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Flashcards in Blood Histology Deck (61):
0

Why is blood considered to be a CT

it contains cells, a liquid ground substane

1

Hematocrit

% of blood that is RBCs usually about 44% of blood sample

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Buffy coat

Composed or WBCs and platelets (cell fragments) less then 1% of blood sample

3

Plasma

fluid component of blood minus the formed elements
55% of blood

4

What is plasma composed of?

water, proteins, other solutes
water is 92% of plasmas total volume

5

serum

When the proteins are removed from the plasma

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Plasma proteins (4)

albumin
globulins
fibrinogen (for clotting)
regulatory proteins (enzymes and hormones)

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Albumin

transports small molecules in the blood
important in maintaining oncotic pressure
SYNTHESIZED in LIVER

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Decreases in serum albumin indicate what?

Could be a result of liver disease, since albumin is synthesized in liver
can also be a result of kidney disease, which allows albumin to escape in the urine
malnutrition/ low protein diet

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Fibrinogen

blood clot formation
converted into long insoluble strands of fibrin for blood clot

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Globulins

immunoglobulins,
smaller alpha and beta globulins bind, support and protect,
certain hormones and ions

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Formed elements in the blood (3)

RBCs (transport gasses in blood)
WBCs (defense)
platelets (clotting)

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RBCs are composed of

plasma membrane, underlying cytoskeleton, Hgb and a few other glycolytic enzymes
lack nuclei

13

Things involved in the junctional complex in the Cell membrane of RBCs

involves many proteins and spectrin
Spectrin is a large dimer and hooks up with junctional complex
allows RBCs to maintain biconcave shape

14

Spectrin

larger dimer that helps RBCs maintain biconcave shape

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glycophorin

helps RBCs move through and not stick to vessels.

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Cytoskeletal Abnormalities - Elliptocytosis

Autosomal dominant disorder
oval shaped RBCs
caused by defectiv self association of SPECTRIN subunits,
if anything in the COMPLEX IS DEFECTIVE

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Cytoskeletal abnormalities - Spherocytosis

autosomal dominant
DEFICIENCY IN SPECTRIN
small dense cells lacking central pallor

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Clinical features of cytoskeletal abnormalities

anemia, jaundice, spenomegally.
splenectomy is usually curative.
polychromasia usually a sign of bone marrow stress as well as immature RBCs released too early

19

How many protein globins does each HgB have?

4
Alpha or B chains.

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What does each Hgb globin chain contain

non protein heme group in the shape of a ring, with an Fe in its center.

REMEMBER each Hgb can bind 4 irons. meaning capable of binding 4O2s.

21

Hemoglobin Abnormalities - Sickle Cell anemia

point mutation --> glutamic acid to valine at 6th positino in B globulin chain
defective HgB (HbS) tetramers aggregate and polymerize in O2- RBCs, changing biconcave disc shape
rigid, less deformable. sickle shaped cell
SEVERE CHRONIC HEMOLYTIC ANEMIEA AND OBSTRUCTION OF POST CAP VENULES. CELLS STUCK IN CAPILLARY BED BLOCK O2 DELIVERY

22

HgB Abnormalities - Thalassemia syndromes

heritable anemias
defective synthesis of either A or B chains of normal HgB tetramer (a2b2)
hydrops fetalis= most sever alpha form, usu intrauterine fetal death
B thalassemia major= most sever B form= sever transplant dependant anemia = abnormal growht of facial features

23

RBC volume disorders - anemia

low # RBCs
inadequate production or survival
lethargy, shortness of breath, pallor, fatigue heart palpitations
strain on heart

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RBC volume disorders - Polycythemia

#RBCs higher than normal
may have normal blood volume
blood thick, viscous
STRAIN ON HEART

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Congenital hemolytic anemia

increased destruction
abnormal protein with increased fragility of PM

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Pernicious anemia

decreased absorption of Vit B12 bc
decreased IF in gastric secretions

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Fe deficiency anemia

most common, bur rarely due to diet
most common cause= excessive menstral bleeding, ulcers, colon cancer

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Aplastic anemia

decreased formation of RBCs and Hgb
defective bone marrow

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Compensatory polycythemia

result of chronic hypoxia
smoking
damage due to long term exposure to tobacco and CO

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Erythrocytosis

Increase #RBCs due to increased EPO

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Polycythemia Vera

RBC growth in Red marrow not regulated
RBC precursors continue to grow/ mature independent of EPO

32

Blood doping

attempt to enhance athletic performance bin increasing #RBCs
removal and reinfusion with own blood
increase #RBCS also increase viscosity and work heart must do
also acheived by using recombinant humnan EPO rhEPO

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EPO

hormone released by kidney
stimulates synthesis of RBCs

34

HbF

fetal hemoglobin. has higher affinity for O2 than does HbA

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Erythroblastosis Fetalis

Hemolytic disease in the newborn. when mom is Rh- and baby is Rh+. If mom exposed to Rh+ , will start to make antibodies against. problems in subsequent pregnancies.
TREATED with Rhogam - prevents long term sensitization to Rh antigens.

36

Leukocytes

WBCS
may leave bloodstream via diapedesis and enter CT by homing
immunity
larger cells.

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Granulocytes - definition

have primary and specific or secondary cytoplasmic granules
phagocytic cells with multilobed nucleus

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A granulocytes - definition

contain only primary granules.

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leukocytopenia

decreased circulating WBCs due to bacterial or viral infection. exposure to toxins, lukemia

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leukocytosis

increased WBCs can be indicative of dehydration, allergy or infection

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Types of Granulocytes (3)

Neutrophils, Eosinophils, Basophils

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Neutrophils

Most abundant. multilobed nucleus
eliminate opsonized bacteria or limit extent of inflammatory reactions
specific receptors for integrins for HOMING
1ST to arrive in areas of tissue damage
PHAGOCYTOSIS of bacteria and dead cells.

43

Eosinophils

red granules
nucleus= 2 lobes
PARASITIC infections
dampen severity of allergic reactions
role in bronchial asthma

44

Basophils

Bilobed nucleus, and blue-violet granules
resemble mast cells
histamine, heparin
role in Delayed hypersensitivity

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heparin

anticoagulant

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Types of Agranulocytes (2)

Lymphocytes
monocytes

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Lymphocytes

round nucleus, occupies most of cell. thin sliver of cytoplasm
T-cells - manage and direct immune response. some attack foreing cells and virus infected cells
B-cells - stimulated to become plasma cells and produce antibodies

48

Monocytes

Nucleus kidney shaped or u shaped
stay in blood 12-100 hrs then enter CT
in CT differentiate into Macrophages, involved in bacterial PHAGOCYTOSIS/ antigen presentation/ clean up of CELL DEBRIS

49

Homing and inflammation steps (4)

Rolling and attachment
adhesion
transendothelial migration
activation of macrophages

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Rolling and attachment

leukocytes establis reversible binding with endothelial cells (CHO ligands - selectins)

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adhesion

strong interaction of endothelial cells and leukocytes
ICAM and LFA-1

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Transendothelial migration

PMNS migrate across endothelium along IL8 gradient, disrupt erythrocyte interaction

53

Activation of MQ

MQ secrete Tnf-a and IL-1 to stimulate expresion of selectins by endothelial cells to keep neutrophils homing
+feedback

54

Leukocyte adhesion deficiencies
(clinical significance of homing)

characterized by defect in wound healing, recurrent infections, and marked leukocytosis
LAD I
LAD II
no leukocyte migration into the CT

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Platelets

cytoplasmic fragments of the megokaryocytes
under control of TPO- produced in KIDNEYS and liver
megakaryocyte--> proplatelet--> fragment into platelets
BLOOD CLOTTING

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self regulatory mechanism of platelets

Platelet formation stimulated by TPO
platelets then bind and degrade TPO

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Hemostasis

Trauma --> blood to coagulate or clot
components in the plasma produce a web of FIBRIN that traps RBCS and platelets in the web to halt blood flow.

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Thrombocytopenia definition

reduction in number of platelets leading to increased susceptibility to bleeding

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Thrombocytopenia causes

decrease in production of platelets
increase in destruction of platelets
drugs - penicilin, sulfonamides, digoxin

60

purpura

small reddish purple blotches
associates with thrombocytopenia.