What is different about lymphocytes from all other blood cells?
come from a diff stem cell from other blood cells
Normal platelet count?
150,000 - 400,000
Where are non-circulating platelets stored?
What causes the release of platelets?
damage to the capillary endothelium
form a platelet plug
Where are plasma proteins formed?
mainly in the liver
3 plasma proteins that contribute to colloid osmotic pressure and blood pressure?
How does this occur
albumin, serum globulin, fibrinogen
they hold water in the vascular space due to colloid osmotic pressure
Serum albumin function?
essential to maintain blood volume and pressure
Serum globulin functions to transport ____, ____, _____, ____, & _____ in the plasma and contains _______molecules.
bilirubin, lipids, steroids, iron, and copper
inactive precursor of fibrin whih forms the framework for blood clots
Where does hematopoiesis occur in embyo?
liver and spleen
Where does hematopoisis occur in adults?
in the red bone marrow
3 serum globulin fractions?
alpha, beta, and gamma
2 stages in hematopoiesis?
When and how does mitosis of hematopoiesis occur?
immature stem cells undergo mitosis when stimulated by a biochemical signal that is released when the number of circulating cells is decreased
2 functions of erythropoeitin?
1. stimulates maturation/differentiation of blood cells in adults
2. stimulates marrow conversion from yellow to red
What type of hematopoiesis is abnormal in adults?
extramedullary (outside bone marrow
differentiation of immature lymphoid stem cell into mature lymphocytes
Why might an adult have extramedullary hematopoiesis?
long-term chronic anemia overworks the bone marrow and it cannot meet demands of the body so spleen and liver start performing hematopoiesis
Lymphocytes differentiate into ____ & _____.
b cells and t cells
What controls erythropoiesis?
amnt of HgB in the blood
Why does HgB level affect erythropoiesis?
decreased O2 transport stimulates increased RBC production
What stimulates the release of erythropoietin?
Renal hypoxia -> release of erythropoieting ->_____.
RBC production is stimulated
Where does hemolysis occur?
spleen and liver
Broken down RBC's ae removed from the circulation by _____.
When hemolysis occurs what happens to HgB?
1. broken down to heme and globin
2. heme is converted to bilirubin -> transported to liver by serum globulin and albumin -> liver excretes bilirubin into intestine as part of bile -> bacteria in intestine convert bilirubin to urobiligen ->excreted in feces and some in urine
2 parts of HgB?
heme and globin
What is necessary for the production of HgB?
67% of body's iron is ______, 30% is bound to ____, ____, and ___ _____, and 3% is ____.
bound to heme in RBC and muscle cells
stored bound to ferritin, some macrophages, and hepatic cells
lost daily in urine, sweat, and via intestines
heme = _____.
Why does liver dysfunction cause jaundice?
bilirubin (yellow - colored) builds up in the body b/c it is normally excreted into the intestines by the liver as part of bile
What is O2 sat a reflection of?
% of HgB that is saturated with oxygen
Normal Hct in men and women?
men - 45%
women - 42%
Normal relationship of Hct to HgB?
Hct usually HcT usually 3X that of HgB
If a pt has a severely depleted H&H with O2 sat of 100% are they OK?
What would be a more accurate reflection?
no, because they don't have much HgB so even if all of it is saturated with O2 they don't have enough O2 either way
PaO2 - amount of O2 in the blood (on ABG)
defecit of RBC's that is not a disease but a manifestation of a pathologic process
Pt with decreased RBC has decreased _______ and can have ______ and tissue ______.
hypoxemia, and hypoxia
3 reasons for anemia?
1. decreased RBC production
2. blood loss
3. increased RBC desruction
Main concern with a pt with anemia?
decreased O2 carrying capacity of blood
Manifestations of anemia stem from _____ and include _____.
decreased O2 carrying capacity of the blood
mech to compensate for tissue hypoxia
First manifestations of anemia?
Second S/S of anemia?
due to compensation - tachycardia, DOE, pallor, vasoconstriction, shunting of blood flow to vital organs (AWAY from skin and kidneys)
S/S of severe anemia?
chest pain, fainting, and possible heart murmur
Why chest pain with severe anemia?
infarction of heart tissue due to hypoxia from anemia
Major complication of severe anemia?
MI due to hypoxia
Why have a heart murmur with anemia?
severe anemia - tachycardia and increased CO due to compensation causes murmur
Iron deficiency anemia?
lack of iron necessary for HgB synthesis
2 main causes of iron deficiency anemia in men and women?
men - GI bleed
women - menorrhagia
2 causes of Fe deficiency anemia?
decreased intake or absorption by the duodenum or loss via hemorrhage
2. iron replacement (ferrous SO3 PO, IV replacemtn for severe cases)
3. dialysis pt should have optimal serum iron and ferritin levels
Why do dialysis pt need good Fe and ferritin levels?
give dialysis pt procrit (synthetic erythropoiten) - if there is no Fe or ferritin to carry Fe then RBC will be produced but they will not contain HgB
itracellular protein that stores and transports Fe in the body
genetic disorder most prevalent among Asians and ethnic groups near Mediterranean sea that causes anemia
Patho of thalassemia major?
insufficient production of normal HgB due to inherited problem with either the alpha or beta globin protein fraction - mutant gene replaces normal fraction -> the non-effected globin protein is over-produced and the RBC are oddly shaped and prone to hemolysis
labs with thalassemia major?
1. very low HgB
2. MCV, MCH, MCHC are all decreased - RBC are small and pale due to lack of HgB
S/S of thalassemia major?
1. S/S of anemia
2. splenomegaly - r/t excessive filtering of deformed RBC's
3. hepatomegaly - r/t Fe overload
4. down's syndrome appearance
5. bone deformities
due to overworked bone marrow - bone marrow will overgrow
Tx of thalassemia major?
1. blood tranfusions to maintain accetable H&H in children
2. bone marrow transplantation
3. chelation/vitamin C for Fe overload
therapy to remove heavy metals from the blood
Why is it necessary to maintain acceptable blood levels with blood transfusions in thalassemia?
RBC are being destroyed
Why does Fe build up in thalassemia major?
RBC destruction releases iron and causes overload
Only way to cure thalassemia?
bone marrow transplantation
Who does thalassemia major present in most?
Why is it necessary to ONLY get blood levels to acceptable levels?
will stifle their body's own RBC production if get levels too high
genetic stem cell disorder that causes all blood cell types to be decreased
3. immunosuppresive therapy if caused by autoimmune disorder
4. maintain acceptable levels of HgB and platelets
5. bone marrow transplatation with umuunosuppresive therapy is curative
6. vit B12 or folate deficiency
Tx for prevention and management of infection in aplastic anemics?
______ medications can cause aplastic anemia?
What is the result of anemia caused by deficiencies in folate and B12?
disrution of DNA synthesis of blast cells of the bone marrow -> funky shaped RBC's
3 causes of folate and B12 deficiencies?
1. dietary deficiency
2. lack of intrinsic factor produced by parietal cells of the stomach (gastrectomy)
3. possibly a genetic, autoimmune disease causing antibodies against intrinsic factor
Functions of B12?
mylenation and DNA synth of blast cells in bone marrow
What is necessary for B12 absorption?
classic B12 deficiency anemia caused by lack of intrinsic factor
Labs in pernicious anemia?
1. large RBC
2. decreased H&H
3. decreased serum cobalamin/B12
2 diagnostic tests for pernicious anemia?
1. + Schilling test - indicates low levels of excretion of radioactive vit B12
2. gastric acid analysis - may be negative for HCL acid
Why is gastric acid low in pt with pernicious anemia?
because parietal cells that produce intrinsic factor also produce HCL acid
Problem that occur in gastric bypass?
low levels of intrinsic factor = pernicious anemia
2 Tx gastric bypass ppl have to do for life
intrinsic factor replacement and B12 supplements
diagnostic test for pernicious anemia IM injection of B12 and oral B12 that is radioactive then test urine for B12
S/S of pernicious anemia?
1. general S/S of anemia
2. neuromuscular S/S: weakness, parethesias, reduced position sense, impaired thought processes
Why are there neuromuscular S/S with pernicious anemia?
B12 is involved in nerve myelination
Tx of pernicious anemia?
1. IM B12 injections + oral folate until cause is ID'd
2. blood transfusions may be necessary for elderly pt
3. manage possible hypokalemia associated with early B12 therapy
2 effects of deficient B12?
anemia and neuromuscular effects
Major concern when pt is taking B12 supplements?
Sickle cell anemia?
autosomal recessive genetic disorder with abnormal form of HgB produced - HgB S
What occurs in sickle cell anemia?
RBC become deformed and crescent shaped when O2 levels are low
Approx. _____ African Americans are carriers of sickle cell anemia.
1 in 10
Prognosis for sickle cell anemia?
incurable - often fatal by middle age form renal and pulmonary failure
Labs with sickle cell anemia?
1. severe anemia
2. sickled cells on blood smears
3. increased serum bilirubin due to high rates of RBC hemolysis
S/S of sickle cell anemia are all r/t what?
Results of this?
all r/t sickled shape of HgB
sickled cells cannot pass through blood vessels and may get stuck and occlude vessels causing thrombosis and/or sickled cells are damaged by running into vessel walls which causes increased RBC hemolysis in spleen and causes severe anemia
Sickle cell crisis?
mass sickling of RBC
2 S/S of sickle cell crisis?
1. vaso-occlusion anywhere
2. severe pain
7 factors that can cause sickle cell crisis?
1. hypoxia of RBC
2. lung infection
3. dehydration (cells clog vessels more)
4. high altitudes
5. emotional/physical stress
6. surgery & blood loss
7. extreme cold
S/S of sickle cell anemia?
mainly s/s are caused by what?
S/S mainly caused by clots due to clogging of vessels:
2. cardiomegaly -> congestive heart failure
3. renal infarcts -> hematuria
4. bone marrow hyperplasia
5. aseptic bone necrosis -> osteomyelitis
6. CVA -> mental retardation
7. pulmonary embolism -> pneumonia
8. splenomegaly -> splenic atrophy
9. infarcts of extremities
11. ulcers (on legs)
12. severe pain
Tx of sickle cell anemia?
1. oxygen2. pain meds
3. bed rest
4. IV fluids
5. blood transfusion if needed
6. bone marrow transplant
Why is pain a big priority with sickle cell anemia?
pain is severe and can cause stress that increase crisis
Teaching for sickle cell anemia?
1. avoid high altitudes
2. adequate fluid intake
3. prevent/treat infections: vaccines important
ASA and tylenol is sickle cell anemia?
avoid ASA - salicylic acid - acidity can lead to crisis
tylenol can increase liver probs that can occur in sickle cell
Acquired hemolytic anemia?
caused by abnormal breakdown of RBC due to physical trauma, immune disorders, or infections/toxins
4 EX of physical traumas that could cause acquired hemolytic anemia?
hemodialysis, CPB, prosthetic heart valves, burns
3 EX of infections/toxins that can cause acquired hemolytic anemia?
malaria, arsenic or lead poisoning, snake venom
Anemia of acute blood loss?
present after major trauma or secondarty to a disease process such as a GI bleed
Effect of anemia of acute blood loss?
rapidly decreases overall blood volume
Anemia caused during cardiac bypass surgery?
heart and lung machine used during cardiac bypass surgery that pumps blood through the machine and acts as artificial heart - can destroy RBC
Clinical manifestations of anemia of acute blood loss?
1. 10% loss - asymptomatic
2. tachycardia/hypotension with exercise, cold/clammy skin at rest
3. 50% loss - shock and death
Tx for anemia of acute blood loss?
1. Stop blood loss2. replace lost volumes: IV fluids (crystalloids and colloids) - usually NS initially
3. replace blood volume with blood transfusions
too many RBC
blood circulation may be impaired by hypervolemia and hyperviscosity of blood
2 types of polycythemia?
primary - polycythmia vera
Polycythemia vera cause?
caused by chromosomal mutation of a single stem cell into an abnormal cell which multiples at very high rates
When does polycythemia vera start?
aroung age 60
Development of polycythemia vera?
dev slowly and follows a chronic course
Labs in polycythemia?
increased RBC, WBC, and platelets
O2 sat is normal
Secondary polycythemia cause?
hypoxia due to an outside process
Some conditions that can cause secondary polycythemia?
COPD, anything that causes chronic hypoxia
Why does hypoxia cause polycythemia?
not enough O2 will increase RBC production
Labs in secondary polycythemia?
increased RBC, O2 sat will be reduced
Clinical manifestations and potential complications of polycythemia?
1. CVA due to thrombosis2. thomboses
5. pronounced pruritis
6. hemorrhage r/t destruction of vessels due to excess blood volume
7. hepatomagaly and splenomegaly
Most serious complication of polycythemia?
CVA due to thrombosis
Tx for polycythemia?
phlebotomy to keep Hct at around 48%
3. ROM to prevent clots
4. possibly myelosuppresive therapy to suppress bone marrow
arrest of bleeding/ prevention of blood loss
How is hemostasis achieved/dysfunctional?
acheived through interactions between vessel wall, platelets, and plasma coagulation proteins
if any of the 3 are dysfunctional will alter hemostasis
Labs for coagulation disorders?
What will occur is the pt has thinner blood/ blood that is not clotting normally?
1. PT- prothrombin time
2. INR - international normalized ratio
3. aPTT - activated partial thromboplastin time
increases in these values mean "thinner" blood that will take longer to clot than normal
international normalized ratio
activated partial thromboplastin time
heparin and lovenox
What would you expect the aPTT to look like for a person on heparin?
should be higher than normal
therapeutic - 55 to 75
What should be monitored if pt is taking the drugs heparin and lovenox?
What should be monitored in pt taking coumadin?
PT & INR
3 drugs where increased clotting time/ thinness of blood is expected and desired?
coumadin, lovenox, and heparin
platelet count < 100,000
#1 reason ppl are on coumadin?
S/S of thrombocytopenia?
no S/S until gets < 50,000
< 50,000 - increased bruising/prolonged bleeding after minor trauma
Why does everyone put on heparin have to have a baseline CBC?
have to have baseline platelet level to monitor for HITS - will be cut in half after admin of heparin
EX of a drug that can cause thrombocytopenia?
S/S of thrombocytopenia?
1. bleeding most common - epistaxis
2. petechia, purpura, ecchymosis
3. bleeding into joints, retina, brain
4. s/s of internal bleeding
Contraindication if a pt is on heparin or has severely low platelet levels?
IM injections will cause bleeding
flat, pinpoint, non-blanching red or purple spots caused by capillary hemorrhages in the skin and MM's
petechiae that occur in groups or patches
platelet count >400,000 that is usually a secondary response to hemorrhage, inflammatory disease, trauma, malignancy, infection, hemolysis (anything that causes bleeding and increases platelet production)
Meds that can cause thrombocytosis?
Tx for thrombocytosis?
treat with antiplatelet drugs
How do they work?
ASA, plavix, hydroxyurea, agrylin
ASA and plavix prevent platelet aggregation
agrylin inhibits maturation of platelets
What is aspirin used for in the hospital?
Not used for?
used as anticoagulant med
not for pain or fever
Hemophilia and von willebrand disease?
inherited disorders of coagulation where pt is lacking a clotting factor
What clotting factors are deficient in hemophilia A, hemophilia B, and von willebrand disease?
hemophilia A - Facor VIII and fibrinogen
hemophilia B - Factor IX and fibrinogen
vwd - deficiency of von Willebrand coagulation protein
Clinical manifestations of hemophilia A&B and von Willbrand disease?
1. prolonged bleeding from even minor injuries
2. uncontrolled bleeding after dental procedures
4. GI bleeding
5. ecchymoses and hematomas
7. hemophilia and von willebrand disease
Where does it occur most?
bleeding into joints causes pain and possible deformitiy
mostly in knees, ankles, elbows, shoulders, and hips
Tx/prevention of hemophilia A&B and von Willebrand disease?
1. replacement of deficient clotting factor with FFP
2. avoidance of aspirin
3. joint bleeding controlled with immobilization and ice
4. prophylaxis before dental procedures
5. DDAVP (desmopressin)
What does it do?
stim release of clotting factors from endothelial cells
How is coumadin toxicity treated?
fresh frozen plasma
disseminated intravascular coagulation - life-threatening syndrome in which clotting and bleeding occur simultaneously
2 triggers of DIC?
1. anything that causes damage to vascular wall and initiates the inflammatory response
2. clotting response is initiated by presence of pro-coagulation substances in the blood or stagnant blood flow
Patho of DIC?
coagulation cascade is initiated by inflammatory response or presence of pro-coagulation substances in blood or stagnant blood flow -> accelerated clotting is initiated -> clotting factors are depleted and the fibrinolytic system is over-activated to break down the clots -> bleeding
#1 cause of DIC?
2 EX of things that cause DIC through inflammation?
3 things that can cause DIC through pro-coagulation substances?