EXAM 2 - The Heart, Lymphatic and Immune System Flashcards
cardiac output
heart rate x stroke volume
blood pressure
cardiac output x peripheral resistance
cardiodynamic autonomic control: sympathetic
nerve from cardioacceleratory center (medulla) synapses in spinal cord
preganglionic axons release Ach onto ganglia
postganglionic axons synapse on SA node, AV node, and left ventricle and release NE
NE activates B1-adrenergic receptors coupled to Gsa GPCR
Gsa increases cAMP production and increases HR
where do the sympathetic postganglionic axons synapse on?
SA node, AV node, left ventricle
sympathetic synapse on heart
increase cAMP, increase HR
NE binding to Gsa
adenylate cyclase –> cAMP –> to PKA and HCN channels
effects of PKA
activates troponin
inactivates phospholamban
activates ryanodine receptors
activates L-type Ca2+ channels
effect of increasing troponin
increases contractile strength
effect of binding to HCN
increases heart rate
effect of decreasing phospholamban
phospholamban typically inactivates SERCA – by disinhibiting SERCA, Ca2+ gets pumped into SR quicker allowing for quicker repolarization –> quicker cardiac myocyte AP
effect of activating RyR
increases contractility due to Ca2+ eflux
effect of L-type Ca2+ activation
more depolarized plateau phase to permit contraction
hydrostatic pressure near heart in arteries
high; 80-120 mmHg
hydrostatic pressure in capillaries
low (15-25)
hydrostatic pressure in veins
0-20
parallel circulatory systems
pulmonary circulation
systemic circulation
two pumps for two loops
coronary arteries
arise from coronary sinus in aorta and delivers oxygenated blood to cardiac muscle tissue itself
cardiac veins
drain into coronary sinus and opens into right atrium
arteries and arteriole functions
distribution
arteries and arteriole constraints
distribution vessels must be able to handle pressure during contraction and store pressure during diastole
capillary function
exchange
capillary constraints
exchange vessels must permit bidirectional flow of substances
vein functions
collection
vein constraints
collection vessels must be able to deal with low pressure upon returning to the heart
path of circulation
arteries carry blood away from heart
branch into arterioles
branch into capillaries
capillaries do exchange
later rejoin into venules
venules deposit into veins
which vessels do not have elastic fibers
veins, capillaries
which vessels do not have smooth muscle
capillaries, veins
which vessel has the greatest wall thickness
aorta, artery
which vessel has the thinnest thickness?
vein,,capillary (smallest is venule)
arteries
hold 13%
elastic
muscular
arterioles
elastic arteries
conducting
buffer changes in pressure
muscular arteries
distributing
most common
arterioles
resistance
small diameter
no externa
can affect BP
veins
hold 64%; volume reservoir
venules
medium diamater
large
venules
collect blood from capillary to deposit into veins
no media
medium diameter veins
return blood expand easily (high compliance) valves
large veins
return blood back to the heart
thin 3 layers
capillaries
hold 9%
microcirculation
large SA
continuous
fenestrated
sinusoid
thoroughfare channels
provide direct flow b/w arterioles and venules (capillary)
metarterioles
precap sphincters to regulate blood flow
arteriovenous anastomaoes
alternative blood pathway
continuous capillaries
exchange of small molecules in most tissues
fenestrated capillaries
fenestrations in endothelium that allow peptide exchange
hypothalamus, kidney, intestine, pituitary
sinusoid capillaries
allow exchange of large proteins
larger diameter, large sinuses
liver, bone marrow, spleen
B1 AR
NE binds to this, adenylate cyclase, cAMP PKA etc etc etc
B2 AR
epi binds to this, increases cAMP and inhibits MLC in smooth muscle
M3 cholinergic
Ach binds to this and decreases cAMP to relax smooth muscle
A1 AR
gq coupled; NE binds to this and increases IP3 for more contraction in smooth muscle
also binds:
angiotensin
endothelin
thromboxane
NO smooth muscle
endothelial gets NO from blood flow, it diffuses into smooth muscle
guanylate cyclase to cGMP to PKG
- inhibit IP3 (dilation)
- stimulate MLC phosphatase; decreases MLC (dilation)
- stimulates K+ channel; ends contraction
- inhibits L-type Ca2+; decreases contraction
- stimulates pump to get rid of Ca2+
compliance
how easily a heart chamber or blood vessel expands when filled with blood (pressure)
veins
high compliance
low elasticity
arteries
low compliance
high elasticity
LARGE volume change but small pressure change
veins
LARGE pressure change but small volume change
artery
venous blood reserve
central reflexes can decrease compliance of veins to supply more blood to the arterial circulation as needed
structures for venous circulation
skeletal pump
valves
respiratory pump
skeletal pump
veins pass through here and when muscles contract they press on veins and blood moves
respiratory pump
drop in pressure in chest cavity during inhalation reduces pressure on the veins and allows blood to flow back up to the heart
flow =
(change in) pressure / resistance
change in pressure =
P artery - P venous
systemic circulatory pressure > total peripheral resistance
flow
why is the flow in the capillaries not zero?
the systemic circulatory pressure is greater than the total peripheral resistance
resistance is proportional to
length
viscosity
turbulence
resistance is inversely proportional to
radius
vascular networks
parallel vessel circuits
vessel series
parallel vessel circuits
lower resistance (capillaries)
vessel series
high resistance
flow =
velocity x area
if flow is constatn
velocity = 1/area
poisseuille’s law
predicts blood flow rate in a vessel
viscosity and length dictate this
filtration
removal of solutes from blood to deliver to tissues
driivng force of filtration
hydrostatic pressure forces fluid OUT of the capillaries
reabsorption
wastes and water into capillaries
driving force of reabsorption
oncotic pressure brings fluid BACK into the capillaries
net filtration pressure =
net hydrostatic pressure (NHP) - net colloid oncotic pressure (NCOP)
sigma for NFP
adjustment for pressure; reflection coefficient
1 < s < 0
high: low protein permeability, concentration is important
low: high permeability, more even and less important
filtration > reabsorption
net leakage of fluid
Kf
filtration rate
high Kf
high water permeability
low Kf
low water permeability
lymphoid tissues
nodules, tonsils, adenoids, MALT
tonsils
germinal centers for B cell proliferation
lymph organs
nodes, thymus, spleen ; immune function site
first line of defense
prevention of infection
second line of defense
targeted destruction of pathogens
third line of defense
specific targeting of pathogens (immunomemory)
bacteria protists parasites fungi
living cells with biochem machinery needed
control points nonspecific defenses
point of entry
disruption of life cycle
interfere w toxins
point of entry control point
block receptor binding
disruption of life cycle control point
slow growth of pathogen until immune system can destroy it
interfere w toxins
block toxin release
physical / chemical barriers
1st
skin and linings
protective chemicals (acidity, lysozyme, antimicrobial peptides)
mucous membranes (traps particles and organisms, transports)
phagocytes
2nd
microphages: neutrophils, eosinophils
macrophages
macrophages
monocytes (bone marrow and blood)
langerhaans cells (skin and mucosa)
osteoclasts (bone)
microglia (CNS)
red pulp (spleen)
immunological surveillance
2nd
monitor cells for abnormal markers (AB and complement proteins)
attack and kill abnormal cells (pathogens and self cells w bad marker)
interferons
2nd
small proteins released in response to viral infection
complement system
2nd
3 pathways for protease cleavage but end at MAC
MAC
pokes holes in membranes to kill pathogens
inflammatory response
2nd
increased flow of plasma and leukocytes to tissue
elevated phagocytosis, activated hemostasis, activation of complement, response termination
fever / pyrogenesis
pathogen inactivation
elevate body temp
increased leukocyte movability, increased phagocytosis, increased T cell proliferation, increased interferon activity, DECREASE endotoxins
can damage cell
naturally acquired passive immunity
transfer of maternal antibodies across placenta
induced passive immunity
administration of AB to combat infection (booster shot)
induced active immunmity
develops after admin of antigen to prevent disease (vaccines)
naturally acquired active immunity
develops after exposure to antigens in environment
humoral response
B cells + MHCII + CD4 on Th
neutralization
agglutination
opsinization
cell mediated response
Tc regulate and kill infected cells + nucleated cells + MCH1 + CD8
BCR
Fab and Fc portion can be secreted as AB
TCR
alpha and beta chains never secreted; CD3
somatic recombination
in bone marrow when making WBC
germline DNA – SR – DJ rearranged – SR – VJ and VDJ joined – transcription
IgM
all areas in response to infection
secreted as pentamer
IgA
mucosa linings, dimer, fight off microbes in body secretions
IgG3
blood plasma placenta to fetus
signals macrophage in infection
IgD
least prevalent
IgE
epithelia, mast cells histamine, inflammation
primary diversification (during development)
somatic recombination
junctional diversity
combinatorial diversity
junctional diversity
VDJ and VJ shuffling: nucleotides randomly insert
combinatorial diversity
different heavy and light chains can pair
secondary diversification (after activation, B cells)
somatic hypermutation
isotype switching
somatic hypermutation
selects for AB that binds tighter to pathogen
isotype switching
constant region switch
MCH1
1 bound domain, short
MCHII
2 domains, medium
anergic
no response need antigen and sitmulatory proteins
