Lecture 23 Flashcards

(25 cards)

1
Q

describe the composition of blood

A
  • 7% of total body weight
  • 5L (male) 4L (female)
  • loose connective tissue
  • watery extracellular matrix (plasma) makes up 1/4 of bodies ECF
  • cellular elements include
    -> red blood cells (erythrocytes) = gas transport
    -> white blood cells (leukocytes) = immune function
    -> platelets (thrombocytes) = clotting and hemostasis
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2
Q

what are the types of WBC

A

N - neutrophils
L - lymphocytes -> in lymph nodes
M - monocytes -> macrophages in tissues
E - eosinophils
B - basophiles -> mast cells in tissues = release histamine in response to antigens

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3
Q

what does centrifugation of blood reveal (what are the components)

A
  • fractional composition of blood
  • 42% packed red blood cell volume
  • 58% plasma volume
  • <1% white cells
  • hematocrit = fraction of blood volume that is RBC
  • hemoglobin = oxygen carrying proteins
  • red cell count (4-6 million)
  • total white count = all the types of leukocytes
  • differential white cell count
  • platelets
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4
Q

what is the buffy layer

A
  • platelets and white cells between plasma and RBCs
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5
Q

describe the process of hematopoeisis

A
  • synthesis of blood cells in the bone marrow from pluripotent hematopoietic stem cell
  • occurs in the bone marrow of the pelvis, spine, ribs, cranium, and proximal ends (closest to torso) of long bones
  • within active bone marrow 25% of the developing cells become RBC
  • 75% become WBC
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6
Q

what explain the ratio difference of RBC and WBC production from hematopoiesis

A
  • due to difference in lifespan and turnover
  • RBC = 120 days
  • WBC 6-12 hours
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7
Q

what are cytokines and what do they control

A
  • proteins released from one cell that affect the activity of another
  • control the production and development of blood cells
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8
Q

what are the cytokines involved in hematopoiesis, their site of production, and what they influence growth or differentiation of

A
  • erythropoietin (EPO) -> site of production = kidney cells primarily -> influences growth of RBC
  • thrombopoietin (TPO) -> site of production = liver primarily -> influence growth of megakaryocytes (platelets)
  • colony stimulating factors -> site of production =endothelium, fibroblasts of bone marrow, leukocytes -> influences all types of blood cells, mobilizes hematopoietic stem cells
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9
Q

what is hypoxia and how is it fixed

A

= low levels of O2 in arterial blood
-> sensed by cells in kidney
-> kidney makes EPO
-> EPO acts on progenitor cells in bone marrow to stimulate erythropoiesis
- increased # of RBCs and increased O2 transporting capability in the blood

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10
Q

describe RBCs

A
  • 120 days lifespan
  • biconcave and bendy
  • no nucleus
  • no mitochondria
  • no membrane bound organelles
  • contains hemoglobin
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11
Q

what is hemoglobin

A
  • tetramer composed of 4 protein globular chains (2 alpha, 2 beta)
  • centered around a heme group
  • each heme group consists of a porphyrin ring with an iron atom in its center
  • 1 hemoglobin binds 4 oxygen, 1 per iron
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12
Q

how does O2 binds to Fe

A
  • weakly so it can release in the tissues
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13
Q

what is anemia

A
  • low RBC count
  • decreased hemoglobin content and reduced O2 carrying capacity of the blood
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14
Q

what results in accelerated RBC loss

A
  • blood loss
  • hemolytic anemia
    -> RBC degradation > production
    = genetic (sickle cell anemia)
    = acquired (malaria)
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15
Q

what results in decreased RBC production

A
  • aplastic anemia (drugs or radiation)
    -> not changing, unable to make RBC
  • dietary insufficiencies
    -> iron deficiency
    -> folic acid deficiency
    -> vitamin B12 deficiency
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16
Q

what is hemorrhage

A
  • loss of blood from the vessels
17
Q

what is hemostasis

A
  • keeping blood inside the blood vessels
18
Q

what are the 4 steps of hemostasis in response to damage

A
  1. vasoconstriction (upstream of damage)
  2. platelet plug formation
  3. coagulation (formation of clot)
  4. dissolution of clot (fibrinolysis)
19
Q

explain formation of a platelet plug

A
  • the edges of the megakaryocyte break off to form cells fragments called platelets
  • intact endothelium releases prostacyclin and NO which prevents platelet adhesion
  • but
    1. exposed collagen binds and activates platelets
    2. release of platelet factors
    3. factors attract more platelets
    4. platelets aggregate into platelet plug
  • plug is then converted into fibrous clot via coagulation cascade
20
Q

explain the coagulation cascade

A
  • cascade of reactions in the plasma that sequentially activates enzymes leading to production of fibrin
    intrinsic pathway
  • cascade involving plasma proteins and initiated by exposure of collagen
  • factor 12 activated by collagen
  • activates factor 11
  • activates factor 9
  • activates factor 10
    extrinsic pathway
  • initiated due to release of tissue factor (protein and phospholipid) from damaged tissue
  • activates factor 7
  • activate factor 10
  • converts prothrombin -> thrombin
  • both pathways result in activation of thrombin
    -> converts fibrinogen in the plasma to fibrin
  • fibrin cross links to from mesh that stabilizes the platelet plug
21
Q

summary of hemostasis

A
  • prevention of blood loss and repair of vascular tissue
    1. vasoconstriction due to paracrine signals from endothelium
    -> decreased blood flow and pressure in the vessel
    2. platelets adhere to exposed collagen in damaged vessel and aggregate to form platelet plug
    3. activation of coagulation cascade generates fibrin mesh (from fibrinogen) that stabilizes plug to form clot
    4. fibrinolysis
    -> tissue is repaired and clot dissolves due to the actions of enzyme plasmin
22
Q

explain ABO-Rh blood groups

A
  • blood type refers to the antigens that are expressed on your RBCs
  • antigens are inherited surface proteins
  • if you are A type your RBCs have A antigens on their membrane
  • if mixed with plasma containing Antibodies to group A, the antibodies cause the blood cells to clump or agglutinate (squish)
23
Q

explain transfusion compatibility

A
  • donor A, B, and AB RBCs clump (agglutinate) when given to someone with O type blood due to reaction of the RBC antigens with the recipient’s plasma
  • AB (Rh+) = universal acceptor, no plasma antibodies
  • O (Rh-) is universal donor, no membrane antigens
  • Rh- recipients may only receive Rh-
24
Q

explain the Rh factor incompatibility during pregnancy

A
  1. Rh+ father
  2. Rh- mother carrying her first Rh+ fetus. Rh antigens from the developing fetus can enter the mothers blood during delivery
  3. in response to the fetal Rh antigens the mother will produce anti-Rh antibodies
  4. if the woman becomes pregnant with another Rh+ fetus, her anti-Rh antibodies will cross the placenta and damage fetal red blood cells
    -> hemolytic disease of the newborn
25
how can the Rh incompatibility be prevented
- inject mother with Anti-Rh antibodies before birth of first child - attack the contaminating Rh+ fetal blood before mother can develop her own immune response