Blood Typing Flashcards
What is plasma, and what are formed elements?
Plasma - fluid content of blood - H2O, proteins, ions
formed elements: platelets, WBC, erythrocytes
What is the difference between serum and plasma?
serum - plasma minus clotting factors
- albumin, globulin, regulatory proteins
Plasma - serum PLUS clotting factors
What is albumin?
most abundant protein in blood
- made in liver
- regulates plasma osmotic pressure: regulates where water is found in vessels and tissue fluid
- helps transport steroids and bilirubin (lipids)
What are globulins?
some types made by liver
- transports metal ions, lipid, fat soluble vitamins
others made by plasma cells during immune response - antibodies
transferrin
What are the clotting proteins and where are they made?
made in the liver
fibrinogen, prothrombin
- activated by Ca in the blood
- liver damage greatly affects clotting ability
- chelators bind to Ca and prevent binding to clotting proteins - prevent coagulation
What happens when the body needs more oxygen?
kidneys release erythropoietin to increase RBC production
- binds to receptor on the RBC progenitor cell (proerythroblast)
What is erythropoiesis? Describe the steps
RBC development from the hemocytoblast
chromatin becomes uncoiled, DNA separate to allowed transcription for hemoglobin
as hemoglobin builds up, nucleus is condensed
nucleus extruded from the cell prior to leaving the bone marrow
reticulocyte - last stage prior to becoming full erythrocyte
- contains strands of Ribosomal ER: typically not found in whole blood unless body is stressed to make more RBC
What is a reticulocyte?
immature erythrocyte
can be found in circulating blood - eventually mature to erythrocytes within 1-2 days
- contains clumps of ribosomes and mitochondrial material
Describe the life cycle of RBCs. How long do they live, and where do they go when they die?
RBC’s cannot reproduce - no nucleus
membrane becomes more stiff/fragile as they age
macrophages in the liver capture old RBC’s - breakdown with protease and recycle:
- AA’s for hemoglobin
- Fe and pigment excreted via bile to intestines
Where does RBC production occur in the fetus and postnatally?
fetus - liver, spleen and bone marrow of flat/long bones
post natal - ENDS of long bone (epiphyses)
- also in flat bones - sternum
What is hemoglobin structure like?
2 alpha and 2 beta complexes
Fe ion formed the porforin ring - each Fe binds O2
How is hemoglobin tested?
tested by light spectrometry or piece of paper
- deeper red = more hemoglobin
men typically have more hemoglobin
What is hematocrit? What affects it?
hematocrit: % of blood that is formed elements
men have more T, higher density of skeletal muscle, higher requirement for O2 - higher hematocrit %
affected by hydration
What is erythrocyte sedimentation rate?
determined by interactions btw factors that promote (fibrinogen) and resist (- charge of RBC repel each other) sedimentation
normal RBC settle slowly and do not form rouleaux/aggregate
- rouleaux - stacks of RBC that become heavier and sediment faster
- plasma proteins like fibrinogen adhere to RBS and promote rouleaux formation
- increased rouleaux = high ESR
What are some conditions with high ESR?
anemia, cancer, kidney disease, thyroid disease, lupus, RA, infections
What are some conditions with low ESR?
sickle cell disease, spherocytosis, congestive heart failure
What is hemorrhagic anemia
due to sudden/chronic blood loss
sudden decrease in blood volume
hematocrit may be normal/low
high reticulocyte count - trying to compensate
What is hemolytic anemia
caused by autoimmune, parasitic (malaria) infection, transfusion reaction
- rupture of RBC membranes
antibodies can clump and damage RBC’s
- hemoglobin in blood
- high reticulocyte
What is aplastic anemia?
bone marrow no longer producing normal RBCs - something wrong with them cells
can be caused by: chemotherapy, toxic chemical exposure, medications, viral infections (hepatitis, Eptein-Barr), pregnancy
What is iron deficiency anemia?
RBC’s are being produces but do not have sufficient Fe to bind O2
- large circle of paleness in biconcave
What is pernicious anemia?
inability to produce hemoglobin. caused by 2 factors:
absence of Vit B12 - required for hemoglobin synthesis
- found in animal products
- needs to cross epithelial lining to get absorbed
absence of intrinsic factor - need to get vitamin B12 past epithelial lining of digestive system,
- no supplement available - synthesized by body
- can be caused by gastric bypass
- if there is a lack of intrinsic factor, requires B12 shots
What is sickle-cell anemia?
single AA substitution where valine replaces glutamic acid
- low O2 level in blood causes RBC to collapse and form sickle cell shape
- shape does not move as well, causes damage to vessels, organs and joints
symptoms: swelling of extremities, infection, pain in the joints/organs, delayed growth, vision problesm
What are platelets?
fragments of the megakaryocyte (found in bone marrow)
- synthesis increased by throbopoetin in liver
- pitches off pieces of membrane and cytosol
What are the three stages of hemostasis?
vascular spasm
platelet plug formation - involving 5HT, ADP, thromboxane
coagulation
What is the vascular spasm phase of hemostasis?
reflexive reaction of smooth muscle when it is damaged
endothelial cells release: endothelin and 5HT
vasoconstrictive molecules released by endothelial cells and platelets - 5HT and thromboxane A2
narrows opening of blood loss, and shrinks the block that the platelets needs to form
platelets begin to react to damaged vascular epithelial cells due to exposed collagen
What is the platelet phase of hemostasis?
platelets begin to stick to exposed surface and each other
positive feedback - releases 5HT, ADP, thromboxane that increase vasoconstriction and activate other platelets
platelet aggregation - platelet receptor for fibrinogen bind fibrinogen
What is the coagulation phase of hemostasis?
fibrin proteins come together to form mesh network that traps movement of H2O
- traps RBC/WBC in blood
- coagulation can occur in plasma
What are the extrinsic pathway for coagulation?
requires chemical outside blood vessel
- tissue thromboplastin: from damaged CT around blood vessels
- with Ca, activates clotting factor X
- clotting factor X + Ca = prothrombinase activated
What is the intrinsic pathway for coagulation?
no added outside chemical
- test tubes without heparin, damaged platelets
- eventually activated clotting factor X
After the extrinsic/intrinsic pathway for coagulation, what is the common pathway?
starts with activation of prothrombinase
- with Ca, activates thrombin
- thrombin causes fibrinogen to polymerase into strands of fibrin
- fibrin interacts and trap H2O - stops blood flow
What is required for prothrombin synthesis? Why do we give babies aquamephyton?
prothrombin requires Vitamin K - comes from bacteria in large intestine
- shots given to baby bc they do not have it in their digestive system
Describe the clot reaction
platelets attach to fibrin threads
platelets release fibrin-stabilizing factor - increases cross linking between fibrin threads
platelets contract to compress clot into a tight mesh and pull edge of sounds together
fibroblast in CT surrounding damaged vessel and growth factors from the blood heal damaged blood vessel
Describe the repair of blood vessel after the clot reaction
growth factors from platelets stimulate fibroblasts
- fibroblasts form CT mesh of collagen
- endothelial cells replace vessel lining
- clot is removed by t-PA
