heart, hormone, immuno Flashcards
cardiac output formula
CO = SV x HR
how to increase CO?
Increase heart rate
increase contractile strength of muscle
Frank-Starling law: increase ‘stretch’ of heart muscle by increasing amount of venous return
how to increase venous return?
increase total blood volume (this is done by retaining water in nephrons)
and contraction of large veins can increase venous return too
order of events in cardiac action potential
Depolarization when fast sodium channels open
Slight dip when Na closes and K channels open, causing k to leave
Plateau maintained by slow calcium channels opening
Repolarization when Ca channels close
RMP when K channels finally close and the ATPase gets to work.
action potential of the SA node (this is the pacemaker, not the AV node)
Self-depolarization: slow influx of NA through leak channels
Depolarization: Ca rushes in when voltage gated channels open
Repolarization: K rushes out when voltage gated channels open
where do APs travel in heart?
SA node > atria depolarize and contract > travel down INTERNODAL TRACT > AV node (where it is delayed) > AV bundle (bundle of His) > R and L bundle branches > Purkinje fibers (only now do ventricles contract)
autonomic reg of HR
vagus nerve synapse near the SA node and release ACh. This provides a constant level of inhibition called VAGAL TONE
As for symp, there are sympathetic neurons dropping NE directly on heart. Also, epinephrine from adrenal medulla binds to receptors on muscle cells
Lastly, there are BARORECEPTORS in carotid arteries and aortic arch that measure bp and hence adjust HR
blood pressure
directly proportional to CO and peripheral resistance.
local autoregulation
blood flow control on a local level. Certain metabolic wastes cause arteriolar smooth muscle to relax, thus increasing perfusion
erythropoeitin
made in kidney, stimulates RBC production in bone marrow
hemolytic disease of the newborn
when Rh- mother has an RH+ baby, during birth some Rh+ cells will sensitize mother, who’ll produce anti-Rh Abs. The second Rh+ baby will be killed, because these Ab can cross placenta
chemotaxis
movement of WBCs directed by chemical signals
megakaryocytes
give rise to platelets, RBCs, and WBCs
thrombin
converts fibrinogen to fibrin (the clotting protein)
what can decrease Hb’s affinity for O2?
binding fewer O2 (cooperativity) more acidity increased PCO2 increased temperature ^ as you can see, the last 3 are all hallmarks of a tissue during exertion. Therefore the O2 falls off Hb for the cell's use
3 ways CO2 is transported
it turns to bicarbonate by carbonic anhydrase, an enzyme inside RBCs
Some can be bound to hemoglobin
And some can simply be dissolved in plasma (it is more soluble than O2)
which 2 WBCs can squeeze through intracellular clefts?
macrophages, neutrophils because they are capable of amoeboid motility
why is oncotic pressure important?
Proteins dissolved in plasma draw water back into capillaries. Salts are no substitute because their ions can also diffuse out
chylomicrons
a lipoprotein package used to transport fats in the bloodstream
the complement system
proteins called complements in blood bind to specific motifs on bacteria, leading to their destruction
IgM
involved in initial immune response. Pentameric in blood; monomeric on B cell surfaces
IgG
the main enzyme. Located in blood and it alone can cross placenta
IgD
serves alongside IgM as the antigen receptor on B cell surfaces
IgA
located in secretions including breast milk. Dimer structure.
IgE
located in blood, used in allergic reactions
epitope
the part of an antigen which Abs recognize
hapten
the smaller molecule bound to a large molecule like a protein
Abs have these functions against pathogens
binding to antigen may physically inactivate pathogen, such as preventing virus from entering cells
The antibody’s binding can also induce phagocytosis
The antibody binding can also activate complement system to punch holes in cell membrane
B cells
these are what produce antibodies
Plasma cell - these actively produce antibody
Memory cell - remains dormant in lymph nodes for the same infection in future
T cells
T helpers - CD4. These activate B cells, killer cells, and others. It communicates with lymphokines and interleukins
T killers - CD8. It destroys certain cell types: virus-infected, cancerous, and foreign cells from a transplant
MHCI and II
MHC I are found on the exterior of every nucleated cell. They randomly bind peptides from inside the cell to display on the surface (so T cellscan find them)
MHC II, whereas, are only found on the APCs. They phagocytose cells and display the fragments using MHC II. This will activate B cells
bone marrow
synthesizes all blood types
spleen
a lymphoid tissue, where B and T cells surveil lymph. Spleen also recycles aged RBCs
thymus
the site where T cells mature
difference btw Ab light and heavy chains?
while both have constant and variable domains, its only the heavy chains that define the class of antibody (IgM, IgA)
Hb - O2 curve
it shifts LEFT in conditions of low acidity and CO2 and temp
it shifts RIGHT when high acidity, CO2, temp
However, PO2 does not shift the curve
