Blood Flashcards

1
Q

Blood tissue type

A

Connective tissue

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2
Q

Contains cells suspended in the

A

Matrix fluid

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3
Q

Formed elements

A

Cellular components of the blood
1)RBCs
2)WBCs
3)platelets (thrombocytes)

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4
Q

Components of whole blood

A

1) plasma: 55%
-least dense

2)Buffy coat
-WBCs and platelets (<1% of whole blood)

3)RBCs: 45% of whole blood
-most dense

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5
Q

Hematocrit

A

Ratio of volume of RBCs to total volume of blood

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6
Q

Plasma proteins

A

Formed by hepatocytes in the liver

1) albumin (60%)
2) globulins (35%)
3) fibrinogen (4%)

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7
Q

Albumin

A

-contribute to colloid osmotic pressure(pressure plasma proteins in blood exert, pulling fluid back into capillaries)
-has buffering potential
-transports substances
1)fatty acids
2) bilirubin
3) thyroid hormones
4) steroid hormones

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8
Q

Globulins

A

“Immunoglobulins”
“Gamma globulins”
-antibodies (protein produced in immune system to fight harmful substances, or antigens)
-synthesized immune cells (b lymphocytes (b cells-WBCs) plasma cells)

-transport globulins (small molecules):
-synthesized in liver
1) hormone-binding proteins
2)metalloproteins
3)lipoproteins
4)steroid-binding proteins

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9
Q

Fribrinogen

A

Inactive clotting protein
-fibrin (active form converted by thrombin)
-fibrin is long and insoluble

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10
Q

Non-protein nitrogen sources (NPN)

A

Present in the blood and primarily derived derived from breakdown of proteins in the body

NPNs are excreted by the kidney and their appearance and quantity in the urine is an important indicator of renal function. Kidney disease is often indicated by an elevated NPN.

1)urea
2)Uric acid
3)creatinine

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11
Q

Urea

A

NPN

Metabolic waste produced from deanimation of amino acids

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12
Q

Uric acid

A

NPN

Metabolic waste produced from catabolism of nucleic acids

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13
Q

Creatinine

A

Metabolic waste from metabolism of creatinine and creatinine phosphate

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14
Q

Nutrients of the blood

A

1) monosaccharides- mostly glucose
2) AAs
3) fatty acids
4) lipoproteins (chlyomicrons (large, transport dietary fat and fat-soluble vitamins from intestine to the body), HDL, LDL, IDL, VLDL)
5) vitamins

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15
Q

Na+ importance

A

Maintains BV- osmotic tone
-strongly associated with Cl- and HCO3-

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16
Q

Hb structure

A

-complex quaternary structure
-4 globular protein subunits (each similar to myoglobin, known as globulin)
-2 alpha chains and 2 beta chains
-these globular (protein) subunits are what binds CO2
-each heme (nonprotein, synthesized in mitochondria(of immature RBC which does contain mitochondria), 4total) contains 1 iron which can bind to 1 O2 molecule➡️ 4 O2 can bind
-iron easily associates with O2 (oxyhemoglobin)
-and dissociates w/ O2 (deoxyhemoglobin)

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17
Q

Properties of Hb

A

-heme binds to O2
-globin binds to CO2
-result: Hb can transport O2 and CO2 at the same time

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18
Q

Fetal Hb

A

-strong (O2 binding) form of Hb found in embryos
-steals O2 from mother’s Hb

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19
Q

RBC recycling

A

1) RBC death and phagocytosis
-in liver, spleen, or Red bone marrow
2) Hb ➡️Heme + globin
3)Heme➡️ Biliverdin + Fe3+
4) Fe3+ is stored and transported
-liver stores Fe3+ in ferritin, then transports it to bone marrow in transferring. Fe3+ used to make new Hb (erythropoiesis)
5)biliverdin➡️bilirubin
6)bilirubin➡️urobilin or stercobilin
-in the colon: bilirubin➡️urobilinogen
-then converted into urobilin (makes urine yellow) or stercobilin (makes feces brown)
7) globin➡️AAs
-used to make new proteins of Hb

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20
Q

RBC maturation- erythropoiesis

A

-occurs only in Red bone marrow (myeloid tissue)
-stem cells mature to become RBCs

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21
Q

Hematopoietic stem cells (hemocytoblasts)

A

Stem cells in bone marrow divide to produce:
■ myeloid stem cells:
■ become RBCs, ​some WBCs
■ lymphoid stem cells:
■ become lymphocytes

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22
Q

Lymphoid stem cell pathway (lymphopoiesis)

A

Lymphoid stem cell➡️lymphoblastic➡️prolymphocyte➡️lymphocyte

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23
Q

Results of myeloid stem cells pathways

A

1)Mostly RBCs
2) platelets
3) WBCs
-basophil
-esoinophil
-neutrophil
-monocyte

24
Q

Stages of RBC maturation

A

■ Myeloid stem cell
■ Proerythroblast
■ Erythroblasts
■ Reticulocyte
■ Mature RBC
■ Takes about 15 days

25
Q

Building RBCs requires

A

-AAs
-iron
-vitB12 and 6
-folic acid

26
Q

Megakaryocytes produce (become)

A

Platelets

27
Q

EPO release

A

By kidneys when ⬇️O2
-➕RBC production
-RBCs carry O2➡️⬆️O2 ((-) feedback)

28
Q

A blood type

A

-surface antigen A

Anti-B antibodies

29
Q

B type blood

A

Surface antigen B

Anti-a antibodies

30
Q

Type AB blood

A

Surface antigens A and B

Neither anti-A or anti-B antibodies

31
Q

Type O blood

A

Neither A or B surface antigens

Anti-A and anti-B antibodies

32
Q

Rh (+)

A

Can receive + or -

33
Q

Rh (-)

A

Can only receive - blood

34
Q

Erythroblastosis fetalis/ fetal hemolytic disease

A
  • results from and incompatibility between mother and fetus and only occurs when Rh - mother gives birth to Rh + baby (IGG antibodies attack fetal blood supply; IGM initially made during first pregnancy but to large to cross the placenta)
    -can cause complete destruction of fetal RBCs
35
Q

Circulating WBCs

A

-migrate out of bloodstream
-have amoeboid movement
-attracted to chemical ➕((+) chemotaxis)
-some are phagocytes:
-neutrophils
-eosinophils
-monocytes

36
Q

Pernicious anemia

A

-low RBC production
- due to unavailability of vit B12 due to:
1) vitB12 deficiency
2) lack of intrinsic factor
3) absorption problem

37
Q

5 types of WBCs

A

-Granulocytes
1)neutophils
-multi lobed; phagocytes- pathogens➡️ release prostaglandins and leukotrienes
2)eosinophils
-bi-lobed; phagocytes- attack large parasites and “antibody marked” objects➡️ exctrete NO and cytotoxic enzymes; sensitive to allergen; control inflammation
3) basophils
-bi-lobed; release histamine (dilates blood vessels); release heparin(prevent clotting); release chemotatic factors (inflammatory promoters)
-agranulocytes
4) monocytes
-phagocyte
5) lymphocytes (B and T)
-part of body’s specific defense system; non-phagocytic

38
Q

B cells

A

■ 20% B-Lymphs
■ responsible for humoral or Antibody Mediated Immunity (AMI) Differentiate into plasma cells
■ Synthesize antibodies
■ Tend to increase in number in acute viral infection or in lymphocytic leukemia

39
Q

T cells

A

■ 80% T-Lymphs
■ Cell-mediated immunity (CMI) - Lymphokine production
■ Attack foreign cells by directly killing infected cells, or cancer cells
-targeted response based on antigen recognition

40
Q

Most common WBCs numeric

A

Never
Let
Monkeys
Eat
Bananas

41
Q

Degranulation

A

-removing granules from cytoplasm
-cause by fusion w/ lysosomes
-occurs in granulocytes, mast cells and some lymphocytes
-defensins:
-peptides from lysosomes
-attack pathogens membranes

42
Q

NK cells

A

-nonspecific
-first line of defense
-kills “nonself””

43
Q

Cytotoxic T cells

A

Destroy infected cells (virus and cancer)

44
Q

T helper cells

A

-produced in thymus
-mature in spleen and lymph nodes
-detect infections
-activate other immune cells

45
Q

Lymphocyte levels⬆️➡️

A

Viral infection

46
Q

Neutrophil levels⬆️➡️

A

Bacterial infection

47
Q

Acute viral infection WBC

A

Lymphocytosis (⬆️lymphocyte)
W/ neutropenia(⬇️neutrophils)

48
Q

Platelets function

A

Clotting
1) release of important clotting chemicals
-granules contain serotonin, Ca2+, enzymes, ADP, platelet-derived growth factor(PDGF)
2)temporarily patch damaged walls
3)actively contract tissue after clotting formation

49
Q

Hemostasis phases

A

1) vascular phase
2) platelet phase
3) coagulation phase

50
Q

Vascular phase

A

Contraction of blood vessel

Lasts about 30 minutes after injury.
Endothelial cells contract & release endothelins.

Stimulates smooth muscle contraction & endothelial division.
Endothelial cells become sticky & adhere to platelets & eachother.

51
Q

Platelet phase

A

Plug is formed

Platelets stick to endothelial surfaces, basement membrane, exposed collagen fibers & to each other.

When activated, platelets release chemical that promote aggregation, vascular spasm, clotting & vessel repair.

52
Q

Coagulation phase

A

extrinsic: faster; breaking blood vessel
-intrinsic: slower (➕injury or bleeding); exposure to walls of damage blood vessel
1. Protein prothrombin is converted into the active enzyme thrombin.

  1. Active enzyme thrombin converts the protein fibrinogen (soluble) into the protein fibrin (insoluble).
  2. As fibrin network grows, blood cells & additional platelets are trapped in fibrous tangle, forming a blood clot.
53
Q

Fibrinolysis

A

-slow process of dissolving clot:
-thrombin and t-PA
-activate plasminogen
-plasminogen produces plasmin
-digests fibrin strands

54
Q

Anticoagulant therapy

A

-prevents clot formation and/or extension of existing clot
-they do not dissolve existing clots

55
Q

Testosterone effect on EPO

A

⬆️testosterone➡️⬆️EPO