chapters 13,14,11 Flashcards
Whole blood consists of: %’s
55% plasma
45% formed elements
55% of whole blood is plasma, which consists of
water 91.5% solutes 1.5% proteins 7% - albumin - fibrinogen - globulins
45% of whole blood consists of formed elements which consists of
erythrocytes: 4.2-6.2 million
Platelets: 140,000-340,000
Leukocytes: 5,000-10,000
Leukocytes breaks down into
neutrophils: 57-67% eosinophils basophils lymphocytes: 25-33% monocytes
alpha globulin transports
bilirubin
lipids
steroids
beta globulin transports
iron
copper
gamma globulin
contains anitbody molecules
fibrinogen
inactive precursor of fibrin, which forms framework of bloodclots.
1/3 of platelets reserved in
spleen
erythrocytes functions
transport O2
Remove CO2
buffer blood pH
no cytoplasmic organelles, nucleus, mitochondria, or ribosomes
live 80-120 days
reversible deformity: biconcave and torpedo-like
platelets are fragments..
cytoplasmic fragments of megakaryocytes.
hematopoiesis
developmental process of pluripotential stem cells.
RBC. neutrophils
eosinophils. basophils
monocytes. platelets
hematopoises occurs
in bone marrow
hematopoiesis can be accelerated by
increase in differentiation of daughter cells
increase number of stem cells
conversion of yellow bone marrow to red marrow.
erythropoietin
hormone secreted by kidney to stimulate erythrocyte production
erythrocyte development stages
erythroblast
reticulocyte
erythrocyte
reticulocyte
small disk with no nucleus
leaves bone marrow and enters blood stream to where it matures to an erythrocyte.
hemoglobin synthesis
2 pairs of polypeptide chains; globins
- each with an attached heme molecule composed of iron
where is iron found in body
67% total body iron bound to heme
30% stored bound to ferritin
3%: lost daily
nutrition requirements for erythropoiesis
iron: hemoglobin
vitamins: b12, folate, b6
how is b12 absorbed
required intrinsic factor in stomach
- secreted by parietal cells
stimulant of erythopoiesis
low oxygen saturation
red cell destructions
80%-90% in spleen and liver
broken down into amino acids and iron is recycled
byproduct is bilirubin
-conjugated in liver and excreted in bile
- increased RBC destruction = increased bilirubin = jaundiice
anemia clinical manifestations
decreased O2 carrying capacity tissue hypoxia compensatory mechanisms - inc. pulmonary and cardiac function -inc. O2 extraction selective tissue perfusion (short-term) increased RBC production long-term
anemia s/s
fatigue
weak
tachycardia
exertional dyspnea
moderate to severe anemia s/s
hypotension. tachycardia
vasoconstriction. murmur
pallor. angina
tachypnea. heart failure
dyspnea muscle cramps
headache. dizzy
aplastic anemia
normocytic-normochromic anemia
stem cell disorder
dec. in hematopoietic tissue in bone marrow
pancytopenia
acquired aplastic anemia comes from
ebstein-Barr
HIV
Dengue
Familial aplastic anemia
fanconi constitutional pancytopenia
pancreatic deficiency in children
putative hereditary defect in cellular uptake of folate.
pancytopenia (aplastic anemia) s/s
RBC: weakness fatigue pallor dyspnea palpitations, murmurs WBC: fever, chills bacterial infections PLATELETS: petechiae bruising bleeding
aplastic anemia treatment
bone marrow transplant
maintenance of essential hemoglobin and platelets
prevention and management of infection
no transplant: immunosuppression, stimulation of hematopoiesis, bone marrow regeneration.
anemia of chronic renal failure
impaired erythropoietin production
impaired excretory function
- hemolysis, bone marrow depression, blood loss
anemia of chronic renal failure treatment
dialysis
administer erythropoietin
monitor hct and hgb
replacement of b12, iron, and folate (restricted diet)
where are clotting factors synthesized
liver
granulocytes
phagocytes:
- neutrophils
- eosinophils
- basophils
- mast cells
All granular
agranulocytes
phagocytes:
- monocytes
-macrophages
Immunocytes:
- lymphocytes (B & T)
- natural killer cells (granular)
granulocytes
digestive enzymes: - kill microorganisms - catabolize debris Biochemical mediators - inflammatory - immune functions
Eosinophils
allergic reactions
parasites
basophils
vasoactive amines:
- histamin
- serotinin
- heparin
mast cells
histamine, chemotactic factors and cytokines
acute/chronic inflammation, fibrotic disorders, wound healing
monocyte/macrophage
ingest and destroy microorganisms and foreign material, debris, and defective/ dead cells.
lymphopoiesis
B cells
T cells
fully mature in blood stream
stimulation of platelets
thrombopoiten
pediatric blood cell counts
higher than adult levels at birth
lymphocytes count higher at birth
platelets normal
3 main components of hemostasis
vasculature: endothelial cells
platelets
clotting factor
primary hemostasis
vascular damage
vasoconstriction
platelet plug
secondary hemostasis
coagulation cascade
blood clot
tertiary hemostasis
clot dissolution
fibrinolysis
extrinsic system
tissue factors
vitamin K
VII
intrinsic system
platelets XII Xi Vitamin K IX VIII
where extrinsic and intrinsic meet
Factor X
prothrombin
inactive precursor to thrombin
thrombin
acts upon fibrinogen to make active form fibrin.
Prostaglandin derivatives: positive hemostasis regulation
thromboxane
- platelets
- inc. fibrinogen receptors, cause degranulation, vasoconstriction
- aggregation
Negative hemostasis regulation
prostacyclin - endothelial cells - inhibit degranulation - vasodilation Nitric oxide - endothelial cells - vasodilation , inhibits adhesion/ aggregation
lysis of blood clots
t–PA
plasminogen-> plasmin
- degrading enzyme
fibrin degradation
megaloglastic anemia
large stem cells
defective DNA synthesis
- dec. vitamin b12 or folate
pernicious anemia
Macrocytic- normochromic Lack of IF from gastric parietal cells - no vitamin b12 absorption slow onset - nerve demyelination
sickle cell anemia
hypochromic anemia
genetic defect of hemoglobin synthesis
sickled cells cause vascular occlusion
severe anemia, RBC of different shapes, sizes, and recurrent painful episodes
iron deficiency anemia
microcytic hypochromic anemia most common world wide inadequate dietary intake/ blood loss insufficient iron delivery/use brittle, thin, coarsely ridged, and spoon-shaped nails red, sore and painful tongue
sideroblastic anemia
microcytic-hypochromoic
anemia due to mitochondiral metabolism of Fe, unable to use iron.
splenomegaly and hepatomegaly
ringed sideroblasts within the bone marrow
- RBC contain Fe granules that have not been synthesized into Hb
thalassemia
microcytic-hypochromic
increased RBC destruction
alpha or beta globin synthesis impaired
polypeptide chain with deficient synthesis of alpha or beta globins
faconi anemia
normocytic-normochromic anemia
genetic alteraion
defects in DNA repair
hemolytic anemia
normocytic-normochromic anemia accelerated destruction of RBC - inherited - autoimmune - drug- induced -- penicillin, cephalosporins -- Quinidine - a-methyldopa
Anemia of chronic disease
reduced response to EPO AIDS rheumatoid arthritis lupus hepatitis renal failure - dec. RBC life span - ineffective bone marrow response - altered iron metabolism
polycythemia
overproduction of RBC
relative polycythemia
dehydration
fluid loss
absolute polycythemia
1st: abnormality of bone marrow stem cells (vera)
2nd: increased EPO in response to chronic hypoxia
Polycythemia vera stages
1: prediagnostic by symptomatic
2: initial remission with treatment
3: myeloid-metaplasia (myelofibrosis)
4: acute leukemia
hypervolemic: reactive to increased RBC
qualitative leukocyte disorders
disruption of cellular function in cellular defense
- phagocytes, respond to antigen
hematologic leukocyte disorders
infectious mononucleosis
leukemia
lymphoma
infectious monomucleosis
acute: self-limiting infection of B lymphocytes.
- eventually develop an immune response.
caused by Epstein-Barr virus
leukemia
malignant disorder of blood/blood forming organs (bone marrow)
increased proliferation
genetic: translocation between 9 and 22
acute leukemia
presence of undifferentiated usually blast cells
chronic leukemia
predominant cell is mature but does not function normally
acute lymphocytic leukemia (ALL)
> 30% lymphoblasts in bone marrow/ blood
most common in children
acute myelogenous leukemia (AML)
abnormal proliferation of myeloid precursors
- immature blast replacement of normal cells
Chronic myelogenous leukemia (CML)
myeloproliferative disorder
- polycythemia vera
Chronic lymphocytic leukemia (CLL)
accumulation of B lymphocytes
failure to develop into plasma cells
hodgkin lymphoma
localized to single axial group
reed-sternberg cells in the lymph nodes
mesenteric nodes rarely involved
orderly spread
non-hodgkin lymphoma
chromosome translocations viral and bacterial infections environmental agents immunodeficiencies autoimmune disorders Clonal expansion of B, T, and NK cells multiple periphery nodes mensenteric nodes commonly involved sporatic spread
thrombocytopenia
platelet count less than 100,000
immune thrombocytopenic purpura (ITP)
autoimmune
increased platelet destruction
thrombotic thrombocytopenic purpura (TTP)
platelets aggregate and occlude arterioles and capillaries
all platelets are being used up
- less circulating
Disseminated intravascular coagulation (DIC)
widespread activation of thrombin - activates fibrin - clot formation multiple thrombi release of TF or thromboplastic agents injury to endothelial cells acute bleeding vs chronic thrombotic complications
geriatric blood cell findings
RBC life span normal RBC replaced less quickly - less iron Lymphocyte function decreased with age Platelets more sticky
protein C and S are pro-thrombotic
false
anti-thrombotic
synthesis of coagulation factors occurs
liver
with the exception of factor III, all coagulation factors are plasma proteins that circulate in the blood stream in an inactive state T/F
True
heparin inactivates
thrombin
- inhibition of clotting factor function
- useful in DIC
fibrinolysis occurs in response to
plasmin
philadelphia chromosome is diagnostic for
CML
benign growth of cells is characterized by?
hyperplasia
protooncogene
portion of gene controlling protein synthesis
-off position
oncogene
activated protooncogene
- one mutation: continuous cell growth and division in cancer
P53
initiates DNA repair
tumor suppressor genes
produce proteins that inhibit cellular division
-mutation: requires 2 gene mutations to trigger a role in cancer
challenges to treating cancer
traditional cancer therapies target all proliferating cells in the body
cancer is very heterogeneous disease
genetic instability
- adapt to new conditions, drug resistance.
