Term
| what is the phrenic motorneuron pool? |
|
Definition
| just what it sounds like. probably located at c3,4,5. |
|
|
Term
| what are the crossed synaptic pathways? |
|
Definition
| rarely used pathways between contralateral nerves in the spinal cord |
|
|
Term
| in the baker herman article, the scientists did something completely counterintuitive. they took a man who couldnt breathe, and gave him LESS oxygen. why? |
|
Definition
|
|
Term
| does intermittent hypoxia increase or decrease ipsilateral phrenic nerve activity? |
|
Definition
|
|
Term
|
Definition
|
|
Term
| what happens 60 minutes post hypoxia in control patients? |
|
Definition
| you get long term facilitation |
|
|
Term
| where did baker-herman et al measure BDNF levels? |
|
Definition
|
|
Term
|
Definition
| artificial cerebro spinal fluid |
|
|
Term
| what is methysergide? how does this relate to BDNF levels? |
|
Definition
| it is a seretonin inhibitor/antagonist, and it blocks BDNF metabotropically |
|
|
Term
| what is emetine? how does this relate to BDNF levels. |
|
Definition
| inhibitor of protein synthesis. which means BDNF was newly synthesized to cause the long term facilitation |
|
|
Term
| What is CSNX? what happens to BDNF when we do this? |
|
Definition
| carotid nerve cut. when we do this, we decrease BDNF levels. |
|
|
Term
| what is hypercapnia? what happens when we do this |
|
Definition
| high CO2. this increases breathing RATE (not tidal volume like hypoxia. |
|
|
Term
| baker herman et al, what did they show between BFND and long term facilitiation? |
|
Definition
| they were strongly positively correlated. when bdnf increases, ltf increases. |
|
|
Term
| what is siRNA? how did the researchers use this in the BDNF study? |
|
Definition
| small interference RNA. it blocks the mRNA that is used to synthesize BDNF |
|
|
Term
| what happens when you just inject someone with BDNF? |
|
Definition
| you get the same pLTF. so you don't have to make them hypoxic to get this result |
|
|
Term
|
Definition
| it is a molecule that acts on (inhibits) the BDNF receptor which is a tyrosine kinase. if you inject these together, you don't get the same pLTF (BDNF has to bind to its receptor) |
|
|
Term
|
Definition
|
|
Term
| what do the siRNA parts of the experiment purport to show us? |
|
Definition
| this change is happening at the transcriptional/translational level. |
|
|
Term
| what is the sequence of events from spinal cord injury to hypoxia? |
|
Definition
| SCI @ c2 --> cut descending path to spinal cord -->decrease phrenic nerve drive --> decrease diaphragm activity--> hypoxia |
|
|
Term
| how does intermittent hypoxia lead to increased phrenic drive? |
|
Definition
| intermittent hypoxia -->sensed by carotid bodies (doesnt work if you cut it CSNX)-->this signal goes to the respiratory generators in brainstem-->increase drive to phrenic motor pool through ligand gated channels (excitatory: glutamate). |
|
|
Term
| how does serotonin work in the CNS |
|
Definition
| reticular systems in your brainstem release serotonin. this makes your cns more excitable or aroused in the same way that epinephrine does in the peripheral nervous system. this serotonin modulates the motor pool activity by making the phrenic nerve more excitable by decreasing activity of potassium leak channel permeability. |
|
|
Term
| what happens when we decrease permeability of K+ leak channels? |
|
Definition
| the resting potential of the membrane would increase, making it easier to get an action potential. |
|
|
Term
| what increases Ca+2 permeability? |
|
Definition
|
|
Term
| what increases BDNF synthesis? |
|
Definition
|
|
Term
| once bdnf is made, does it just work inside the cell? |
|
Definition
| no. its an autocrine response, so it leaves the cell and has to then attach to the K252a receptor (we know this because if we block k252a, it doesnt work!) |
|
|
Term
| so over 90 minutes, we can modulate excitability and get new/more synaptic vesicles. These long term cascades will decrease the membrane potential which would increase inward Na+/Ca+2 |
|
Definition
|
|
Term
| is rest important in this BDNF system? |
|
Definition
| yes! if you gave sustained hypoxia, the system doesnt get time to recover and improve. |
|
|
Term
| what are the general functions of blood? |
|
Definition
Distribution of nutrients/gases to
or from appropriate places
Chemical messenger/transport
system
Regulation of body temp., pH,
electrolytes, glucose, etc .
Maintenance of interstitial and
vascular fluid volume
Immune responses/protection
against infectio |
|
|
Term
|
Definition
RBCs - anuclear (not “true”
cells |
|
|
Term
|
Definition
granulocytes vs
agranulocytes |
|
|
Term
|
Definition
cell fragments of
megakaryocytes |
|
|
Term
| where are megakaryocytes located? |
|
Definition
|
|
Term
| what is the packed cell volume distribution of blood? |
|
Definition
acked cell volume (42-45%)
99% RBCs – Hct ~ O2
-carrying |
|
|
Term
| what is plasma made of, and what does it do? |
|
Definition
90% H2O + proteins – absorbs and
distributes heat |
|
|
Term
| what other inorganic/organic substances are in blood? |
|
Definition
electrolytes – composition of interstitial
fluid ~ sea water
nutrients, wastes, hormones |
|
|
Term
| what plasma proteins are in blood? |
|
Definition
albumin - genereated by the liver, to exert an osmotic pressure and regulate fluid volume.
-globulins
alpha,beta – bind/transport products (cholesterol)
alpha– inactive proteins that become active
gamma– immunoglobulins - antibodies
fibrinogen |
|
|
Term
| how are parts of blood produced in bone marrow? what is its structure |
|
Definition
highly cellular in red (active) vs.
yellow (inactive)
connective tissue matrix - reticular cells
multipotent stem cells
variable adipose tissue pockets
large vascular sinusoid |
|
|
Term
| what are the functions of bone marrow? |
|
Definition
hemopoiesis
phagocytosis
iron storage/recycling
antibody production
cellular reserve storage |
|
|
Term
| what are the steps in regulation of hemopoiesis? |
|
Definition
| pluripotent hemopoietic stem cells (these cells can either be lymphoid cells or myeloid cells. these then become colony forming units (committed). immature cells are produced. there is growth factor regulation that is done with glycoproteins that are produced locally. others eg interleukins, stem cells, colony stimulation factors, EPO |
|
|
Term
|
Definition
| hemoglobin is cranked out at this stage. |
|
|
Term
| what is a reticulocyte and how do they mature? |
|
Definition
| they are immature RBCs. they extrude their nuclei, and they increase their levels of granular RNA so they can still crank out hemoglobin |
|
|
Term
| low O2 levels detected at kidney -stimulates....... |
|
Definition
|
|
Term
tem cell interaction –
2-3 million/sec
time frame??
gender differences??
environment? |
|
Definition
time frame - 1 week,
gender differences - men have higher % hematocrit
environment - colorado training |
|
|
Term
| what is the structure of hemoglobin? |
|
Definition
globin – four folded
polypeptide chains
heme – four non-protein, Febinding groups |
|
|
Term
| how is CO2 transported on hemoglobin> |
|
Definition
| 30% is bound to Hg, but 60% is converted to bicarbonate. |
|
|
Term
| what would a % hematocrit be for an anemic? |
|
Definition
|
|
Term
| what would a hematocrit level be for someone with polycythemia? |
|
Definition
| 60% or more becomes dangerous. |
|
|
Term
| when you are dehydrated what happens to your percentage of hematocrit? |
|
Definition
| it increase to 70% or so. thats why dehydration is dangerous! |
|
|
Term
| what are some different type of anemia? |
|
Definition
| iron deficient anemia (same number of RBC's, but no iron to bind the O2), RBC production anemia can be an issue with low folic acid or b12 |
|
|
Term
| what causes sickle cell anemia and what is the problem with it? |
|
Definition
| a single nucleotide change in the DNA makes it so deoxygenated RBC's sickle. can cause problems with clotting and O2 |
|
|
Term
|
Definition
destruction of bone
marrow
Related to marrow disease (leukemias –
overproduction of immature leukocytes)
Secondary to radiation therapie |
|
|
Term
|
Definition
emolytic-uremic syndrome
verotoxin (E. coli) attaches to vascular
endothelium, non-inflammatory coagulation
Causes mesh of activated platetes, RBC
shearing
malaria –parasite protozoan
replication/RBC destruction
Sickle cell is a hemolytic anemia |
|
|
Term
| what are some clinical signs and symptoms of anemia? |
|
Definition
skin pallor (palms, nailbeds)
fatigue, listlessness
dyspnea on exertion - increased heart rate, palpitations
CNS symptoms - headache, drowsiness, dizziness: pernicious anemia)
Sickle cell – painful ischemic episodes, CVAs |
|
|
Term
| what are some clinical signs and symptoms of polycythemia? |
|
Definition
dizziness, fatigue, blurred vision
cyanosis
clubbing
hypertension, feeling of “fullness” in head |
|
|
Term
| leukocytes (white blood cells) are either granular or agranular. what types of WBC's are in each group? |
|
Definition
Granular - (neutrophils, eosinophils,
basophils) - granules =
lysosomes/vacuoles with
heparin/histamine
agranulary - monocytes/macrophages, lymphocytes. |
|
|
Term
| what are neutrophils? what is their function? |
|
Definition
olymorphonuclear (PMN) leukocytes
phagocytotic – engulf bacteria,
dead/damaged tissue
1st responders (margination, adhesion,
emigration)
prolonged attacks – liquefy hosts
elevated number with bacterial
infections |
|
|
Term
|
Definition
| dead neutrophils and their phagocytosed bacteria/damaged cell parts |
|
|
Term
| what are some properties and function of eosinophils? |
|
Definition
1-3%; lifespan ~ 8-12 days
Primary function –
parasite destruction
allergic/inflammatory responses
phagocytosis of antigen-antibody complex
suppression of other WBCs |
|
|
Term
| what are some properties and function of basophils? |
|
Definition
% - lifespan ~ hours-days
Primary function – allergic reactions
degranulation/rupture
allergens bind to IgE receptors
release of heparin/histamine
dilation/ leakage
bronchoconstricution
granulocyte attraction
mast cells in CT |
|
|
Term
| what are some properties and function of monocytes/macrophages |
|
Definition
lifespan ~ 3 days – depends on status
primary functions
settle in tissues – macrophages
capture antigens for presentation –
cell and humoral immunity
synthesize interleukins -attraction/activation of WBC |
|
|
Term
| what are some properties and functions of lymphocytes? |
|
Definition
Primary function – immunity
B-type –bone marrow - antibody-mediated
immunity
T-type – Thymus cell-mediated
cytoxic, helper, suppressor, regulatory |
|
|
Term
|
Definition
| regulation or stopping the flow of blood |
|
|
Term
| what are some of the steps of hemostasis? |
|
Definition
1. vascular spasms
2. formation of a hemostatic plug by platelet aggregation at endothelial collagen damage. there are some local chemical mediators of this process. |
|
|
Term
| what are the three roles of the hemostatic plug? |
|
Definition
1) platelet contraction (filamentous
interaction)
2) chemical release (norepinephrine,
serotonin)
3) assist in coagulation (3rd step) |
|
|
Term
| how does coagulation work? |
|
Definition
solid gel transformation (supporting platelet plug)
conversion of fibrinogen to fibrin
catalyzed by enzyme thrombin at injury site
12 different “clotting factors” responsible for
process
most proteins synthesized in liver
two pathways
simultaneous/amplified
intrinsic vs. extrinsic pathway |
|
|
Term
| what is the intrinsic pathway of coagulation? |
|
Definition
happens within the bloodstream
Inactive factor XII →Active factor XII (Hageman)
damaged vessel surface
foreign substance
↓
Inactive factor XI →Active factor XI
↓
Inactive factor IX →Active factor IX
↓
Inactive factor X →Active factor X
↓
Prothrombin →Thrombin |
|
|
Term
| what is the extrinsic pathway of coagulation? |
|
Definition
Tissue thromboplastin (factor III; tissue damage)
↓
Inactive factor X →Active factor X
↓
Prothrombin →Thrombin
↓
Fibrinogen →Fibrin
Fibrin (loose network) + Factor XIII →Fibrin (stabilized
network) |
|
|
Term
| how does this clot eventually dissolve? |
|
Definition
platelets secretion attract fibroblasts from surrounding tissue. lot dissolved by plasmin activation (plasminogen
derivative)
activation at lungs by tissue plasminogen activator. assisted by basophils, mast cell secretions. |
|
|
Term
| what are some clotting disorders? |
|
Definition
excessive/abnormal clotting - generation of thrombus – embolus
damaged endothelial lining
slow-moving blood (atria, venous system)
trauma (tissue thromboplastin into blood)
decreased clotting
genetic disorders of clotting factor generation (Factor VIII or IX – Xlinked)
platelet deficiency (thrombocytopenia – also seen in leukemias)
Vitamin K deficiency |
|
|
Term
| what are some signs/symptoms of thrombocytosis? |
|
Definition
thrombosis (signs of ischemia)
easily bruised
typically asymptomatic |
|
|
Term
| what are some signs/symptoms of thrombocytopenia? |
|
Definition
Petechiae (purple, pinpoint hemorrhages)
External hematomas, severe bruising
GI, CNS bleeding are life-threatening |
|
|
Term
| what are some signs/symptoms of hemophilia? |
|
Definition
Hemarthrosis (1st
yr. and just afterwards
with ambulation)
Muscle hemorrhages (increase blood loss)
– nerve impingement
Signs of increased bruising |
|
|
Term
| what are the general functions of the immune system |
|
Definition
| infection, wound healing, opposition of foreign matter |
|
|
Term
| what is the innate immune system? |
|
Definition
non-specific, no memory
First line of defense - Physical/chemical mediators
Second defense – cellular mediators
phagocytes and natural killer cells
soluble factors |
|
|
Term
| what is the adaptive or acquired immune system? |
|
Definition
pecificity and memory against antigens
active
requires prior antigen exposure
relatively permanent; natural vs. artificial (vaccine)
passive
presence of antibodies
temporary; natural (mothers milk) vs. artificial |
|
|
Term
| is the epidermis part of the immune system? |
|
Definition
yes. its innate immunity. hin outer layer,
waterproofed
(keratinized) dead cells
Langenhans cells |
|
|
Term
| is the dermis part of the immune system? |
|
Definition
| yes. innate immunity. thick inner layer, massive CT, mainly elastin. massive amount of vasculature. |
|
|
Term
| where are your mucuous membranes part of the immune system? |
|
Definition
GI, GU, respiratory tracts
Secretion of mucous (goblet
cells), propulsion (cilia) |
|
|
Term
|
Definition
it is one of the first chemical lines of defense. Oily, protective layer
Fatty acids inhibitor some bacterial/fungal growth |
|
|
Term
| how is pH part of the immune system? |
|
Definition
| decrease ph on the skin and GI inhibit bacterial growth. |
|
|
Term
|
Definition
destroys various bacteria (saliva,
nasal secretions, tears) |
|
|
Term
| What is the second line of defense, the cellular mediators? |
|
Definition
neutrophils
macrophages/monocytes
antigen presenting cells
release interleukins/cytokines – stimulate specific immunity
eosinophils - parasitic, allergic reactions, also modulatory
basophils – histamine/heparin release
natural killer cells
non-specific lysis of virus-infected ormalignant cells |
|
|
Term
|
Definition
| soluble mediators released from virus infected cells. blocks viral replication of neighboring cells. stimulate B, T, and NK Cells. |
|
|
Term
| what are complement proteins? |
|
Definition
| plasma protein cascade active with antibodies, foreign cells. these form membrane attack complexes. serve as chemotaxins and opsonins. |
|
|
Term
| how do antibodies activate the complement system |
|
Definition
| antigen antibody complex starts it, ends with membrane attack complexes |
|
|
Term
| what is the alternative pathway to the complement system> |
|
Definition
| bacterial microbial surface polysacharrides signal the start of this pathway, and then it ends with the formation of membrane attack complexes |
|
|
Term
|
Definition
| something that coats a surface to inactivate it. |
|
|
Term
| how does the acquired immunity work? |
|
Definition
| we need to recognize self vs nonself. we do this by recognition of antigens. |
|
|
Term
|
Definition
| its a protein or lipid. it has a subunits called an epitopes. these epitopes are all places that can be recongnized by other cells. when these are foreign, they will bind to antibodies and then to t-cell receptors |
|
|
Term
| what is the major histocompatitbility complex? |
|
Definition
HLA
class I - all nucleated cells, viral antigen presentation
Class II - on AntigenPreventingCells, serve as platform |
|
|
Term
| what is antibody structure like? how are they produced? |
|
Definition
| there are heavy chains + light chains. made in bone marrow and lymph. antibodies are similar to t-cell receptors |
|
|
Term
| give an overview of humeral mediated immunity |
|
Definition
B-cell binding/ingestion of antigen
antigenic fragments on MHC II platforms
memory cells – retain specificity
plasma cells – clones to release antibodies
Functions:
Increase phagocytosis + stimulate T cells
Activate complement system |
|
|
Term
| what are the subtypes of antibodies/immunoglobulins? |
|
Definition
IgM- produced first, secreted early
IgG - major AB of secondary responses
- newborn protection for first 6 mo.
IgA - mucosal defense, transmitted in breast milk
IgD – B-cell surfaces
IgE – parasitic, allergic reactions |
|
|
Term
| IGM --> IGG. which one is more active? |
|
Definition
| IGM is relatively inactive. once it attaches to its antigen, it changes to IGG which is very much more active |
|
|
Term
|
Definition
| also known as packed cell volume (PCV) or erythrocyte volume fraction (EVF), is the volume percentage (%) of red blood cells in blood. |
|
|
