Blood Typing Flashcards

1
Q

What is plasma, and what are formed elements?

A

Plasma - fluid content of blood - H2O, proteins, ions

formed elements: platelets, WBC, erythrocytes

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2
Q

What is the difference between serum and plasma?

A

serum - plasma minus clotting factors
- albumin, globulin, regulatory proteins

Plasma - serum PLUS clotting factors

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3
Q

What is albumin?

A

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)

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4
Q

What are globulins?

A

some types made by liver
- transports metal ions, lipid, fat soluble vitamins

others made by plasma cells during immune response - antibodies

transferrin

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5
Q

What are the clotting proteins and where are they made?

A

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

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6
Q

What happens when the body needs more oxygen?

A

kidneys release erythropoietin to increase RBC production
- binds to receptor on the RBC progenitor cell (proerythroblast)

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7
Q

What is erythropoiesis? Describe the steps

A

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

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8
Q

What is a reticulocyte?

A

immature erythrocyte
can be found in circulating blood - eventually mature to erythrocytes within 1-2 days
- contains clumps of ribosomes and mitochondrial material

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9
Q

Describe the life cycle of RBCs. How long do they live, and where do they go when they die?

A

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

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10
Q

Where does RBC production occur in the fetus and postnatally?

A

fetus - liver, spleen and bone marrow of flat/long bones

post natal - ENDS of long bone (epiphyses)
- also in flat bones - sternum

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11
Q

What is hemoglobin structure like?

A

2 alpha and 2 beta complexes
Fe ion formed the porforin ring - each Fe binds O2

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12
Q

How is hemoglobin tested?

A

tested by light spectrometry or piece of paper
- deeper red = more hemoglobin

men typically have more hemoglobin

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13
Q

What is hematocrit? What affects it?

A

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

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14
Q

What is erythrocyte sedimentation rate?

A

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

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15
Q

What are some conditions with high ESR?

A

anemia, cancer, kidney disease, thyroid disease, lupus, RA, infections

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16
Q

What are some conditions with low ESR?

A

sickle cell disease, spherocytosis, congestive heart failure

17
Q

What is hemorrhagic anemia

A

due to sudden/chronic blood loss
sudden decrease in blood volume
hematocrit may be normal/low

high reticulocyte count - trying to compensate

18
Q

What is hemolytic anemia

A

caused by autoimmune, parasitic (malaria) infection, transfusion reaction
- rupture of RBC membranes

antibodies can clump and damage RBC’s
- hemoglobin in blood
- high reticulocyte

19
Q

What is aplastic anemia?

A

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

20
Q

What is iron deficiency anemia?

A

RBC’s are being produces but do not have sufficient Fe to bind O2
- large circle of paleness in biconcave

21
Q

What is pernicious anemia?

A

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

22
Q

What is sickle-cell anemia?

A

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

23
Q

What are platelets?

A

fragments of the megakaryocyte (found in bone marrow)
- synthesis increased by throbopoetin in liver
- pitches off pieces of membrane and cytosol

24
Q

What are the three stages of hemostasis?

A

vascular spasm
platelet plug formation - involving 5HT, ADP, thromboxane
coagulation

25
Q

What is the vascular spasm phase of hemostasis?

A

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

26
Q

What is the platelet phase of hemostasis?

A

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

27
Q

What is the coagulation phase of hemostasis?

A

fibrin proteins come together to form mesh network that traps movement of H2O
- traps RBC/WBC in blood
- coagulation can occur in plasma

28
Q

What are the extrinsic pathway for coagulation?

A

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

29
Q

What is the intrinsic pathway for coagulation?

A

no added outside chemical
- test tubes without heparin, damaged platelets
- eventually activated clotting factor X

30
Q

After the extrinsic/intrinsic pathway for coagulation, what is the common pathway?

A

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

31
Q

What is required for prothrombin synthesis? Why do we give babies aquamephyton?

A

prothrombin requires Vitamin K - comes from bacteria in large intestine
- shots given to baby bc they do not have it in their digestive system

32
Q

Describe the clot reaction

A

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

33
Q

Describe the repair of blood vessel after the clot reaction

A

growth factors from platelets stimulate fibroblasts
- fibroblasts form CT mesh of collagen
- endothelial cells replace vessel lining
- clot is removed by t-PA