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Flashcards in LO Fluids Deck (26)
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Body water content, including major components

Total body water is 42L, intracellular is 28L (cl 20mM) , extracellular is 14L wiith interstitial(cl 116mM), plasma (cl 102,) and transcellular (variable solute) fluid inside it :)
Measure water content with diluted dyes


COmpare and contrast units used to express body fluid solute

*write this on cheat sheet with the cranial nerves*
mOsm/kg/hso osmolality (no temp dependent)
mOsm/L h20 osmolarity (temp dependent) active solute per h20 unit.
Active particle: can cause movement within sodium

Na+: 1mmol, 1mEQ, 1Osm
Ca2+ 1mmol, 2 mEQ, 1 OSM
NaCl: 1mol, 2 Eq, 2 Osm


explain gibbs donnan effect and how it accounts for subtle differences in ionic compositions of plasma and interstitial fluid

when its permeable to some but not all molecules. the liquid will shift to make it work for osmolarity gradient.


discuss transport of body fluids between different fluid compartments and consider how differences in selective periability are involved in regulating transport

Between plasma and interstitial: across endothelial cells (blood capillaries and lymphatic capillaries

Between Cells and Interstitial: across cell membrane

Between transcellular and interstitail: across epithelial cells.
determined by permeability and small solutes (regulated by ATPase and it takes up 20% of your daily calories to do this)


Describe plasma and plasma water and major body solutes

Plasma water has more solute in mEq/L than plasma volume itself. same amount of sodium just expressed differently.

Major solutes: extracellular: Na, Ca, Cl, Hco3
intracellular: K, Mg2+, po4, protiens.


outline composition of blood and describe its functions

erythrocytes (RBC)
monocytes (WBC)
granulocytes (WBC)- basophils, neutrophils, eosinophils, all have granules-
lymphocytes (WBC- immune response)
thromocytes (Platelets)

and plasma

Blood is important for respiration, nutrition, excretion, homeostasis, communication, hemostasis, immune function :)


define hemeatocrit and discuss how changes in hematocrit show blood idsorders

Blood volume. Red blood cells.
- plasma 55 percent, RBC 40 percent, buffy coat < 1

anemia: not enough hemocrit (30) hard to get 02 to tissues
polycythemia: too much hemocrit (70) makes blood viscous


discuss roles of proteins found in plasma

albumin, 55%, globulins 38% (larger weight) , fibrinogens 7%

albumin: oncotic pressure and transport
lipoproteins: lipid transport
glycoproteins: transferrin, haptoglobins, cerulopoasmin (cu binding)
Coagulation factors

Erythrocytes have a 120 day life, different maounts in males and females (more in males)

neutrophils bacetrial fungi, lymphocytes, immune function b cells immunoglobulin, natural killer cells,


explain process of hematopoeisis and identify factors involved in differentiation. specifically erythropoesis?

*something you wanna put on a cheat sheet girl*

Long term hematopoietic stem cell to short term to common myeloid progenitor to MEP and then PFUE and then ERYTHROPOETIN and IL3 make it CFU-E and turns into RBC :) d

Hemoglobin is synthesized
once a reticulocyte released into bloodstream, its mature in2 days. theres a long period of it losing the nucleus (reticulocyte) then mitochondria and ribosomes
Erythrocytes: biconcave dis 8um long, high SA to volume ratio. No nucelus. deformable. rouleaux formation (they stack) high permeability to ions and high carbonic anhydrase [ ]. hemoglobin and gas content high.


explain erythropoietin and describe how it promotes erythropoiesis.

hormone that regulates new erythrocytes. hypoxia sensed in the kidneys and hif1a and b promote EpO synethesis.
epo inhibits apoptosis in burst forming and colony forming erythroids


where do we produce blood cells?

hematopoietic organs vary across lifespan.
before birth its mostly bone marrow, and then as you get older its mostly vertebrae pelvis, then sternum then ribs then arm/slegs


hemolysis and crenation?

hemolysis: low ECF solute [] leads to water coming in
crenation: high ECF solute [] leads to water going out


what are the factors involved in erythropoeisis?

1. tissue oxygen (due to hemorrahge or high altitude)
2. erythropoetin (produce din kindey)
3. cytokines il3
4metals: iron for heme and copper for ceruloplasm
5. folic acid and b12
6. sex steroids: testosterone INCREASES
estrogen DECREASES


what are the factors involved in erythropoeisis?

1. tissue oxygen (due to hemorrahge or high altitude)
2. erythropoetin (produce din kindey)
3. cytokines il3
4metals: iron for heme and copper for ceruloplasm
5. folic acid and b12
6. sex steroids: testosterone INCREASES
estrogen DECREASES


outline handling of iron and describe its incorporation into heme during hemoglobin synthesis

Iron Metabolism
1. absorbed via stomach and recycled (most of it)
2. oxidation (ceruloplasmin oxidizes fe2 to fe3)
3. transferrin binds fe3 and takes it to blood
4. iron delivered to tissues with transferrin receptors (bone marrow)
5. fe3+ encorporated into erythroblasts. fe3 reduced to fe2 and put into heme = which goes into hemoglobin
- fe3+ in cytosol is reduced to fe2 by ferrireductase for entry into mitochondria
- OR stored as fe3 in cytosol
- ferrochelatase puts fe2 into protoporphyrin (mitochon) to make the heme. iron IN the poryphorin RING.
-poryphorin ring is made by gylcin and succinyl coA and vit B to make the ring in the mitochondria.
6. excess is stored in bone marrow and liver.


describe structure of hemoglobin and differentiate adult and baby hemoglobin

heme joined with polypeptide chain. to form hemoglobin chain alpha or beta)
Adult hemoglobin (HbA) 4 hemoglobin chains, 2 of each kind. and a heme group.
- each can bind 4 o2 molecules, each to the ferrous iron in the heme groups

= when one binds, makes the others easier
= when o2 needs to be delivered, it will unbind and it can also interact with other gases!
= low pressure: better dissocation

2 parts found in blood HbF (fetal): and HbA
Fetal has a different shape, and can bind at a lower partial pressure meaning that baby gets all the blood !!

Alpha: chromosome 16 (main hemo)
Beta: chromosome 11 (main hemo)

by 18 weeks, mostly a and b hemoglobin but
fetus is mostly using alpha and gamma chains.


discuss disorders associated with abnormal hemoglobin synthesis and factors influencing their severity

POLYPHYRIAS; too much porphyrin precursors in marrow (erythropoetic) and liver (hepatic). An absence of any 8 enzymes can cause this.
- cant form heme groups
Vampire disease: (sunlight, gums, garlic, can't get enough blood)

THALASSEMIAS: reduced synthesis of a polypeptide chain alpha, or beta. this reduces o2 binding. fatal in utero. promote too much EPO cause you think you have decreased o2, but thats not true you just can't bind it! Treatment: blood transfusion.

SICKLE CELL DISEASE: hemoglobin changed structure of the beta chain. causes long aggregates of RBC and they can cause blockages. carrying the gene is actually beneficial against malaria. can't form actin!!


explain pathway of erythrocyte degradation and excretion, outline rates of various components of hemoglobin metabolism.

120 days later...

weakening of the membrane, trying to fit through small spots and it ruptures (especially in the spleen)
Hemoglobin undergoes phagocytosis by tissues and macrophages (reducoloendothelial system)
- monocytes enter tissue and become macrophages (bone marrow and spleen), they break away in degradation with kupffer cells from the liver.

Globin broken down into amino acids
The heme releases Fe2 which goes in plasma by transferrin
Poryphoryn broken into chain of 4 nuclei which is made into biliruben.
BIliruben binds albumin for transport to plasma.
Biliruben is taken up and conjugated with glucuronic acid to form biliruben glucuronide. secreted from bile duct into small intestine for excretion.
50% of conjugated bilirubin is converted to urobilinogen is reabsorbed into blood.
Urobilinogen re-excreted by liver or to kidneys to become urine.


Outline maturation of megakaryocytes and generation of platelets

TPO from the liver stimulates this in bone marrow.
Platelets break off of the megakaryocytes (in fragments)
Platelet formation occurs in bone barrow and then goes into circulatino

- disc
-no nucleus
- 2-3um
- can alter shape
contain granules (alpha - coagulation factors etc (more of these in the slides) .) and dense - adp atp ca and serotonin )


outline the three components of the hemostatic response and discuss how these components influence each other

1. Vasoconstriction
2. Platelet pathway : primary (influences the other two through phospholipids and serotonin and thromboxane and adp)
3. Blood coagulation cascade

Vasoconstriction: immediate response: local (neurogeneic/myogenic spasm with short and long response) to increase pressure in tissues.
also release humoural substances (serotonin, endothelins, clotting factors) serotonin and endothelins promote vasoconstriction.


describe platelet response to vascular injury and explain how the response is isolated to the site of injury

When vessel wall is damaged, it platelets adhere to VMP mediated by glycoproteins on the platelet surface
and exposed collagen

Platlets undergo a change and release their alpha and dense granules (ADP and fibrinogen)

Psuedopodia makes them spiky and sticky to other platelets.

ADP stimulates thrombozane A which vasoconstricts and makes more platelets (positive feedback)

THis forms an unstable plug. (might stop little injuries)
localized due to PROSTACYCLIN.

PROSTAGLANDINS: prostacyclin and thoomboxane A.
In healthy tissue: prostacyclin (in endothelial cell) inhibits platelet aggregation by reducing ca with high Camp levels
In damaged tissue: thomboxane A (in platelet) makes aggregation.


describe the initiation and amplification of clotting/coagulation cascade

Create stable fibrin clot to strengthen the plug and complete the seal. Requires THROMBIN which acts on FIBRINOGEN to make a clot.
localized and maintained through negative feedback loops. 3 enzyme complexes (extrinsic (10a), intrinsic (10a) and prothrombinase (thrombin)) all have calcium all have phospholipid membrane.


outline the factors involved in the prevention of hemostasis (anticoagulation)

Physical factors: smooth vessels
Vasodilators (noepinephrine as a dilator) PgI
Endogenous anticoagulants (so many on the slides plz put on sheet)
Exogenous anticoagulants: heparin, ca chelators,


describe the common disorders of hemostasis and consider the complications associated with these factors.

Platelet abnormalities
Thrombocytopenia (platelet deficiency)
Thrombocyosis (excess platelets)

PA1 deficiency

Coagulation defects
- vit K (clotting factors )
Hemophilia: deficiency of specific factors injury results in uncontrolled bleeding
- type a: factor 8
-type b: factor 9
both intrinsic ..

Von Willebrand Disease: no good platelet adhesion (vacor 8 and vwF)


whats thrombin for?

platelet aggregation
conversion of fibrinogen into fibrin monomers and polymers
activation of 13 into 13 a to make stable fibin mesh
intrinsic Xase activation :)
* this concept is a little fuzzy, if time watch the lecture again.


whats thrombin for?

platelet aggregation
conversion of fibrinogen into fibrin monomers and polymers
activation of 13 into 13 a to make stable fibin mesh
intrinsic Xase activation :)
* this concept is a little fuzzy, if time watch the lecture again.