-
neutrophil
granulocyte that is usually first on scene of inflammation/infection and releases enzymes that kill microbes
-
eosinophil
granulocytes that are released in response to allergies and parasites
-
basophils
granulocytes that respond in allergic/inflammatory reactions
- release histamine = vasodilation
- release heparin = thin blood
-
hematopoiesis?
formation of blood cells
-
HgB?
oxygen transport protein of the RBC
-
Hct?
% of RBC in the blood
-
methemoblobin
form of HgB where iron in the heme groups is in the ferrous state (Fe3+) instead of ferrous state (Fe2+) that is naturally produced in the body
cannot bind oxygen
-
Anemia?
decreased RBC's or HgB in the blood
-
Polycythemia?
increased proportion of RBC for blood volume
-
Pancytopenia?
reduced amount of RBC, WBC, and platelets
-
Granulocytopenia?
What are the 3 granulocytes?
decrease in amount of granulocytes
neutrophils, eosinophils, and basophils
-
Megaloblasts?
unusually large erythroblast
-
erythroblast?
nucleated precursor cell for RBC
-
-
hypochromic?
RBC's are paler than normal due to decreased HgB of the cell
-
reticulocyte count?
Why may it rise?
measures how fast RBC are made by the bone marrow and released into the blood
will rise anytime negative feedback shows the need for more RBC: hypoxia, RBC destruction, hemorrhage, etc
-
-
acrocyanosis
blue fingers and toes
-
hematology
study of blood and blood forming tissues
-
4 major organs of blood formation and their functions?
- 1. bone marrow - blood forming organ
- 2. spleen - filters micro-org from blood; RBC destruction
- 3. lymph system - maturation of T lymphocytes
- 4. liver - formation of plasma proteins
-
Composition of the blood?
45% cells, 55%plasma
-
platelets AKA?
thromocytes
-
How much blood is in the body?
5-6L
-
Composition of plasma?
mostly water with plasma proteins and inorganic compounds
-
Normal RBC count?
4.2 - 6.2 million/mm3
-
2 functions of RBC?
- 1. transport O2 and CO2
- 2. assist in maintaining acid-base balance
-
Normal WBC count?
5000-10,000/mm3
-
2 functions of WBC?
- 1. phagocytosis
- 2. immune antibody formation
-
2 types of neutrophils?
bands and segs
-
Bands?
baby neutrophils - indicates acute bacterial/viral infection
-
-
2 types of agranulocytes?
monocytes and lymphocytes
-
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?
spleen
-
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?
AKA?
essential to maintain blood volume and pressure
-
Serum globulin functions to transport ____, ____, _____, ____, & _____ in the plasma and contains _______molecules.
bilirubin, lipids, steroids, iron, and copper
antibody
-
Fibrinogen?
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?
- 1. mitosis
- 2. maturation/differentiation
-
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
-
Lymphopoiesis?
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
-
Erythropoiesis?
RBC production
-
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
-
Renal hypoxia -> release of erythropoieting ->_____.
RBC production is stimulated
-
hemolysis?
RBC destruction
-
Where does hemolysis occur?
spleen and liver
-
Broken down RBC's ae removed from the circulation by _____.
the spleen
-
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?
iron
-
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
-
-
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)
-
Anemia?
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 ______.
O2-carrying ability
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?
fatigue, weakness
-
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
-
Labs for iron de
decreased H&H, RBC, serum Fe,
RBC are small and pale
MCV, MCH, MCHC are decreased
-
RBC indices?
part of CBC with differential
description of size, weight, and width of the RBC
-
S/S of iron deficiency anemia?
- 1. most assymptomatic
- 2. may display general s/s of anemia
- 3. classic clinical manifestations: glossitis (smooth red tongue), chelitis (dry, cracked lips), PICA
-
glossitis?
smooth, red tongue
-
Chelitis?
dry, cracked lips
-
Treatments of iron deficiency anemia?
- 1. treat underlying causes
- 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
-
Ferritin?
itracellular protein that stores and transports Fe in the body
-
Thalassemia major?
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
-
Thalassemia minor?
carrier only
-
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
-
Chelation?
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?
children
-
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
-
Aplastic anemia?
genetic stem cell disorder that causes all blood cell types to be decreased
-
2 causes of aplastic anemia?
congenital or acquired
-
4 possible causes of acquired aplastic anemia?
EX 2 drugs that can cause it?
radiation, toxins, drugs, and infection
tegretol/carbamazepine and anti-neoplastics
-
Labs in aplastic anemia?
pancytopenia on CBC
-
S/S of aplastic anemia?
- 1. general S/S of anemia
- 2. bacterial infections
- 3. signs of bleeding: epistaxis, increased bruising, increased menstrual flow, retinal hemorrhage)
-
2 major concerns in aplastic anemia?
- prone to infection
- prone to bleeding
r/t reduced WBC and platelets
-
6 Tx for aplastic anemia
- 1. Tx the underlying cause
- 2. prevention and management of infection
- 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?
neupogen
-
______ medications can cause aplastic anemia?
anti-convulsants
-
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?
intrinsic factor
-
Pernicious anemia?
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
-
Schilling test?
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?
hypokalemia
-
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:
- 1. retinopathy
- 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
- 10. vaso-occlusion
- 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
- 7. teaching
-
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
-
Polycythemia?
too many RBC
-
Polycythemia results?
blood circulation may be impaired by hypervolemia and hyperviscosity of blood
-
2 types of polycythemia?
primary - polycythmia vera
secondary polycythemia
-
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
- 3. hypertension
- 4. angina/CHF
- 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%
- 2. hydration
- 3. ROM to prevent clots
- 4. possibly myelosuppresive therapy to suppress bone marrow
-
Hemostais?
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
-
PT?
PT normal?
Drug?
prothrombin time
10-14 seconds
coumadin
-
INR?
INR normal?
Drug?
international normalized ratio
0.8 -1.2
coumadin
-
aPTT?
aPTT normal?
Drugs?
activated partial thromboplastin time
35-45 seconds
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?
aPTT
-
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
-
Thrombocytopenia?
platelet count < 100,000
-
#1 reason ppl are on coumadin?
atrial fibrilation
-
S/S of thrombocytopenia?
no S/S until gets < 50,000
< 50,000 - increased bruising/prolonged bleeding after minor trauma
<20,000 spontaneous hemorrhage
-
HITS?
heparin induced thrombocytopenia
-
4 causes of thrombocytopenia?
1. idiopathic thrombocytopenic purpura - immune mediated thrombocytopenia
2. drugs - heparin (allergic reaction), digoxin, thiazide diuretics, dilantin, tegretol
3. alcohol intake
4. radiation/chemotherapy
-
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?
lopressor
-
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
-
Petechiae?
flat, pinpoint, non-blanching red or purple spots caused by capillary hemorrhages in the skin and MM's
-
Purpura?
petechiae that occur in groups or patches
-
-
-
Thrombocytosis?
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?
estrogen/oral contraceptives
-
Tx for thrombocytosis?
treat with antiplatelet drugs
-
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
- 3. hematuria
- 4. GI bleeding
- 5. ecchymoses and hematomas
- 6. hemarthrosis
- 7. hemophilia and von willebrand disease
-
Hemarthrosis?
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)
-
DDAVP?
What does it do?
desmopressin
stim release of clotting factors from endothelial cells
-
How is coumadin toxicity treated?
FFP
-
-
DIC?
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
-
-
2 EX of things that cause DIC through inflammation?
sepsis, burns
-
3 things that can cause DIC through pro-coagulation substances?
snake venom, malignancy, incompatible blood tranfusion
-
EX of a condition that causes DIC through stagnant blood flow?
shock
-
6 potential causes of DIC?
sepsis, burns, snake venom, milignancy, incompatile blood transfusion, shock
-
What is the ultimate result of DIC?
massive hemorrhage
-
Clinical manifestations of DIC?
clotting and bleeding issues
- 1. clot to any organ: MI, kidneys and lungs are mainly affected
- 2. hemorrhagic: bleeding may occur from various sources: petechiae, bruising, internal bleeding
-
How would the nurse recognize if DIC has caused renal failure?
Hct, daily weights, I&O, BUN
-
How would the nurse recognize if DIC has caused pulmonary infarct?
- 1. dyspnea
- 2. decreased O2 sat
- 3. anxiety
-
Labs for DIC?
+ D dimer and elevated anti-thrombin complex
1 of them positive does not indicate DIC but if both are postivie it is indicitive of DIC
-
D-dimer?
specifically measures excessive fibrinolysis
-
anti-thrombin complex
small protein that inactivates several enzymes of the coagulation system
-
Tx of DIC?
- 1. removal of underlying cause and support of major organs
- 2. replacement of depleted clotting factors
- 3. anti-fibrinolytics for life=threatening hemorrhage
- 4. controversial - begin heparin drip on at risk pt to prevent clots from ever forming
-
How are clotting factors replaced for DIC?
FFP, PRBC's
-
Amicar?
anti-fibrinolytic that is used in DIC to treat life-threatening hemorrhage
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