells are sources of estrogen?
granulosa cells
what part of the mature follicle gets bigger during follicular development
fluid-filled antrum
how often is a mature follicle formed
one per month
division of mature follicle
divides mitoticly and divides into secondary oocyte with 23 chromosomes, it begins but stops in metaphase
doesn’t occur unless oocyte is fertilized
corpus luteum formation
remanants of follicle
after mature follicle ruptures and oocyte expelled
corpus luteum secretes
sex hormones progesterone and estrogen to stimulate buildup of uterine lining (endometrium) and prepare uterus for possible implantation of fertilized oocyte
what structure releases GnRH
hypothalamus
GnRH release stimulates release of
FSH and LH
FSH and LH play a major role in
events in ovarian cycle
phases of ovarian cycle
- follicular phase (days 1-13)
- ovulation (day 14)
- luteal phase (days 15-38)
ovulation
- release of secondary oocyte from mature follicle
- occurs on day 14 of 28 day cycle
- antrum increases in size and swells with increased fluid
- expands until ovarian surface thins, eventually rupturing and expelling secondary oocyte
ovulation is induced with increased
LH secretion
order of oocyte release on ovaries
- infundibulum (has to catch oocyte, contains fimbriae)
- ampulla (where fertilization occurs)
- isthmus
- uterine part
uterine wall is mostly
smooth muscle
contains
- endometrium
- myometrium
- perimetrium (thin connective tissue covering on outside)
from deep to superficial
uterine cycle
changes in endometrial lining
uterine cycle is influenced by
estrogen and progesterone - secreted by follicle and then corpus luteum
uterine cycle phases
menstrual phase (1-5)
proliferative phase (6-14)
secretory phase (15-28)
menstrual phase
1-5
sloughing off of functional layer
lasts through period of menstrual bleeding
proliferative phase
days 6-14
development of new functional layer of endometrium
overlaps time of follicle growth and ovarian estrogen secretion
secretory phase
days 15-28
increased progesterone secretion from corpus luteum
results in increased vascularization and uterine gland development
estrogen secretion happens in
proliferative phase of uterine cycle
progesterone secretion happens in
secretory phase of uterine cycle
if fertilization doesn’t occur in secretory phase
- corpus luteum degenerates
- drop in levels of progesterone (causing functional layer to slough off)
levels of hormones during follicular phase of ovarian cycle
high FSH and estrogen levels
low LH and progesterone
mammary glands
exocrine glands
divided into lobes and then into lobules composed of alveoli
lactiferous ducts
bring materials to the nipple
breast milk release
- occurs in response to internal and external stimuli
- starts to produce after giving birth
prolactin
produced in anterior pituitary gland
stimulates milk production, with increase mammary gland forms more and larger alveoli
oxytocin
produced by hypothalamus and released from posterior pituitary gland
responsible for milk ejection
primary male reproductive organs
testes
accessory reproductive organs of male reproductive system
ducts and tubules lead from testes to penis
male accessory glands
penis
epididymis
responsible for storage of sperm
where are gametes produced in MRS
inside seminiferous tubules
internal components of testes are organized into
lobules divided by septum
components of seminiferous tubules
within tubule lumen of seminiferous tubules sperm or germ cells are found
seminiferous tubules are making haploid gametes so meiosis is going to start dividing toward lumen
sperm within lumen
spermatids line the lumen
spermatagonia on outside border of seminiferous tubule
sustentacular cells
provide strength to germ cells, support them, provide nutritional support, and influence rate of sperm cell production
maturation of sperm cells
spermatogonia (2n) - primary spermatocyte - secondary spermatocyte - spermatids - spermatogonia (sperm) (n)
hormone regulation on spermatogenesis and androgen production
- GnRH stimulates anterior pituitary gland to secrete FSH and LH
- LH stimulates interstitial cells to secrete testosterone, FSH stimulates sustentacular cells to secrete androgen-binding protein (ABP)
- Testosterone stimulates spermatogenesis but inhibits GnRH secretion and reduces the anterior pituitary glands sensitivity to GnRH
- Rising sperm count levels causes sustentacular cells to secrete inhibin, further inhibiting FSH secretion
- testosterone stimulates libido and development of secondary sex characteristics
androgen binding protein keeps
testosterone levels high in testes
seminal fluid
- alkaline secretion need to neutralize vaginal acidity
- gives nutrients to sperm traveling in female reproductive tract
- produced by accessory glands
a) seminal vesicles
b) prostate gland
c) bulbourethral glands
semen
- formed from seminal fluid and sperm
- called ejaculate when released during intercourse
- contain 200-500 million spermatozoa
- transit time from seminiferous tubules to ejaculate is about 2 weeks
puberty
- period in adolescence where reproductive organs become fully functional
- external sex characteristics become more prominent
timing of puberty affected by
genetics, health, environmental factors
puberty initiation
- hypothalamus secretes GnRH
- stimulates anterior pituitary gland to secrete FSH and LH
- sex hormone levels increase starting the process of gamete and sexual maturation
menarche
about 2 years after first signs of puberty
first period
gender differences of puberty
girls 2 years prior to boys
8-12 for girls
9-14 for boys
racial differences of puberty
african american girls about 1 year earlier than caucasions
onset of puberty has decreased with better nutrition and health care
precocious puberty
- signs of puberty developing much earlier than normal
- may be without known cause
- may be due to pituitary or gonad tumor
perimenopause
time near menopause
irregular or skipped periods
menopause
women stop monthly menstrual cycles for a year
45-55
- atrophy of reproductive organs and breasts with reduced hormones
- decrease vaginal wall thickness
- hot flashes
- thinning hair
- increased risk of osteoporosis and heart disease
- sometimes treated with hormone replacement therapy
fertilization
- 2 gametes fuse to form diploid cell (containing genetic material from both parents)
- restores diploid number of chromosomes
- determines sex of organism
- initiates cleavage
oocyte viable for how long after ovulation
24 hrs
sperm remains viable for
3-4 days
corona radiata penetration
1st phase of fertilization of mature oocyte
when sperm reaches secondary oocyte, it is initially prevented by corona radiata and zona pellucida
sperm can push through these layers
zona pellucide penetration
Acrosome reaction:
- release of digestive enzymes from acrosomes
- allows sperm to penetrate zona pellucida
After penetration of secondary oocyte:
- immediate hardening of zona pellucida
- prevents other sperm from entering this layer
- ensures only one sperm fertilizes the oocyte
labor
physical expulsion of fetus and placenta from uterus
usually 38 weeks
increased levels of estrogen during labor
- increases myometrium sensitivity
- stimulate production of oxytocin receptors on uterine myometrium
contractions become more intense and more frequent with increasing
estrogen and oxytocin
premature labor
prior to 38 wks
undesirable because infant body systems are not fully develop (especially lungs, insufficient surfactant)
initiation of true labor (uterine contractions)
- mothers hypothalamus secretes increasing levels of oxytocin
- fetus’s hypothalamus also secreting oxytocin
- combined maternal and fetal oxytocin initiates true labor
both fetal and maternal release of oxytocin stimulate placenta to secrete
prostaglandins
- help stimulate uterine muscle contraction and soften and dilate the cervix
true labor is a
positive feedback mechanism
positive feedback mechanism of true labor
- oxytocin is released from mother and fetus hypothalamus
- stimulates uterus to contract and placenta to make prostaglandins
- prostaglandings stimulate more frequent and intense contractions of uterus
- uterine contractions cause fetal head to push against cervix, causing it to stretch and dilate
- dilating cervix initiates nerve signals to hypothalamus which causes more oxytocin release from mother and fetus
blood
- regenerated CT
- moves gases nutrients, wastes, and hormones
- transported through CV system
arteries
transport blood away from heart
veins
transport blood toward heart
capillaries
allow exchange between blood and body tissues
components of blood
formed elements and plasma
formed elements of blood
erythrocytes (RBCs)
leuokocytes (white blood cells)
platelets (thrombocytes)
erythrocytes function in blood
transports respiratory gases in the blood
leukocytes function in the blood
defend against pathogens
platelets function in the blood
form clots to prevent blood loss
plasma of blood
fluid portion of blood
contains plasma proteins and dissolved solutes
functions of blood
- transportation
- protection
- regulation of body conditions (maintaining homeostasis)
blood helps transport…
formed elements, dissolved molecules, and ions
- carries oxygen to and from carbon dioxide to the lungs
- transports nutrients, hormones, heat, and waste products
leukocytes, plasma proteins, and other molecules (of immune system) protect against
pathogens
platelets and plasma proteins within blood protect against
blood loss
blood and body temperature
blood absorbs heat from body cells (especially muscle)
heat is released at skin blood vessels
blood and pH
blood absorbs acid and base from body cells
blood contains chemical buffers (e.g., bicarbonate, proteins)
blood and fluid balance
water is added to blood from GI tract
water is lost through urine, skin, and respiration
fluid is constantly being exchanged between blood and interstitial fluid
- blood contains proteins and ions helping maintain osmotic balance
oxygen-rich blood is
bright red
oxygen poor blood is
dark red
volume of blood in body
about 5 L
males have slightly more than females
viscosity of blood
blood is thicker than water (4-5x)
depends on amount of dissolved and suspended substances
viscosity increases if
erythrocyte number increases
amount of fluid decreases
plasma concentration of solutes (e.g., proteins, ions) within blood
typically .09%
determines direction of osmosis across capillary walls
temperature of blood
1 degree high than measured body temperature
pH of blood
between 7.35 and 7.45
crucial for normal plasma protein shape
percentages of blood
Plasma:
- 55% of whole blood
- contains water, proteins, and other solutes
Buffy Coat:
- <1% of whole blood
- contains platelets and leukocytes
Erythrocytes:
- 44% of whole blood
- contains erythrocytes
what type of fluid is plasma
extracellular fluid
has higher protein concentration to interstitial fluid
blood is a
colloid mixture
contains dispersed proteins
plasma proteins examples
albumin
globulins
fibrinogen
other clotting proteins, enzymes, and some hormones
most plasma proteins are produced in
the liver
some may be produced by leukocytes or other organs
colloid osmotic pressure
prevents loss of fluid from blood as it moves through capillaries
- helps maintain blood volume and blood pressure
colloid osmotic pressure can be
decreased with certain diseases resulting in fluid loss from blood and tissue swelling
- liver disease
- kidney diseases
albumins
most abundant
exert greatest colloid osmotic pressure
act as transport proteins for some lipids, hormones, and ions
globulins
- second largest group
- smaller alpha-globulins and larger beta-globulins that transport water insoluble molecules, hormones, metals, ions
- gamma-globulins (immunoglobulins or antibodies) - body defense
fibrinogen
- 4% of plasma proteins
- blood clot formation
serum
plasma with clotting proteins removed
hemopoiesis
production of formed elements
where does hemopoiesis occur
red bone marrow of certain bones
hemocytoblasts
stem cells/pluriopotent - can differentiate into many types of cells
produces myeloid and lymphoid line
myeloid line
forms erythrocytes, all leukocytes except lymphocytes, and megakaryocytes (platelet producing cells)
lymphoid line
only produce lymphocytes
erythrocytes are formed by
erythropoiesis
platelets are formed by
thrombopoiesis
leukocytes are formed by
leukopoesis
platelet formation
megakaryocytes line blood vessels where appendages on megakaryocytes fall into called proplatelets
as blood pushes through proplaets break off forming platelets within blood
erythrocytes
- contain hemoglobin
- biconcave disc structure
- contain spectrin for support and flexibility
- can stack and line up in single file (roleau)
- transport oxygen and CO2 between tissues and lungs
hemoglobin
red pigmented protein
- oxygenated when maximally loaded with oxygen
- termed deoxygenated when some oxygen is lost
- composed of 4 globin proteins with 2 alpha chains and 2 beta chains each containing a heme group with iron in its center
makeup of hemoglobin
oxygen binds to iron in center of hemoglobin, so each hemoglobin can bind to 4 oxygen molecule
oxygen binds to iron
binding is weak
rapid attachment in lungs and rapid detachment in body tissues
carbon dioxide binds to globin protein
binding is weak
attachment in body tissue and detachment in lungs
EPO regulation of erythrocyte production
- decreased blood oxygen levels
- kidney detects decreased blood O2
- kidney cells release EPO into blood
- EPO stimulates red bone marrow to increase the rate of production of erythrocytes
- increased numbers of erythrocytes enter the circulation, during which time the lungs oxygenate erythrocytes and blood O2 levels increase
- increased O2 levels are detected by kidney, stopping EPO release (negative feedback)
erythrocyte recycling
- eryhtrocytes form in red bone marrow
- they circulate in blood for about 120 days
- aged erythrocytes are phagocytized by macrophages in the liver and spleen. the three components of hemoglobin are separated (globin, heme, iron)
- each of separated coponents of hemoglobin have different fate
- globin proteins: broken down into amino acids and enter the blood (potential use to make new erythrocytes)
- iron: small amounts of iron are lost in sweat, urine, and feces daily; also lost during injury or mestruation
- heme: converted to biliverdin then bilirubin which is transported to liver by albumin and released as bile into small intestine. then bilirubin is converted to urobilinogen in small intestine (some urobilinogen absorbed back into blood and converted into urobilin and excreted in urine, most continues in large intense and is converted into stercobilin and expelled in feces)
type A
surface antigen A
anti B antibodies
type B
surface antigen B
anti A antibodies
type AB
surface antigens A and B
no anti A or anti B
type O
no surface antigens
anti A and anti B
Rh blood type
presence or absence of Rh factor (antigen D) deterines if blood is + or -
antibodies to Rh are not usually there (only appear after Rh exposure to Rh+ blood)
agglutination in transfusion reaction
if patient is type B and is given type A blood…
- anti A antibodies in plasma will attach to type A erythrocytes and cause a clumping of erythrocytes creating a blockage in small vessels
leukocytes
defend against pathogen
motile and flexible - most not in blood but in tissues
leukocytes have ability to perform
diapedesis and chemotaxis
diapedesis
process of squeezing through blood vessel wall
chemotaxis
attraction of leukocytes to chemical at an infection site
neutrophils
phagocytize pathogens
most abundant leukocyte
eospinophils
phagocytize antigen-antibody complexes and allergens
present in cases of parasitic infection
basophils
release histamines (vasodilator increasing capillary permeability) and heparin (anticoagulant)
granulocytes
neutrophils
basophils
eosinophils
agranulocytes
lymphocytes
monocytes
lymphocytes
coordinate immune cell acitivty
attack pathogens and abnormal infected cells
produce antibodies
monocytes
exit blood vessels and become macrophages
phagocytize pathogens
Most abundant to least abundant leukocytes
neutrophils
lymphocytes
monocytes
eosinophils
basophils
platelets are stored in
spleen
circulation of platelets
circulate for 8-10 days and then broken down and recycled
platelets play a major role in
blood clotting
hemostasis
stoppage of bleeding
phases of hemostasis
vascular spasm
platelet plug formation
coagulation phase
hemostasis steps
- Vascular spasm
- blood vessel constricts to limit blood escaping - Platelet plug formation
- platelets arrive at site of injury and stick to exposed collagen fibers - Coagulation
- coagulation cascade converts inactive proteins to active forms, leading to production of fibrin strands of a blood clot
vascular spasm
- 1st phase
- lasts from few to many minutes
- greater vasoconstriction with greater vessel damage
platelet plug formation
when blood vessel is damaged collagen fibers are exposed causing platelets to stick to collagen with help of von Willebrand factor where they develop long processes allowing for better adhesion where platelets continue to aggregate there
when blood vessel is uninjured platelet activation is
inhibited as a result of prostacyclin which repels platelets and causes endothelial cells and platelets to make cAMP which inhibits platelet activation
platelet activation
platelets cytosol degranulates and releases chemicals causing
- prolonged vascular spasms
- attraction of other platelets
- coagulation stimulation
- reparation of blood vessels
platelet plug is formed typically within
1 minute
prevented from getting to large by prostacyclin
serotonin and thromboxane A2 causes
prolonged vascular spasms in platelet activation
adenosine triphosphate (ADP) and thromboxane causes
attraction of other platelets and facilitate their degranulation (positive feedback)
procoagulants stimulate
coagulation
mitosis stimulating substances trigger
repair of blood vessel
coagulation
blood clotting
network of fibrin (insoluble protein that comes from fibrinogen) forms a mesh that traps erythrocytes, leukocytes, platelets, and plasma proteins to form a clot
subsances involved in coagulation
- calcium, clotting factors, vitamin K
clotting factors
most inactive enzymes
most produced in liver within hepatocytes
vitamin K
fat soluble coenzyme required for synthesiss of clotting factors II, VII, IX, X
intrinsic coagulation pathway
initiated by damage to inside of blood vessel
extrinsic coagulation pathway
initiated by damage to tissue outside of vessel
clot elimination includes
clot retraction and fibrinolysis
clot retraction
actinomyosin (protein with platelets) contracts and squeezes serum out of developing clot making it smaller
fibrinolysis
degradation of fibrin strands by plasmin
begins within 2 days after clot formation
occurs slowly over a number of days
four chambers of the heart
left atrium and right atrium
left ventricles and right ventricles
left atrium and right atrium are superior chambers that
receive blood and send it to ventricles
left ventricle and right ventricles are inferior chambers that pump blood
away
left side of the heart has
oxygenated blood
right side of the heart has
deoxygenated blood
right side
receives deoxygenated blood from body and pumps it to the lungs
left side
receives oxygenated blood from the lungs and pumps it into the body
atrioventricular valves are between
atria and ventricles
semilunar valves are between
ventricle and an arteriole trunk
pulmonary semilunar valve and aortic semilunar valve
right AV is sometimes called
tricuspid
left AV valve sometimes called
bicuspid
mitral
flow of blood through heart and lungs
- deoxygenated blood enters the atrium through IVC and SVC
- blood within right atrium enters right ventricle through right atrioventricular valve (tricuspid)
- blood enters ventricle is pumped through pulmonary semilunar valve into the lungs
- deoxygenated blood enters lungs where it flows through capillaries and becomes oxygenated and enters back into the heart in the left atrium
- blood within left atrium is pumped into ventricles via left atrioventricular valve (mitral, bicuspid)
- blood within ventricles is then pumped out via the aortic semilunar valve throughout the body where further gas exchange occurs as blood is delievered to body systems and deoxygenated blood is then brought back to the heart
pericardium
refers to 3 layers of the heart
outer layer of heart
fibrous periardium
serous pericardium
contains visceral and parietal layer containing with pericardial cavity with serous fluid
layers of the heart wall (from deep to superficial
epicardium
myocardium
endocardium
ventricles have thicker walls than
atria
left ventricle has thicker wall than
right ventricle
left ventricle must generate higher pressure to force blood through systemic circulation; right just pumps to nearby lungs
cardiac muscle contains
striated muscle due to arrangement of contractile proteins and overlapping nature of thin and thick filaments
sarcolemma
plasma membrane containing openings called T-tubules which are infolds of plasma membrane
cardiac muscle contains intercellular junctions that include
desmosomes
gap junctions
desmosomes
proteins that serve to connect two adjacent cells
become embedded in cell membrane
gap junctions
proteins with opening in center that functionally pass ions through
gap junctions are important in
contraction and activation of muscle
stimulate electrical current needed for contraction
storage site for Ca2+
sarcoplasmic T tubules
cardiac muscle contains
intercalated discs
metabolism of cardiac muscle
high demand for energy
- extensive blood supply
- numerous mitochondria
- myoglobin and creatine kinase
creatine + ATP —->
CK – creatine phosphate + ADP
cardiac muscle is able to use
different kinds of fuel molecules like:
fatty acids, glucose, lactic acid, amino acids, and ketone bodies
cardiac muscle metabolism relies mostly on
aerobic metabolism which makes it susceptible to failure when oxygen is low
fibrous skeleton is made up of
dense irregular connective tissue
fibrous skeleton provides
structural support at boundary of atria and ventricles that froms fibrous rings to anchor valves
the fibrous skeleton acts as an
electrical insulator preventing ventricles from contracting at same time as atria
coronary circulation delivers blood to
heart wall
- coronary arteries transport oxygenated blood to heart wall
- coronary veins transport deoxygenated blood away from heart wall toward right atrium
conduction system
initiations and conducts electrical events to ensure proper timing of contractions
conduction system contains specialized cardiac
muscle cells that have action potentials but do not contract
conduction system activity is influenced by
autonomic nervous system
components of conduction system
SA node
AV node
AV bundle (bundle of His)
R and L bundle branches
Purkinje fibers
SA node
pacemaker
tissue in posterior wall of atrium that starts generating action potential
what part of the brain contains the cardiac center
medulla oblongata
the cardiac center of the medulla contains
- cardioacceleratory
- cardioinhibitory centers
the cardiac center of medulla receives signals from
baroreceptors and chemoreceptors in CV system
the cardiac center sends signals via
sympathetic and parasympathetic pathways
the cardiac center ______ cardiac activity
modifies
- influences rate and force of hearts contractions
what influences the rate and force of heart contractions
cardiac center
what kind of nerve innervation decreases heart rate
parasympathetic
what kind of nerve innervation increases heart rate and force of contraction
sympathetic
steps of heart contraction
Conduction system
1. initiation - SA node generates action potential
2. spread of action potential - action potential is propagated throughout the atria and the conduction system
Cardiac Muscle Cell
1. action potential - action potential is propagated across the sarcolemma of cardiac muscle cells
2. thin filaments slide past thick filaments and sarcomeres shorten within cardiac muscle cells
RMP of nodal cells
-60mV
the sodium concentration is great inside or outside of a nodal cell
greater concentration of Na+ outside of cell
SA Node Cellular Activity
- RMP @ -60mV
- increase (depolarization)
- MP reaches threshold (-40mV) - repolarization
- when cell becomes negative enough ation potential is generated
pacemaker potential
time it takes for SA node to go from -40mV to threshold voltage
steps of SA node generating action potential
- Reaching threshold
- slow voltage gated Na+ channels open
- inflow of Na+ changes membrane potential from -60mV to -40mV - Depolarization
- fast voltage gated Ca2+ channels open. inflow of Ca2+ changes membrane potential from -40mV to just above 0mV - Repolarization
- fast voltage gated Ca2+ close. voltage gated K+ channels open allowing K+ outflow. MP returns to -60mV and K+ channels close
RMP of cardiac muscle cell
-90mV
at RMP of cardiac muscle cell, all Na+ is
closed so concentration gradient for ions remains table so ions aren’t moving through creating action potential
electrical events of cardiac muscle cell
- Depolarization
- starts @ - 90mV and rapidly reaches +30mV - Plateau
- almost no change during period of time - Repolarization
why do cardiac muscle cells have a plateau
helps ensure heart is beating synchronously with all of its components so if stimulated, nothing will happen
steps of cardiac muscle cells
- Depolarization
- fast voltage gated Na+ channels open and Na+ flows into cell reversing polarity from -90mV to +30mV. Channels then close - Plateau
- voltage gated K+ channels open and K+ flow out of cardiac muscle cells. slow voltage gated Ca2+ channels open and Ca2+ moves into the cell with no electrical change and depolarized state is maintained - Repolarization
- voltage gated Ca2+ channels close, voltage gated K+ channels remain open and K+ moves out of cardiac muscle cell, and polarity is reversed from +30mV to -90mV
electrocardiogram (ECG/EKG)
- skin electrodes detect electrical signals of cardiac muscle cells
- common diagnostic tools
P wave
atrial depolarization
QRS complex
ventricular depolarization
during QRS complex the atria are
repolarizing
T wave
ventricular repolarization
P-Q segment
atrial cells’ plateau (atria are contracting)
S-T segment
ventricular plateau (ventricles contracting
P-R interval
time from beginning of P wave to beginning of QRS
from atrial depolarization to beginning of ventricular depolarization
P-R interval represents the time to transmit
action potential through entire conduction system
Q-T interval
time from beginning of QRS to end of T wave
reflects time of ventricular depolarization and repolarization
the length of Q-T interval depends upon
heart rate
cardiac cycle
all events in heart from the start of one beat to the start of the next
the cardiac cycle includes both
systole (contraction) and diastole (relaxation)
relationship of contraction and pressure
contraction increases pressure
relaxation decreases it
blood moves ____ its pressure gradient
down (high to low)
valves ensure that
flow of blood is forward (closure of valves prevents backflow)
what is the most important driving force of cardiac cycle
ventricular activity
ventricular contraction raises
ventricular pressure
AV valves pushed closed, semilunar valves pushed open and blood pushed out
ventricular relaxation lowers
ventricular pressure
semilunar valves closed
AV valves open (no pressure pushing them closed)
phases of cardiac cycle
- atrial contraction and ventricular filling
- isovolumetric contraction
- ventricular ejection
- isovolumetric relaxation
- atrial relaxation and ventricular filling
atrial contraction and ventricular filling
- atria contract, ventricle relax
- ventricular pressure is LESS than atrial and arterial pressure
- AV valves open, semilunar valves closed
isovolumetric contraction
- atria relax, ventricles closed
- ventricular pressure is greater than atrial pressure but less than arterial trunk pressure
- AV valves and semilunar valves closed
ventricular ejection
- atria relax, ventricles contract
- ventricular pressure is GREATER than both atrial pressure and arterial trunk pressure
- AV valves closed, semilunar valve open
isovolumetric relaxation
- atria and ventricles are relaxed
- ventricular pressure is greater than atrial pressure but less than arterial pressure
- both valves closed
atrial relaxation and ventricular filling
- atria relax, ventricles relax
- ventricular pressure is less than BOTH arterial and atrial pressure
- AV valves open, semilunar valves closed
cardiac output
amount of blood pumped by single ventricle in one minute
cardiac output is a measure of
effectiveness of CV system
CO increases in
healthy individuals during exercise
formula for cardiac output (CO)
heart rate (BPM) x stroke volume (SV) = cardiac output (CO)
patient HR 75 BPM, stroke volume is 70ml/beat. what is CO
75 beats/min x 70 ml/beat = 5250 ml/min = 5.25 L/min
stroke volume
amount of blood ejected in one beat from one ventricle
what influences stroke volume
venous return
inotropic agents
afterload
venous return
volume of blood returned to the heart
venous return is directly related to
stroke volume
venous return determines amount of
ventricular blood prior to contraction (EDV)
volume of blood determines
preload (pressure stretching heart wall before shortening)
Frank-Starling law (Starling’s Law)
as EDV increases, the greater stretch of heart wall, results in more optimal overlap of thick and thin filaments
starling’s law suggests that the heart
contracts more forcefully when filled with more blood so SV increases
what factors increase venous return
increased venous pressure
increased time to fill
venous pressure increases during
exercise as muscles squeeze veins
slower heart rates impact on venous return
time available to fill increases with slower heart rate (high-caliber athletes with strong hearts)
steps of venous return
- increased venous return (occurs with greater venous pressure or slower heart rate
- increases stretch of heart wall (preload) which results in greater overlap of thick and thin filaments within sarcomeres of myocardium
- additional crossbridges form and ventricles contract with greater force
- stroke volume increases
inotropic agents effect on stroke volume
- positive inotropic agents
- increased Ca2+ levels in sarcoplasm results in greater binding of Ca2+ to troponin of thin filaments within sarcomeres of myocardium
- additional crossbridges form, and ventricles contract with greater force
- stroke volume increases
inotropic agents
substances that act on the myocardium to alter contractility
positive inotropic agents
e.g., stimulation by sympathetic nervous system
venous returns ____ stroke volume
increases SV
inotropic agents _____ stroke volume
positive inotropic agents increases SV
afterload
resistance in arteries to ejection of blood
afterloads effect on stroke volume
- artherosclerosis, deposition of plaque on inner lining of arteries is typically only a factor as we age
- arteries become more narrow in diameter
- increases the resistance to pump blood into arteries
- stroke volume decreases
chronotropic agenets
alter SA node and AV node activity
positive chronotropic agents increase or decrease cardiac output
increase by increasing heart rate
negative chronotropic agents increase or decrease cardiac output
decrease cardiac output by decreasing heart rate
increase in heart rate increases or decreases CO
increases
decrease in heart rate increases or decreases CO
decreases
venous return is directly correlated with
stroke volume
increase venous return and increase inotropic agents effect on CO
increase SV which increases CO
afterloads effect on CO
increase in afterload would decrease SV causing a decreased in CO
decrease in afterload would increase SV causing an increase in CO
inotropic agents alter
Ca2+ levels in sarcoplasm
foramen ovale
structure in fetal heart that transports deoxygenated blood from right atrium to left atrium where it becomes oxygenated
ductus arteriosus
connection in fetal heart that connects aorta and pulmonary trunk
arteries
convey blood from heart to capillaries
capillaries
microscopic porous blood vessels
exchange substances between blood and tissues
veins
transport blood from capillaries to heart
walls of arteries and veins from deep to superficial
tunica intima
tunica media
tunica externa
what blood vessel contains valves
veins
branching of arteries
branch into smaller vessels extending from the heart where they decrease in lumen diameter, decrease in elastic fibers, and increase in amount of smooth muscle
3 types of arteries
elastic
muscular
arterioles
capillary characteristics
small vessels connecting arterioles to venuoles
average length = 1mm
deiamter = 8-10 micrometers
thin wall and small diameter make it optimal for exchange between blood and tissue fluid
three types of capillaries
continuous
fenestrated
sinusoid
continuous capillaries
endothelial cells form a continuous lining with tight junctions
tight junctions
connect cells but don’t form a complete seal
found within continuous capillaries
tight junctions contain
intracellular clefts which are gaps between endothelial cells of capillary wall
allow smaller particles to pass through, and blocks large particles
continuous capillaries are most commonly found in
muscle, skin, lungs, and CNS
fenestrated capillaries
endothelial cells form a continuous lining but cells have fenestrations
fenestrations allow for
movement of smaller plasma proteins
where are fenestrated capillaries found
intestinal capillaries absorbing nutrients
kidney capillaries filtering blood to form urine
sinusoids (discontinuous capillaries)
endothelial cells form an incomplete lining with large pore gaps
basement membrane is incomplete or absent
openings allow for transport of large substances (formed elements, large proteins)
where are sinusoids found
bone marrow, spleen, liver, and some endocrine glands
venuoles
smallest veins
companion vessels with arterioles
merge to form veins
smallest venuoles are
postcapillary venuoles
largest venuoles have
all 3 tunics
small and medium-sized veins are companion vessels with
muscular arteries
largest veins travel with
elastic arteries
most veins have numerous
valves preventing blood from pooling in limbs to ensure blood flow toward heart
valves are made of
tunica intima and elastic and collagen fibers
similar to heart’s semilunar valves
pulmonary arteries transport
deoxygenated blood to heart
systemic arteries transport
oxygenated blood away from heart
elastic arteries
stretch to accomodate the pulses of blood ejected from heart and recoil to propel blood through the arteries
muscular arteries
regulate distribution of blood through vasoconstriction and vasodilation
arterioles
regulate blood distribution through vasoconstriction and vasodilation
precapillary sphincters regulate
blood flow through capillary beds
when sphincter contracts, it closes off blood flow
when relaxed, it allows blood to pass through
large veins serve as
a blood resovior (at rest - 55% total blood)
small/medium veins
receive blood from venuoles; blood drains into small/medium veins and then into large veins
venules
receive blood from capillaries
valves in veins prevent
backflow of blood
bulk flow
fluid flows down presentation gradient
large amounts of fluids and dissolved substances move
movement direction of bulk flow depends on
net pressure of opposing forces
(hydrostatic vs colloid osmotic)
filtration
fluid moves out of blood
- fluid and small solutes easily flow through capillary openings (intercellular clefts; fenestrations)
filtration occurs on what end of capillary
arterial
reabsorption
fluid moves back into blood
reabsorption occurs at what end of capillary
venous end
colloid osmotic pressure
the pull on water due to the presence of protein solutes
hydrostatic pressure
force exerted by fluid
blood hydrostatic pressure (HPb)
force exerted per unit area by blood vessel on wall
promotes filtration from capillary
blood colloid osmotic pressure (COPb)
draws fluid into blood due to blood proteins (e.g., albumins)
promotes reabsorption (opposes dominant hydrostatic pressure)
clinically called oncotic pressure
on arterial end of blood capillary…
- blood hydrostatic pressure is > than osmotic pressure
- net pressure moves from blood into interstitial fluid
- filtration
on venous end of capillary
- osmotic pressure is > than blood hydrostatic pressure
- net pressure move from interstitial fluid back into blood
- reabsorption
formula for NFP on arterial end
net hydrostatic pressure - net colloid osmotic pressure = net filtration pressure (NFP)
NFP on arterial end
14 mmHg
NFP on venous end
-5 mmHg
blood pressure
force of blood against vessel wall
blood pressure gradient
change in pressure from one end of vessel to other
- propels blood through vessels
pressure is highest in
arteries and lowest in veins
arterial blood pressure
blood flow in arteries pulses with cardiac cycle
systolic pressure
occurs when ventricles contract (systole)
recorded as upper number of blood pressure ratio
highest pressure generated in arteries (they are stretched)
diastolic pressure
occurs when ventricles relax (diastole)
lower number of BP ratio
pulse pressure
pressure in arteries added by heart contraction
pulse pressure formula
difference between systolic and diastolic BP
BP = 120/80 PP= 120-80= 40mmHg
pulse pressure allows for palpitation of
throbbing pulse in elastic and muscular arteries
what influences pulse pressure
elasticity and recoil of arteries
- tends to decline with age and disease
blood pressure gradient in systemic circulation
systemic gradient is difference between pressure in arteries near heart and inferior vena cava
- mean BP in arteries = 93 mmHg
- blood pressure in vena cava 0
- BP gradient = 0 mmHg
increasing BP gradient is the
driving force to move blood through vasculature
increasing BP graident increases
total blood flow and cardiac output
resistance
friction that blood encounters
resistance is due to
contact between blood and vessel wall
peripheral resistance
resistance of blood in blood vessels
resistance is affected by
- viscosity
- vessel length
- lumen size
total BF equation
total blood flow = pressure gradient (established by heart)/resistance (experienced by blood as it moves through the vessels)
factors the increase blood flow
increased cardiac output
less resistance ( vasodilation, reduction in blood vessel length, or decrease in viscosity)
steeper pressure gradient
factors that decrease total blood flow
decreased cardiac output
greater resistance (vasoconstriction, increase in vessel length, or increase in blood viscosity)
skeletal muscle pump
venous side of blood vessels struggle to bring blood back to the heart and needs assistance to be propelled upwards
when muscles contract, it compresses venous walls and blood is going to go in both direction with one way valves having blood be forced upwards
respiratory pump aids in
increasing venous pressure and propelling it to the heart
inspiration increases blood flow to
thoracic veins
expiration increases blood flow into
heart and abdominal veins
during inspiration there is more pressure in
intra-abdominal pressure than intrathoracic pressure causing blood flow up toward thoracic veins
during expiration there is more pressure in
intrathoracic pressure than intra-abdominal pressure
inferior vena cava is released of compression and blood flows into heart and abdominal veins
blood pressure must be kept high enough to
maintain tissue perfusion but not so high that it damages blood vessels
BP depends on
- cardiac output
- resistance
- blood volume
regulated by nervous and endocrine systems
autonomic reflexes regulate BP only
short-term
involves nuclei in medulla oblongata
quickly adjust cardiac output, resistance, or both
autonomic reflexes meet
momentary pressure needs (standing up from supine position)
cardiovascular center of medulla contains
2 autonomic nuclei: cardiac center and vasomotor center
cardiac center influences
BP by influencing cardiac output
vasomotor center influences BP by
influencing vessel diameter (vessel constriction influences resistance)
baroreceptors
nerve endings that respond to stretch of vessel wall
barorecptors firing rate changes with
BP changes
where are baroreceptors found
tunica externa of aortic arch and carotid sinuses
aortic arch baroreceptors transmit signals to
cardiovascular center through vagus nerve (CN X)
- important in regulating systemic BP
carotid sinuses transmit nerve signals to
CV center via glossopharyngeal nerve (CN IX)
- monitor BP in head, neck (vessels that serve the brain)
- more sensitive to blood pressure changes than aortic arch receptors
autonomic reflexes for BP are
baroreceptor reflexes
baroreceptor reflexes are initiated by
decrease or increase in BP
if blood pressure decreases vessel stretch..
declines and baroreceptors firing rate decreases
- this activates the cardioacceleratory center to stimulate sympathetic pathways to increase CO
- it inhibits cardoinhibatory center to minimize parasympathetic activity
- it activates the vasomotor center to stimualte the sympathetic pathways to increase vasoconstriction; parasympathetic stimulation inhibited
- the increase in cardiac output and resistance raises BP
if BP increases
- vessel is stretch and baroreceptor firing rate increases
- cardioacceleratory center sends less signals along sympathetic pathways
- stimulates cardioinhibatory center to activate parasympathetic pathways to SA and AV nodes
- it causes vasomotor center to send fewer signals along the sympathetic pathways to blood vessels (vasodilation); parasympathetic output enhanced
- decrease in cardiac output and resistance lowers BP
baroreceptor reflexes are best for
quick changes in BP but are inneffective for long term BP regulation
chemoreceptor reflexes
influence BP
stimulation of chemoreceptors brings about negative feedback reflexes to return blood chemistry to normal
- responses in respiratory and CV systems
main peripheral chemorecptors are in
aortic and carotid bodies
aortic and carotid bodies send input to
cardiovascular center
aortic bodies send signals via
vagus nerve
carotid bodies send signals via
glossopharyngeal nerve
what stimulates chemoreceptors
- high carbon dioxide
- low pH
- low oxygen
chemoreceptor firing stimulate
vasomotor center which
- increases nerve signals along sympathetic pathways to vessels
- shifts blood from venous resovoirs to increase venous return
- raises BP and increases blood flow (including pulmonary)
- allows for increased respiratory gas exchange in lungs
hormones also regulate
BP
epinephrine and norepinephrine work with
sympathetic nervous system
hormones with effect on BP
angiotensin II
ADH
aldosterone
ANP
- influence BP through resistance, blood volume or both
renin angiotensin system
- kidney receptors detect low BP or are stimulated by sympathetic division; renin is released
- renin converts angiotensinogen that is produced by liver into angiotensin I
- ACE converts angiotensin I into angiotensin II
- angiotensin II increased BP by
- vasoconstriction
- stimulating thirst center
- decreasing urine formation
aldosterone helps maintain
blood volume and pressure
release of aldosterone is triggered by
several stimuli inclduing angiotensin II
aldosterone increases absorption of
sodium ions and water in kidneys
- decreases urine output
ADH helps maintain and elevate
BP
ADH is released from
posterior pituitary gland
release of ADH is triggered by
nerve signals from hypothalamus
stimulated by increased blood concentration or angiotensin II
ADH effects
increased water reabsorption in kidney (less fluid loss, maintaining blood volume)
stimulates thirst center to increase fluid intake (raising blood volume)
in large amounts, causes vasoconstriction (increasing resistance and pressure)
ADH is sometimes termed
vasopressin
ANP decreases
BP
what stimulated ANP release
stretch of atrial heart wall from high blood volume
ANP effect on vessel diameter
causes vasodilation decreasing resistance
ANP effect on urine output
increases urine output decreasing blood volume
mechanisms of BP homeostasis
cardiac output
resistance
blood volume
cardiac output, resistance, and blood volume are directly related to
blood pressure; increase in any of these will raise BP
heart rate effect on cardiac output and BP
increased heart rate increases cardiac output and BP
decreased heart rate decreases cardiac output and BP
stroke volume effect on cardiac output and BP
increase SV increases CO and BP
decreases SV decreases CO and BP
vasocontriction narrows vessel and forces blood through narrower lumen causing
increase in resistance and BP
vasodilation widens vessel and forces blood through wider lumen causing
decrease resistance and BP
the longer the vessel..
the larger resistance which raises BP
shorter vessels …
decreases resistance which lowers BP
increased blood viscosity increases
peripheral resistance and BP
decreased blood viscosity decreases
peripheral resistance and BP
fluid intake _____ blood volume and BP
increases
fluid output _____ blood volume and blood pressure
decreases
function of lymphatic system
transport and house lymphocytes and other immune cells
return excess fluid in body tissues to blood to maintain blood volume
lymph
fluid transported within lymph vessels
components of lymph
water
dissolved solutes
small amounts of protein
- sometimes cell debris, pathogens, or cancer cells
anchoring filament
components of lymphatic capillary that anchors and stabilizes the position of the capillary and prevents walls from collapsing
thoracic duct
drains everywhere except upper right side
right lymphatic duct
drains right arm, right side of chest, and right side of head and neck
primary lymphatic stuctures
red bone marrow
thymus
primary lymphatic structures are involved in
formation and maturation of lymphocytes
secondary lymphatic structures do not
form lymphocytes but house them and other immune cells
site of immune response initiation
secondary lymphatic structures
secondary lymphatic structures include
lymph nodes, spleen, tonsils, and lymphatic nodules
MALT
red bone marrow
located between trabeculae of spongy bone
site of hemopoiesis; production of blood’s formed elements (includes production of T-lymphocytes and B-lymphocytes
t lymphocytes migrate to
the thymus to complete maturation
the thymus grows until
puberty, then regresses
cortex of thymus contains
immature T-lymphocytes
medulla of thymus contains
mature T-lymphocytes
lymph nodes
filter lymph and remove unwanted substances
occur in cluster
cervical lymph nodes
receive lymph from head and neck
axillary lymph nodes
receive lymph from breast, axilla, and arms
inguinal lymph nodes
receive lymph from legs and pelvis
afferent lymphatic vessels
bring lymph to node
an efferent vessel
drains a lymph node (located @ hilum)
components of lymph node
cortex
medulla
afferent vessels
efferent vessels
hilum
lymph is monitored for
presence of foreign material
macrophages remove
foreign debris from lymph
lymphocytes may initiate
immune resopnse
proliferative in germinal centers
cause enlarged nodes that can be felt in neck
spleen
largest lymphatic organ
contains white and red pulp
white pulp
clusters of T and B lymphocytes and macrophages around central artery
red pulp
contains erythrocytes, platelets, macrophages, and B lymphocytes
red pulp is the storage site for
erythrocytes and platelets
spleen monitors
blood not lymph
white pulp monitors lymph for
foreign materials and bacteria
macrophages lining sinusoids of red pulp..
remove particles, phagocytize bacteria, debris, defective erythrocytes, and platelets
summary functions of spleen
- remove foreign particles
- clear defective erythrocytes and platelets
- store erythrocytes and platelets
in first 5months of fetal life, spleen makes
blood cells
can be reactivated under certain conditions (extra medullary hemopoeisis)
- hematological disorders
tonsils
immune surveillance of inhaled and ingested substances
tonsillar crypts
invaginations that trap material
pharyngel tonsils
in nasopharynx
called adenoids when enlarged
palatine tonsils
in oral cavity
lingual tonsils
along posterior 1/3 of tongue
malt
located in GI, respiratory, genital, and urinary tracts
helps defend against foreign substances
the immune system protect us from
infectious agents and harmful substances
composed of cellular and molecular structures that function together to provide immunity
types of immunity differ based on
- cells involved
- specificity of cell response
- mechanisms of eliminating harmful substances
- amount of time for response
innate immunity
immediate response to wide array of substances
adaptive immunity
delayed response to specific antigens
characteristics of innate immunity
- responds non specifically to range of substances
first line of denfense in innate immunity
skin and mucosal membranes
second line of defense in innate immunity
internal processes like
- activation of neutrophils, macrophages, dendritic cells, eosinophils, basophils, mast cells, and NK cells
- chemicals such as interferon and complement
- inflammation and fever
phagocytic cells include
- neutrophil
- macrophages
- dendritic cells
basophils and mast cells
- proinflammatory chemical-secreting cells
- releases histamine, heparin, and aicosanoids
NK cells
apoptosis initiating cells
releases perforin and granzymes
eosinophils
parasite destroying cells
release cytotoxic chemicals
interferon
synthesizes enzymes that interfere with viral replication
result in apoptosis
complement
group of over 30 plasma proteins that are synthesized by liver, continuously released in inactive form
activation of complement
occurs by enzyme cascade
complement activation follows
pathogen entry
classical pathway (complement activation)
antibody attaches to foreign substance and then complement binds to antibody
alternative pathways for complement activation
- binds to polysaccharides of bacterial or fungal cell wall
opsonization
complement protein (opsonin) binds to pathogen and enhances likelihood of phagocytosis or pathogenic cell
inflammation is enhnaced by
complement as it activates mast cells and basophils and attract neutrophils and macrophages
cytolosis
complement triggers destruction of target cell
complement proteins form membrane attack complex (MAC) that creates channel in target cell’s membrane (fluid enters causing lysis)
elimination of immune complexes
complement link antigen-antibody complexes to erythrocytes where cells are moved to liver and spleen where complexes are stripped off
complement is what kind of imunity
nonspecific innate immunity
inflammation
an immediate response to ward off unwanted substances
- local nonspecific respsonse of vascularized tissue to injury, part of innate immunity
steps of inflammation
- Release of inflammatory and chemotacic factors
- mast cells
- basophils - vascular changes include
- vasodilation of arterioles
- increase capillary permeability
- display of CAMs - recruitment of immune cells
- margination
- diapedesis
- chemotaxis - delivery of plasma proteins
cardinal signs of inflammation
- redness (increased blood flow)
- heat ( increased blood flow and increased metabolic activity within the area)
- swelling (increase in fluid loss from capillaries)
- pain (stimulation of pain receptors)
- loss of function
duration of acute inflmmation
8-10 days
fever (pyrexia)
abnormal temperature elevation
1 degree or more from normal
results from release of pyrogens from immune cells or infectious agents
events of fever
- pyrogens circulate through blood and target hypothalamus
- in response, hypothalamus releases prostaglandin E2
- hypothalamus raises temperature set point leading to fever
benfits of fever
- inhibits reproduction of bacteria and viruses
- promotes interferon activity
- increases activity of adaptive immunity
- accelerate tissue reapair
- increase CAMs on endothelium of capillaries in lymph nodes
- recommended to leave low fever untreated
adaptive immunity involves
specific lymphocyte responses to an antigen
immune response consists of
lymphocytes and their products
adaptive immunity is considered
3rd line of defnese
branches of adaptive immunity
cell mediated immunity involves T-lymphocytes
humoral immunity involving B-lymphocytes, plasma cells, and antibodies
cell-mediated immunity
t lymphocytes (effective against APC)
produces cytotoxic T-lymphocytes and helper T-lymphocytes
destroy cells through apoptosis
humoral immunity
B-lymphocytes
plasma cells
produce antibodies
pathogens are detected by
lymphocytes because they contain antigens
antigen
substance that binds a t-lymphocyte or antibody
examples:
- protein capside of virus
- cell wall of bacteria or fungi
- bacterial toxins
- abnormal proteins or tumor agents
antigens are usually
large proteins or polysaccharide
antigenic determinant
also known as epitope
- specific site on antigen recognized by immune system
- each has different shape
- pathogenic organisms can have multiple determinants
immunogen
antigen that induces immune response
immunogenicity
ability to trigger responses
increases with antigen’s degree of foreignness, size, complexity, or quanitity
haptens
small foreign molecules that induce immune response when attached to carrier molecule in host
e.g., poison ivy
what accounts for hypersensitivity reactions
haptens
e.g., drugs like penicillin
B-lymphocytes make
direct contact with antigen
T-lymphocytes have
antigen presented by some other cells
coreceptors on helper T lymphocytes
CD4
coreceptors on cytotoxic T lymphocytes
CD8
B lymphocytes contain receptors that
directly attach to specific antigen
cytotoxic t-lymphocytes release
chemicals that destroy other cells
helper T- lymphocytes
assist in cell mediated, humoral, and innate immunity
(activate NK cells and macrophages)
other types of t-lymphocytes
memory T-cells and regulatory T-cells
antigen presentation
cells display antigen on plasma membrane so T cells can recognize it
two categories of cells present antigens
-all nucleated cells of body
- antigen presenting cells (APC): dendritic cells, macrophages, and B lymphocytes
antigen presentation requires
attachment of antigen to major histocompatibility complex (MHC)
- group of transmembrane proteins
CD4 interacts specifically with
MHC class II molecules
CD8 interacts specifically with
MHC class I molecules
main events in life events of lymphocytes
- formation and maturation
- occurs in primarily lymphatic structures (red bone marrow and thymus)
- becomes able to recognize one specific antigen - activation of lymphocytes
- in secondary lymphatic structures they are exposed to antigen and become activated
- replicated to form identical lymphocytes - effector response: action of lymphocytes to eliminate antigen
- T-lymphocytes migrate to site of infection
- B lymphocytes stay in secondary lymphatic structure (as plasma cells)
plasma cells that stay in secondary lymphatic structures
- synthesize and release large quantities of antibodies
- antibodies are transported to infection site through blood and lymph
activation of lymphocytes
- secondary lymphatic structures house B and T lymphocytes
- site of activation and proliferation of these cells
effector response of lymphocytes
- interaction of T lymphocytes and antibodies to eliminate foreign antigens at site of infection
antigen challenge
first encounter between antigen and lymphocytes
antigen challenge usually occurs in
secondary lymphatic structures
-antigen in blood taken to spleen
-antigen penetrating skin transported to lymph node
- antigen from respiratory, GI, urogenital tracts, in tonsils or MALT
clonal selection
forming clones in response to an antigen
- all formed cells have same TCR or BCR that matches specific antigens
activation of cytotoxic T lymphocytes
- First Signal: CD8 binds with MHC class I molecule of infected cell; TCR interacts with antigen within MHC class I molecule
- Second Signal: IL-2 released from activated helper T-lymphocytes activates cytotoxic T lymphocytes
*activated cytotoxic T-lymphocytes differentiate to form clone of activated and memory cytotoxic T-lymphocytes
activation of helper T-lymphocytes
- First Signal:
- CD4 binds with MHC class II molecule of APC; TCR interacts with antigen within MHC class II molecule - Second Signal:
- other signal receptors interact and helper T-lymphocyte releases IL-2 which binds with helper T lymphocytes
activated helper T cells proliferate and differentiate to form a clone of activated and memory helper T cells
activation of B lymphocytes
- First Signal:
- free antigen binds to BCR; B-lymphocytes engulf and present antigen to activated helper T-lymphocyte - Second Signal:
- IL-4 released from activated helper T cells stimulate B-lymphocyte - activated B lymphocytes proliferate and differentiate into clone of plasma cells and memory B lymphocytes
effector response
mechanism used by lymphocytes to help eliminate antigen
helper T-lymphocyte effector response
- releases IL-2, IL-4, and other other cytokines
- help activate B-lymphocytes
- activate cytotoxic T-lymphocytes with cytokines
- regulate cells of adaptive and innate immunity
cytotoxic T-lymphocyte effector response
destroy unhealthy cells by apoptosis
releases perforin and granzyme to induce apoptosis
plasma cells (differentiated B-lymphocytes)
produce antibodies
most activated B lymphocytes become
plasma cells
plasma cells synthesize and release
antibodies
plasma cells remain in
the lymph nodes
plasma cells produce
millions of antibodies during 5-day life span
they circulate in lymph until encountering an antigen
antibody titer
circualting blood concentration of antibody against a specific antigen
- measures immune response
antibodies
immunoglobin proteins produced against a particular agent
antibodies tag
pathogens for destruction by immune cells
antibody structure
- 4 polypeptide bounds together
- 2 light chains and 2 heavy chains
disulfide bonds in antibodies allows for
linkage between polypeptides
variable regions
gives antibody specificty on antigen binding site
unique to specific antibody
constant region
area among bottom 75% of antibody structure that remains constant
Fc region
fragmented constant
binding of antigen-binding site of a antibody with antigen causes
- neutralization
- agglutination
- precipitation
exposed Fc region portion following antigen binding by antibody promotes
- complement fixation
- opsonization
- activation of NK cells
neutralization
antibody covers biologically active portion of microbe or toxin and neutralizes the organisms ability to be pathogenic
agglutination
antibody cross-links bacteria forming a clump making it easier for organism to be phagocytized
precipiatation
antibody-crosslink circulating particles forming insoluble antigen-antibody complexes and precipetate them out of solution
complement fixation
Fc region of antibody binds to complement proteins; complement activated
opsonization
Fc region of antibody binds to receptors of phagocytic cells, triggering phagocytosis
activation of NK cells
Fc region of antibody binds to an NK cell triggering release of cytotoxic chemicals
IgG
major class
75-85%
most versatile - capable of all Ab actions
IgM
pentamer
best at agglutination
IgA
dimer
areas exposed to environment (mucosal membranes, tonsils) best at neutralization
IgD
activates B cells (BCR)
IgE
allergy and parasitism
degranulation of basophils and mast cells; chemotacic for eosinophils
effector response: cell mediated immunity
- activated helper T lymphocytes release cytokines to stimulate activity of B cells and cytotoxic T cells, and regulate cells of innate immunity
- activated cytotoxic T cells release cytotoxic molecules (perforin and granzymes) causing apoptosis fo foreign or abnormal cells
effector response: humoral immunity
- Fab region of antibody binds to antigen causing several consquences including neutralization of microbial cells, agglutination of cells, and precipitation of particles
- Fc region of antibody serves as point of interaction with several structures including complement activation, bidning of phagocytic cells to cause phagocytosis of unwanted substances, and binding of NK cells to induce apoptosis of unwanted cell
memory results from
formation of long-lived army of lymphocytes upon immune activation
adaptive immunity activation requirs
contact between lymphocyte and antigen
(lag time btwn first exposure of host and direct contact with lymphocyte)
activation of adaptive immunity leads to
formation of many memory cells against specific antigen
with subsequent antigen exposure
- many memory cells make contact with antigen more rapidly producing powerful secondary response (pathogen is typically eliminated before disease symptoms develop)
what is the most effective way to develop memory
vaccines
antibody titer in primary and secondary response
Primary:
lag phase long
IgM increase
then high IgG
then lowers
Secondary:
lag phase shorter
immediate high IgG
lower levels of IgM
active immunity
production of memory cells due to contact with antigen
branches of active immunity
naturally acquired- direct exposure to antigen
artificially acquired- vaccine
passive immunity
no production of memory cells, antibodies from another person or animal
passive immunity branches
naturally acquired - transfer from mother to child across placenta or breast milk
artificially acquired - transfer of serum containing antibody from another person or animal
acute hypersensitivity
- allergy
- overreaction of immune system to noninfectious substance, allergen
autoimmune disorders
immune system is lacking tolerance for specific self-antigen which initiates response as if cells were foreign
due to cross reactivity, altered self-antigens or entering areas of immune privledge
cross reactivity
pathogen is so structurally similar, immune system doesn’t recognize that it is self
e.g., rheumatic heart disease
altered self-antigen
something alters makeup of shape or makeup of antigen (either random mutation or from infection) causing cell to become foreign
e.g., type 1 diabetes
areas of immune privledge
some areas are not involved in immune response
ovaries, testes, etc.
aqcuired immunodeficiency syndrome
life threatening illness that results from human immunodeficiency virus
- destrys helper T cells
- resides in body fluids
- transmitted through intercourse, needle sharing, breastfeedings, placenta
HIV become AIDS when
helper T cells drop below a certain levels
HIV tests look for
HIV antibodies in blood
AIDS patients have many
CNS complications and are prey to opportunistic infections
functions of GI tract
- ingestion
- motility
- secretions
- digestion
- absorption
- elimination
ingestion
introduction of solid and liquid nutrients into oral cavity
first step in process of digesting and absorbing nutrients
motility
voluntary and involuntary muscle contractions
mixing and moving material through GI tract
secretion
process of producing and releasing fluid products facilitating digestion
e.g., digestive enzymes, acid, bile
digestion
breakdown of ingested food into smaller structures
mechanical and chemical
mechanical digestion
materially physically broken down by chewing and mixing
chemical digestion
involves specific enzyme to break chemical bonds
change large complex molecules into smaller molecules
absorption
transport of digested molecules, electrolytes, vitmains, water
move from GI tract into blood or lymph
elimination
expulsion of indigestible coponents that are not absorbed
accessory digestive organs
teeth
tongue
salivary glands
liver
gallbladder
pancreas
GI tract or alimentery canal
where food actually passes through
- oral cavity
- pharynx
- esophagous
- stomach
- small intestine
- large intestine
- anal canal
tunics (deep to superfifical)
mucosa
submucosa
muscularis
serosa
enteric nervous system
- submucosal plexus and myenteric plexus
- baroreceptors and chemoreceptors detect changes in tract wall (stretch) and chemical makeup of lumen content
- sensory and motor neurons
inner circular muscle layer thickened at several points to form
sphincter which closes off lumen and controls movement of material into next section of GI tract
motility involves
peristalsis and mixing
peristalsis
involves wave of contraction that moves bolus along
propels food
mixing
not designed to propel food but initiate mixing with secretions in both directions
peristalsis and mixing both
occur at same time in different areas of GI tract
oral cavity and salivary glands
- where mechanical digestion begins
- saliva secreted from salivary glands in response to food
- contains salivary amylase, enzyme initiating digestion of starch
- mixed with ingested materials to form bolus
pharynx
- bolus moved here where swallowing occurs
- mucus secreted here to facilitate swallowing
esophagous
bolus transported from pharynx to esophagous into stomach
lubricated by mucus secretions
stomach
bolus is mixed with gastric secertions by smooth muscle contractions
secretions produced by epithelial cells of stomach
chyme formed from mixing
duodenum
part of upper GI tract
vestibule
region behind lip and in front of teeth
hard palate
bone covered by mucous membrane
soft palate
located posteriorly and is a soft tissue that forms uvula where it ends
tongue
skeletal muscle under voluntary control
saliva
- mostly produced during mealtime
- 99.5% water and mixture of solutes
- salivary amylase, lysozyme, mucin added
saliva function
- moistens ingested food to help become bolus
- initiates chemical breakdown of starch (chemical digestion)
- food molecules dissolved here so taste receptors stimulated
- cleanses oral cavity structures
- antibacterial subtances inhibit bacterial growth (lysozyme, antibodies)
salivary glands
parotid salivary gland (attaches to roof of mouth)
sublingual salivary glands ( attaches below tongue)
submandibular salivary duct
mechanical digestion
mastication
mastication
chewing
mechanically reducles bulk to facilitate swallowing
requires coordinated activies of teeth, jaw, lips, tongue, cheeks
chewing increases
- surface area to facilitate exposure to digestive enzymes
- salivation
mastication is controlled by
nuclei in medulla and pons
mastication center^
phases of swallowing
- voluntary phase
- pharyngeal phase
- esophageal phase
voluntary phase
bolus of food is pushed by tongue against hard palata and then moves toward oropharynx
pharyngeal phase
involuntary
as bolus moves through oropharynx, soft palata and uvula close off nasopharynx and the larynx elevates so the epiglottis closes over laryngeal opening
esophageal phase
involuntary
peristaltic contractions of esophageal muscle push bolus toward stomach
acidity from esophageal phase in stomach can impact esophagus
stomach performs
mechanical and chemical digestion
where does the digestion of fat and protein begin
within stomach
how long do ingested materials spend in stomach
2-6 hrs
stomach serves as
“holding bag” for controlled release of partially digesting material (chyme) into small intestine (where most digestion and absorption occur)
absorption of nutrients in stomach is
limited to small ,nonpolar substances
gastric folds
rugae that allow for expansion of stomach which will happen as food enters
pyloric sphincrer
where stomach and duodenum meet
controls release of food content into small intestine
stomach wall is composed of 3 layers
mucosa
submucosa
muscularis
serosa
mucosa of stomach
contains simple columnar epithelium with invaginations called gastric pits
gastric pits
lined with secretory cells
collectively called gastric gland
what is responsible for absorption in mucosa of stomach
limina propria
muscularis mucosae
contraction stimulates secretion from gastric glands
muscularis of stomach
oblique layer
circular layer
longitudonal layer
layers of stomach wall deep to superficial
- oblique
- circular
- longitudonal
gastric secretions
- produced by 5 types of secretory cells
- 4 produce gastric juice, fifth secretes hormones
surface mucus cells
- line stomach lumen and extend into gastric pits
- secrete alkaline product containing mucin
- mucous layer helps prevent ulceration of stomach lining (protect from enzymes and high acidity)
mucous neck cells
immediately deep to base of gastric pit
interspresed among parietal cells
produce acid mucin
help maintain acidic conditions
both kinds of mucous cells help
protect the stomach lining from abrasion and injury
parietal cells
intrinsic factor: required for absorption of vitamin B12 in ileum (necessary for production of erythrocytes)
hydrochloric acid: responsible for low pH in stomach (1.5-2.5)
hydrochloric acid functions
- converts inactive enzyme pepsinogen into active pepsin
- denatures proteins, facilitating chemical digestion
- kills most microorganisms entering stomach
- helps breakdown plant cell walls and animal CT
chief cells
- most numerous secretory cells within gastric glands
- produce and secrete packets of zymogen granules that primarily contain pepsinogen, inactive precursor of pepsin
pepsinogen activated by
HCl and other active pepsin molecules
pepsin chemically digests
denatured proteins into oligopeptides
chief cells produce
gastric lipase, playing limited role in fat digestion (10-15% of ingested fat)
G cells
enteroendocrine cells that are widely distributed in gastric glands
secretes gastrin
gastrin stimulates
stomach secretions and motility
what activates pepsinogen
HCl
gastric mixing and emptying
Mixing
1. contraction of smooth muscle in stomach wall mix bolus with gastric secretions to form chyme
2. peristaltic waves result in pressure gradients that move stomach contents toward the pyloric region
Emptying
3. Pressure gradient increases force in pylorus against pyloric sphincter
4. pyloric sphincter open, and small volume of chyme enters the duodenum
5. pyloric sphincter closes and retropulsion occurs
small intestine
small bowel
ingested nutrients reside here at least 12 hrs
absorbs most nutrients and large percentage of water and electrolytes
absorbs vitamins
what is absorbed in small intestine
- most nutrients
- water
- electrolytes
- vitamins
segments of small intestine
duodenum
jejunum
ileum
duodenum
- originates at pyloric sphincter
- C shape around head of pancreas
- continuous with jejunum at duodenojejunal flexure
- most retroperitoneal
the duedenum recieves
accessory gland secretions from liver, gallbladder, pancreas, and chyme from stomach
jejunum
primary region for chemical digestion and nutrient absorption
intraperitoneal and suspended by mesentery
ileum
distal end terminates at ileocecal valve (sphincter controlling entry of materials into large intestine)
intraperitoneal and suspended by mesentary
continues absorption of digested materials
small intestine layers
contains mucosa with circular folds
submucosa
muscularis
and serosa
mucosa of small intestine
shape in circular folds
folds contain villi that extends towards lumen of intestine called intestinal villi
circular folds increase
surface area available for absorption
single intesntial villi
contains mucosa and submucosa
intestinal villi contain
- simple columnar epithelial cells with microvilli)
- goblet cells
- unicellular gland cell
- enteroendocrine cells
simple columnar epithelial cells with microvilli function
absorbs nutrients
microvilli on columnar cells of small intestine make a
brush border
goblet cells
produce mucin
unicellular gland cell
synthesizes eneteropeptidase
enteroendocrine cell
secretes hormones
large intestine
absorbs water and electrolytes from remaining digested material
absorbs vitamins B and K produced by bacteria
watery chyme compacted into feces
stores feces until eliminated through defecation
right colic flexure
bend of colon on right sight from ascending to transverse
left colic flexure
bend of colon on left side from transverse to descending colon
sigmoid flexure
bend of colon on bottom left from descending to signmoid
mesocolon
mesentary attachments (CT holding things in place)
liver
largest internal organ
covered by CT capsule and layer of visceral peritoneum
production of bile is main function in digestion
bile
secreted by liver
contains water, HCO3-, bile pigments, cholesterol, bile salts, lecithin, and mucin
bile salts and lecithin help
mechanically digest lipids
gallbladder
saclike organ attached to inferior surface. of liver
stores, concentrates, and releases bile produced in liver
cystic duct
connects gallbladder to common bile duct
sphincter valve/hepatopancreatic sphincter
controls flow of bile into and out of gallbladder
pancreas
endocrine function: secretes insulin and glucagon
exocrine function: produces pancreatic juice to assit with digestive activies
pancreas regions
head body and tail
alpha cells of pancreas secrete
glucagon
beta cells of pancreatic islet secretes
insulin
acinar cells of pancreatic acinus secrete
-amylase
- lipase
- proteases
- neucleases
duct cells of pancreatic acinus secrete
bicarbonate ions
pancreatic juice
formed from secretion of acinar cells and pancreatic duct cells
alkaline fluid
pancreatic juice is made of
mostly water, HCO3-, digestive enzymes
- pancreatic amylase to digest starch
- pancreatic lipase to digest triglycerides
- inactive proteases that digest proteins when activated
- nucleases for digestion of nucleic acids
gastrin is secreted by
G cells in stomach
gastrin is stimulated for release when
bolus is in stomach (especially if contains proteins)
targets of gastrin
- parietal cells: stimulates secretion of hydrochloric acid
- chief cells: stimulates releases of pepsinogen
- pyloric sphincter: stimulates contraction
cholecystokinin (CCK) is secreted by
enteroendocrine cells of small intestine
stimulated for release when chyme containing amino acids and fatty acids enter small intestine
primary target and effects of CCK
- inhibits stomach motility and gastric secretion
- stimulates release of bile
- stimulates release of enzyme-rich pancreatic juice
- causes relxation of hepatopancreatic sphincter
secretin is secreted by
enteroendocrine cells of small intestine
primarily with increase in acidity of chyme entering small intestine
primary targets and effects of secretin
- inhibits gastric secertions and stomach motility
- stimulates secretion of alkaline solution from pancreatic ducts
- stimulates secretion of alkaline solution
carbohydrate digestion in small intestine
- pancreatic amylase is produced by pancreas and secreted into small intestine
- pancreatic amylase continues digestion of starch that began in oral cavity by salivary amylase
- brush border enzymes complete the breakdown of starch to individual glucose molecules and are responsible for digestion of disaccharides
protein digestion in small intestine
- proteolytic enzymes are released from pancreas
- enteropeptidase activates trypsinogeen to trypsin; trypsin then activates other proteolytic enzymes
- activated pancreatic proteolytic enzymes (chymotrypsin and carboxypeptidase) break proteins into epeptides and aminoacids
- brush border peptidases break peptides into single amino acids to be absorbed through epithelial cells into blood
lipid digestion and absorption in small intesine
- bile silts released from liver and gall bladder emulsify lipid droplets to form micelles
- pancreatic lipase functions within micelles to digest each triglyceride into a monoglyceride and two free fatty acids
- monoglycerides and three fatty acids enter an epithelial cell, while bile salts remain in intestinal lumen to be reabsorbed and recycled
- triglyceride molecules are reassembled within epithelial cells. lipids are then wrapped with protein to form chylomicrons which are then packaged within secretory vesicles and then exocytosed from cells and absorbed into lacteals