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Blood Flashcards

(60 cards)

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1
Q

What are the 2 main components of blood

A

Liquid plasma and formed elements

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2
Q

What are the formed elements

A

RBCS, WBCS, and platelets

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3
Q

What is a hematocrit

A

the percentage of packed RBCs out of the total volume of blood (hard to actually figure out)

  • take blood and centrifuge
    Top: plasma (55%) yellow layer
    Middle: Buffy coat with WBCs and platelets (1%)
    Bottom: RBCs, most dense (45%)
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4
Q

Scarlet blood is …
Dark red blood is….

A

1) oxygenated (artery)
2) deoxygenated (venous)

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5
Q

What is the pH of blood

A

7.35-7.45 (higher pH in arteries)

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6
Q

Average volume of blood in males and females

A

Males - 5-6L

Females - 4-5L

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7
Q

What is the blood plasma made of

A

Proteins (6-8%): albumin, globulin, clotting proteins

Water (90%)

Other solutes: organic (carbs, AA, fats, lactic acid), electrolytes and gases

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8
Q

T or F: plasma proteins all contribute to osmotic pressure and maintain water balance

A

T — don’t leave the bloodstream, pull fluid out of the tissues

  • Albumin: main contributor to osmotic pressure (carry hormones too)

Globulins : alpha + beta (transport lipids), gamma - antibodies

Fibrinogen: fibrin threats for blood clot

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9
Q

What are nonprotein nitrogenous substances in blood

A

by products of cellular metabolism (ex// urea)

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10
Q

T or F: RBCs and WBCs are complete cells

A

F

RBCS: have no nuclei or organelles

platelets : no nuclei, just cell fragments

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11
Q

T or F: most oxygen in the blood is bound to Hb

A

T : bound to Hb in RBCs (biconcave to increase SA, with no nuclei or organelles really)

  • Hb makes up most of the dry weight of RBCs (97%)
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12
Q

What is spectrin and its function

A

linked to the cytoplasmic side of RBCs and allows them to change shape to biconcave
— crosses over and interacts with the inner PM to give shape

** help make them super flexible to get in and out of capillaries due to their shape *

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13
Q

What is Hb and its structure

A

what carries the O2 in the RBCs

  • contains 4 polypeptides (globins): 2 alpha and 2 beta
  • each have a heme group associated with them: each heme has an Iron —- what O2 binds to

1Hb —- 4 O2

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14
Q

Yolks Sac phase of RBC production

A

blood in islands in yolk sac, no WBCs

primarily make epsilon and theta globins

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15
Q

Hepatic spleen phase of RBC production

A

in the fetus (2-3 months); peaks at 5 months and decrease towards birth
- fetal Hb and some nucleated RBCs
- globins: increase in alpha and gamma (greedy, good oxygen binding) and slow increase in beta but low; increase in gamma, decrease in theta and epsilon

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16
Q

Bone marrow phase of RBC production

A

Have mature RBCs and WBCS at 12 weeks
- slowly start producing RBCs here in the marrow (axial and long bones)

  • globins: still high alpha and gamma
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17
Q

adult phase of RBC production

A

RBCs made in bone marrow of pelvis, skull, ribs, vert and long bones

  • switch to alph and beta globins
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18
Q

Phases of erythropoiesis

A

1) stem cell: hemocytoblast (precursor to all blood cells) ; look like normal cell
2) committed cell: proerthroblast —- now will be a RBC, look like normal cell
3) developmental pathway: changes to cell
- Phase 1: ribosome synthesis
- Phase 2: hemoglobin accumulation
- Phase 3: ejection of nucleus

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19
Q

What controls RBC production

A

TO make RBCs, need: proteins, lipids, carbs, iron, vit B and folic acid (B + FA —— rapid DNA synthesis)

—- iron stored in Hb, liver, spleen and bone marrow in iron-protein complexes (ferritin and hemisiderin to stabilize)
— loose iron: bound to transferrin in BS

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20
Q

Steps to RBC regulation

A

1) low O2 in blood causes release of EPO by kidney (increase level in BS)
2) raised EPO and presence of needed products —— promote erythropoiesis in bone marrow
3) enter BS for 120 days
4) old and damaged RBCs taken in by macrophages in liver, spleen, and BM (breakdown Hb to heme and globin)
- Heme: broken to iron (stored intracellular) and bilirubin
globin: broken down to AA and put into BS

5) Bilirubin in blood brought to liver, secreted into intestine bile —- broken down into stercobilin (excreted in feces,what gives them their colour) or released from kidney as bilirubin in urine (gives yellow)

when need iron for RBC production : released from liver into blood while bound to transferrin

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21
Q

What is anemia (general)

A

symptom when blood has low oxygen carrying ability
- fatigue, paleness and shortness of breath

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22
Q

Anemia caused by insufficient RBCs

A

Hemorrhagic: from loss of blood

Hemolytic: premature RBC rupture

Aplastic: destruction/ inhibition of bone marrow — less RBCs made

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23
Q

Anemia caused by decrease in Hb

A

Iron Deficiency: don’t get enough iron from food, or bad absorption, or secondary result of hemorrhagic anemia

Pernicious: deficiency of Vitamin B12 needed for rapid DNA synthesis; lack of intrinsic factor (helps stabilize Vitamin B12 in acidic pH and made by stomach cells) therefore can’t absorb it
—- treat with injections of B12 intramuscular

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24
Q

Sickle cell anemia

A

anemia caused by abnormal Hb (point mutation in beta chain of Hb from Glu to Val )
— need double mutation to have (hetero == chilling)

called HbS

  • mutation causes RBCs to become sickle cell shaped in low O2 environments when unloading O2
  • Normally: RBCs keep shape when going through capillaries and unload O2
  • Sickle Cells: HBS polymers when O2 is released by RBC — give deformed shape that blocks flow of other RBCs

*decrease life span : 20 days

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25
What is Polycythemia
increased proportion of blood occupied by RBCs - can be caused by an increase mass of RBC (absolute) or due to a decrease in blood plasma (relative; can be caused by dehydration ) - extra RBCs increase viscosity
26
Types of Absolute Polycythemia
primary: increase RBC production secondary: elevated EPO via natural or doping
27
T or F: WBCS make up 10% of total blood volume
F - 1%
28
What is leukocytosis
when the WBC is higher than 11,000cells/mL - indicates inflammation of the body
29
Order of WBCS level in blood (highest - lowest)
Never Let Monkeys eat bananas
30
What are granulocytes
WBCs that have cytoplasmic granules that stain acidic (red) or basic (blue) using Wright stain - larger and shorter lived than RBCs - lobed nuclei and phagocytes Ex// Neutrophils, eosinophils and basophils
31
Neutrophils
Multilobed nuclei (worm looking) Granules: acids and basic (contain peroxidases, hydrolytic enzymes and defensins) - BACTERIA killers Extravascularization: chilling in BS and then attracted/activated by chemoattractants —- cause them to roll along BS wall and eventually get captured, spread out and squeeze through capillary wall to attack bacteria
32
Eosinophils
Bi-lobed nucleus Granules: acidic/red (large and coarse) Fxn: fight against multicellular parasites, and certain infections (also control allergy and asthma alongside mast cells)
33
Basophils
Very rare Bi-lobed nucleus (U or S shaped ) - hard to see Granules: basic/purple with histamine (inflammatory that acts as vasodilator and attracts other WBCs
34
What are agranulocytes
lack visible cytoplasmic granules - spherical nuclei (lymphocytes) or kidney shaped (monocytes)
35
Lymphocytes
Large nucleus that takes up most of the cell - normally found in lymphoid tissue Two types of: T and B cells
36
Monocytes
Kidney shaped nuclei - largest leukocytes - when leave circulation (diapedesis: squeeze through BS) they turn to macrophages (mobile and phagocytes that can activate lymphocytes) Blood- monocyte Tissue - macrophage
37
Platelets
not WBCs - produced by megakaryocyte (sites in the BM sinuses and protrudes out to release fragments of itself—— platelets) - have no nucleus, have granules, mitochondria, glycogen and cytoskeleton Granules: alpha (clotting factor) or Dense core granules (histamine) 1) alpha: have serotonin, Ca, enzymes, ADP and PDGF; work to form clots , bind injured BV walls, get RBCs to stick and form plus
38
What keeps platelets inactive
NO and Prostacyclin (PGI2) : prevent their granulation
39
What stimulates the production of leukocytes
interleukins and colony stimulating factor (CSF) - interleukins: numbered - CSF: named for WBC they stimulate
40
Main steps of Leukocytes formation
Precursor for all blood cells: hemocytoblast (pluripotent stem cell) — differentiate into lymphoid stem cell (T and B cells) and myeloid stem cells (all the different WBCs) Myeloid —— granulocyte- macrophage CFU and erythroid CFU , Eosinophils CFU, basophils CFU, and Megakaryocyte CFU
41
Where do WBCs develop
most develop in BM except T cells
42
What are the steps for Hemostasis
- 3 distinct phases to stop bleeding 1) Vascular spasm: vasoconstriction caused by 3 stimuli - direct damage to vascular SM - chemicals released by platelets and cells - reflexes started by local pain receptors *increase in damage —- more spasms * 2) Platelet Plug Formation : form temporary plug normally platelets wont stick to walls due to PGI2 and NO; but if cell wall damage —- stick to walls - exposure of VWF and collagen due to damage: activated platelets -after binding : platelets release ADP (activator), serotonin, and Thromboxane - thromboxane and serotonin : stimulate vasoconstriction to decrease BF to local area - thromboxane and ADP : cause other platelets to stick and bind — limited to immediate area by PO and PGI2 3) Coagulation : set of reactions that transforms blood to gel via intrinsic and extrinsic pathways - form prothrombin — convert to thrombin — catalyze joining of fibrinogen into fibrin mesh (full plug forms)
43
What is clot retraction
stabilization of clot by squeezing serum from the fibrin strands
44
Clot repair
fibroblasts form connective tissue patch PDGF stimulates fixing of BV walls - VEGF (vascular endothelial growth factor) stimulates the endothelial cells to regrow
45
What are the two main mechanisms that limit clot overgrowth
1) swift removal of clotting factors 2) inhibition of activated clotting factors
46
How is thrombin inhibited
Fibrin acts an anticoagulant : binds to thrombin and prevents it from giving postive feedback effects to coagulation , speeding up production of prothrombin activator via Factor V and increasing the intrinsic pathway by activating more platelets - if not absorbed by fibrin, extra thrombin is inactivated by antithrombin III (inactive and binds) - Heparin : 3rd anticoagulant that binds directly to it to deactivate Deactivations of thrombin: fibrin, antithrombin III, and heparin
47
How to prevent un-needed clotting
Prevented by the endothelia cells lining the BV - have NO, PGI2 and heparin secreted and lining them to prevent platelets binding - smooth lining - Vitamin E: anticoagulant
48
Difference between thrombus and embolus
Thrombus: clot that develops and stays in a BV - named based on location (ex// coronary - if BV of heart) - can block circulation and cause tissue death Embolus : free floating thrombus in BS - pulmonary one can impair ability to get O2 around body -cerebral : can cause strokes
49
What is hemophilias
hereditary bleeding disorder caused by lack of clotting factors 1) hemophilia A: most common and lack Factor VIII 2) Hemophilia B: deficiency in Factor IX 3) Hemophilia C: mild, deficiency in factor XI * all defects in intrinsic pathway therefore hard to control microbleeds; but large bleed —- all good to use fast acting extrinsic pathway
50
Antigens on RBCs
glycoprotein; unique to the individual, recognized a foreign if transfused into another - promote agglutination *used to classify blood types
51
T or F: humans have 2 types of antigens on RBCs: ABO and Rh
F- have 30 but ABO and RH cause bad transfusion reactions and used to group
52
Basis of the ABO blood group
- consist of 2 antigens: A and B on RBC surface - Anti-A and Anti-B found in the plasma *agglutinogens and their corresponding AB cannot be mixed —- AB and Ag bind : reaction
53
Type A blood
Named based on the Ag on their surface Antibody in blood: Anti B Antigen on RBC: A Can get blood from A or O
54
Type AB blood
Ag: A and B Antibodies: none universal recipient: can get blood from anyone
55
Type B
Ag: B on RBCs Ab: Anti-A can get blood from B or O (even though O blood has anti A and B antibodies —- only small amount therefore not enough for rxn )
56
Type O blood
Ag: none Ab: A and B antibodies can give blood to anyone in an emergency (such a low volume of blood so antibodies present wont cause much rx)
57
Rh Blood groups
- 8 different Rh Aggultinogens (C, D and E = most common) - presence of RH agglutinogens : + - Anti-RH are not normally made in Rh- people (need prior exposure to make them, once start making them —- always make them) * if Rh- person gets RH+ blood — they will start to form antibodies —— chilling this time but next exposure to Rh+ blood —- RXN
58
Hemolytic disease of newborn
Rh- moms can be sensitized when exposed to Rh + blood (aka if baby is RH+) 1) first exposure : aka first baby is Rh+, they chilling and baby all good ; get exposed to RH+ blood during delivery - now sensitized and make antibodies 2) 2nd baby: also Rh+; Rh+ antibodies of mom can pass placenta and attack RBCs of RH+ baby (sick baby) *aka if no prior exposure : baby good; if prior exposure: baby sick*
59
Treatment to avoid hemolytic disease of newborn
During birth give mom RHoGAM (Rh anitbodies); binds to any baby RH+ RBCs and blocks them so mom RH anitbodies won’t recognize and attack them
60
What are transfusion reactions
donor’s cells are attacked by recipient Antibodies - cause clumping, decreased oxygen carrying ability, and ruptured RBCs that release Hb into BS ** free Hb damages kidney and causes renal failure

pharm 111 (1 decks)

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