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Where do all blood cell types originate from?
pluripotent hematopoietic stem cells
When would you tend to see a high number of reticulocytes? What does this mean?
- In an anemic pt.
- The immature cells are coming out of the BM earlier than normal as a compensatory mechanism.
What is the most important regulator of RBC production?
Tissue oxygenation. RBC function is to carry O2 attached to Hgb.
Normal RBC value for men.
- 4.7 - 6.1 million cells / microliter
- Avg= 5.2 million
Normal RBC value for women.
- 4.2 - 5.4 million cells / microliter
- Avg= 4.7 million
What is MCV?
mean corpuscular volume, aka avg RBC size
What is MCH?
mean corpuscular Hgb, avg amount (mass) of Hgb in a RBC
What is MCHC?
mean corpuscular Hgb concentration
Increased MCV (often from nutritional anemias from B12 and folate deficiency)
characterized by decreased MCH
In low O2 states, ______ will stimulate the production of RBCs.
Where is erythropoietin made (2 sites)
- 90% in the kidney
- 10% in the liver
T or F, in kidney failure the liver can compensate to produce enough erythropoietin for adequate RBC production?
What substances will stimulate erythropoietin production?
NE, epi, and prostaglandins
stimulates erythropoietin production in the kidney
Decreased O2 carrying capacity from any cause
Do RBCs have a nucleus?
Avg RBC lifespan?
RBCs carry a large amount of this enzyme. It catalyzes the reaction of CO2 and water to form carbonic acid. This allows the blood to carry large amounts of CO2 in the form of bicarb ion from the tissues to the lungs. Then it gets converted back to CO2 and is exhaled.
Major buffer found in whole blood?
RBCs, Hbg is a protein, and like other proteins, is a really good buffer.
Avg H+H for a male
45 / 15
Each gram of Hgb can carry about ____ ml of O2.
An individual can carry about ___ ml of O2 per 100 ml of _____.
- Glucose-6-phosphate dehydrogenase is an enzyme in the glycolytic pathway.
- A deficiency in G6PD will disrupt the glycolytic pathway that's needed for RBC metabolism.
- Hemolytic anemia results (G6PD is needed for the stability of the RBC, so without it, RBCs have decreased life span).
- Genetically transmitted.
fractional volume of RBC mass
Major blood components
- RBCs- 45%
- "Buffy coat"- WBCs and Plts- 1%
- Plasma- 54%
stimulation to produce erythropoietin
Optimal erythropoiesis occurs when there is sufficient ____, _____, and ____.
B12, iron, and folate.
SCD involves substitution of ____ for ____ in the beta globulin subunit, making it Hgb S.
valine, glutamic acid
What type of anemia is SCD?
What factors will cause Hgb S to sickle?
hypoxia (PO2< 40 mmHg), acidosis, dehydration, hypothermia
What issues are r/t sickling of cells?
- Cells get stiff clog vessels, organ infarction can occur
- Blood sequestration in the liver and spleen
Is SCD usually the homo or heterozygous form?
Sickle cell trait
- Heterozygous form
- Have 1 Hgb A (normal) and 1 Hgb S (SCD)
- Carrier of SCD
- Rare clinical manifestations
-Type of anemia?
- Early in life
- Severe hemolytic
- Vaso occlusive disease involving the bone marrow, liver, spleen, kidneys, and CNS
Most common cause of M+M in SCD?
Pulm and neuro complications
How does SCD affect the oxyHgb dissociation curve?
- Right shifted, O2 is given up more easily to the tissues.
- Normal P50 = 27, in SCD it's 31 mmHg
PO2 at which the Hgb is 50% saturated
What surgeries are considered low risk for SCD pts?
Inguinal hernia repair, extremity surgeries (except hips)
What surgeries are considered moderate risk for SCD pts?
chole, abd surg
What surgeries are considered high risk for SCD pts?
- intracranial or intrathoracic
- hip surgery
What are peri-op risk factors for SCD pts?
- frequency of hospitalizations or transfusions
- prior organ damage
- concurrent infections
T or F, heterozygous SCD is associated with increased peri-op M+M?
F, homozygous SCD is associated with increased peri-op M+M
Goal pre-op Hct for SCD pts
What should be avoided intra-op with SCD pts?
- Dehydration (1.5 x maint fluid req. for 12h)
- Hypoxemia (minimize pre-op sedation, full reversal at case end, supplemental O2 x 12-18h)
- Hypotension and low flow situations
Acute chest syndrome
- May develop post-op in pts with SCD
- Need aggressive oxygenation, analgesia, and blood transfusions
Why should N20 be avoided in pts with megaloblastic anemias
N20 inhibits methianone synthetase and may worsen the anemia (further impairs B12 activity)
- Due to folate (alcoholism) or vit B12 deficiency
- Deficiency causes BM to be affected
- RBC precursors in the BM become large and can't complete cell division
- These large RBCs are released into the circulation
- Possible neuro issues (peripheral neuropathy, gait disturbances, bilateral paresthesias)
- Tx= replacement of vitamins parenterally
- Due to iron deficiency
- Small RBCs
- Tx= iron replacement
- Inherited defect in globin chain synthesis
- Type of microcytic anemia
- Beta form common in Africa and the Mediterranean
- Alpha form common in SE Asia
Types of thalassemia
- minor- Hgb 10-14
- major- severe and life threatening anemia during the 1st few months of life, require LT transfusion therapy
Anesthesia considerations for thalassemia minor
Chronic compensated anemia, therefore no big considerations.
Anesthesia considerations for thalassemia major
Pts may have splenomegaly, hepatomegaly, CHF, R sided HF, cirrhosis, or various encrinopathies
- Decreased O2 affinity, left shifted oxyHgb dissociation curve
- Little O2 delivery to the tissues
- MetheHgb formed when Fe2+ is oxidized to Fe3+
- Due to mutations or certain drugs
Normal amt of methehemoglobin
Methehemoglobin concentration < 30% of total Hgb
No compromise in oxygenation
Methehemoglobin concentration 30-50% of total Hgb
Pts start to show signs of decreased oxygenation
Methehemoglobin concentration > 50% of total Hgb
Coma and death may result
- Methylene blue 1-2 mg / kg IV as 1% solution over 3-5 minutes
- Requires G6PD to be effective
-what is it?
- decreased RBC production
- causes can include- aplastic anemia due Fanconi's syndrome or drug or radiation induced
decreased production of all blood cell types
- type of aplastic anemia
- exhibits as pancytopenia
Chemo drugs and radiation can produce BM damage associated anemia- is this reversible?
Yes, in most cases
T or F, infectious diseases such as Epstein Barr, HIV, TB, and viral hepatitis can cause BM damage leading to aplastic anemia?
T, usually reversible however
- erythrocytosis or elevated Hct or RBC count
- may be a compensatory response to prolonged hypoxia
Tissue oxygenation is optimal at a Hgb of ____g/dl
Why is O2 delivery decreased in polycythemia?
Blood viscosity increases, flow decreases, and hence less O2 is delivered to the tissues
At what Hct do effects of polycythemia begin to be seen? What s/sx?
- Hct > 50%
- Decreased blood flow to brain and other key organs, may see easy fatigability
At what Hct is polycythemia life threatening?
- Hct > 60%
- Brain is particularly susceptible to decreased perfusion
- Risk arterial and venous thrombosis
What's the difference between primary and secondary polycythemia?
- Primary- due to a stem cell d/o
- Secondary- due to physiologic response to hypoxia, chronic exposure to high altitude, or increased erythropoietin (tumor)
T or F, its with polycythemia vera are at increased risk of both thrombosis and hemorrhage peri-op?
T, increased risk for peri-op hemorrhage due to acquired vWD
Polycythemia anesthesia considerations
- Pre-op phlebotomy
- O2 therapy
- Increased risk for both thrombosis and bleeding
What WBC subtype makes up the majority of WBCs
- neutrophils (PMNs- polymorphonuclear neutrophils)
What are band cells? Normal % of WBCs?
When might an increase in band cells be seen? What is this called?
- With infection, BM putting out younger (immature) neutrophils to try to fight off infection
- Left shift
When might an increase in eosinophils be seen? Normal % of WBC count?
- Allergies or parasitic infections
- 1-4 %
WBC subtype making up the smallest %?
uncontrolled WBC production
Common issues associated with leukemia
- Fatigue (cancerous cells using all the nutrients and energy)
- All due to non functional leukemic cells displacing the BM (so functional cells can't be made)
What are the 2 subtypes of leukemia?
- Lymphogenous (generated in lymph tissues or nodes)
- Myelogenous (generated in the BM)
Chemo - bleomycin and doxyrubicin
General SE of chemo drugs
- Susceptibility to infection or bleeding due to BM suppression
- Tumor destruction increases uric acid load so arthritis and nephropathies can develop
cardiotoxic, even up to 5 years later
- Pulm toxic, causes pulm fibrosis
- PF worsens with increased concentrations of O2, so keep FiO2 < 30%
Vinca alkaloids SE
- chemo agents
- ex: vinchristine, vinblastine
- SIADH or peripheral neuropathy
- paresthesias of the hand
Time to engraphment with BM transplant
- Time for new cells to take hold in the BM
- 10-28 days, pt must be in isolation during this time
Anesthesia considerations for pts with leukemia
- Volume status- N/V
- Use of chemo agents that could have SE (cardiac or pulm)
- viral infection kills helper T cells
- HIV belongs to a retrovirus family
As AIDS occurs, a _____ in the CD4 T cells is seen and a ____ in the viral load, because the virus uses those cells (CD 4 T cells) to gain entry into the T cells.
What CD 4 T cell count is associated with an increased M+M?
< 200 cells / ml
T or F, up to 90% of pts with HIV have an abnormal cardiac echo and pericardial effusion?
- F, 50% have abn echo
- 25% have pericardial effusions
Pneumocystis carinii (PCP)
- PNA associated with HIV
- Occurs when CD 4 count < 200 cells / ml
- Highly active anti-retroviral therapy
- 3 agents
- goal is to have undetectable viral load by 24 weeks
In what bodily fluids can HIV be found?
Tears, saliva, blood, semen, vaginal secretions, CSF, urine, breast milk
How long can HIV live for outside of the host?
Is immunosuppression from GA of concern to a pt with HIV?
- Immunosuppression occurs within 15 mins of induction and may persist for as long as 3-11 days.
T or F, autonomic neuropathy may be associated with HIV?
Why should succ be avoided in HIV pts?
HIV pts may have myopathy or peripheral neuropathy making succ dangerous
Following a hollow needle stick with high risk fluid, how soon should post-exposure prophylaxis be started?
- Within 1-2 hours, but can be as long as 1-2 weeks after.
- You can treat beyond this time frame, but in this case you are limiting the severity, not preventing infection.
What causes VC of the vessel to occur?
BV injury that causes disruption of the normal endothelial lining
What events occur to cause VC of a BV
- 1) Disruption of the endothelial lining of the BV causes endothelin (VC) to be released
- 2) There is also a myogenic spasm (local)
- 3) Thromboxane A-2 (VC) is released from Plts
What is the primary goal of primary hemostasis
Plt plug formation
Plts are fragments of _____ and have no nucleus.
What role do glycoproteins play in Plt action?
- Glycoproteins activate the Plts and cause them to stick onto the exposed endothelial surface when there's a BV breach
- Also prevent Plts from sticking to normal endothelial cells
____ of Plts are sequestered in the spleen
What 3 factors are needed for formation of a Plt plug (hint- A)?
What are some characteristics of Plts that enable them to form clots?
- Contractile proteins (actin & myosin filaments, thrombosthenin)
- Calcium stores (golgi)
- Mitochondria (ATP)
What 2 molecular interactions cause Plts to adhere to the sub-endothelium (collagen)?
- 1) GP1b and VWF (VWF is secreted by activated Plts and injured sub-endothelium)
- 2) GPVI
both attach to collagen
What happens during Plt activation?
- granules are released
- Plts change their shape and get contractile and form pseudopods
In what 2 ways can Plt activation occur?
- 1) exposure of sub endothelial collagen
- 2) Tissue factor (called thromboplastin in clotting cascade)
T or F, the membranes of the activated Plts are really important to a number of critical reactions in the clotting cascade including conversion of prothrombin to thrombin?
What 3 factors mediate Plt aggregation?
- Thromboxane A2
What receptors are essential to Plt aggregation?
What drugs inhibit the GP2b3a receptor?
Integrillin, reopro, aggrastat
What receptor do the anti-Plt drugs plavix, prasugrel, and ticlopidine affect?
P2Y ADP receptor
Essential pieces to the coagulation mechanism
- Prothrombin activator causes prothrombin to be converted to thrombin (need Ca++)
- Presence of thrombin (an enzyme) causes fibrinogen to convert to fibrin
- Thrombin causes activation of fibrin stabilizing factor, cross linked fibrin fibers are formed
What is the rate limiting step in the coagulation process?
- Formation of prothrombin activator
- Formed in response to a damaged BV
Where is fibrin stabilizing factor released from?
What is the significance of fibrin stabilizing factor?
- Without FSF the fibrin fibers are held loosely together by H+ bonds
- With FSF the fibrin fibers are held more tightly b/c the H+ bonds become covalent bonds
After how long does clot retraction occur?
What is needed for clot retraction to occur?
What does clot retraction do?
- Serum is expressed from the clot
- Helps to bring the sides of the vessel together to help in healing
- 1- Plt plug
- 2- clotting cascade
Factors I-IV of the clotting cascade
- I- fibrinogen
- II- prothrombin
- III- tissue factor (thromboplastin)
- IV- calcium ion
What does an "a" mean after a clotting factor roman numeral?
What 3 mechanisms lead to formation of prothombin activator?
- 1) trauma to vessel wall or other tissues
- 2) trauma to blood itself
- 3) contact between blood and damaged endothelial cells
prothombin activator purpose
convert prothrombin to thrombin
In what 2 ways can prothombin activator be formed?
intrinsic or extrinsic pathway
Major events of the extrinsic pathway
- Tissue factor (thromboplastin) released due to vessel wall surrounding tissue trauma
- Factor X is activated
- prothombin activator is formed
Why is thrombin so important to the extrinsic pathway?
Thrombin activates factor V which speeds up the process of converting prothrombin to thrombin
What is the goal of both the intrinsic and extrinsic pathways?
Formation of prothrombin activator
How is the intrinsic pathway initiated?
- By damage to the blood
- Contact of the blood with collagen
T or F, calcium is critical to all steps of the intrinsic pathway except steps 1 and 2
Activation of factor ___ begins the intrinsic pathway.
Trigger for extrinsic pathway to be initiated
Tissue factor released by damaged BV
How quickly can clotting occur in the extrinsic pathway?
How quickly can clotting occur in the intrinsic pathway?
Do the extrinsic and intrinsic pathways occur simultaneously?
- allow vessel to remain patent
- restricted to the site of injury
How is hemostasis achieved by the vessel?
- Balance of pro-coag and anti-coag factors
- Anti-coag factors are secreted by the endothelium (TPA, prostacyclin, anti-thrombin III, proteins C & S)
- Procoag factors tend to be localized to the site of injury
Plt count < 150 K
Does Plt count give qualitative or quantitative assessment of primary hemostasis?
Quantitative, only tells you how many, not how well they're working
Intra-op bleeding can be severe if Plt count is between ___ - ____.
What tests can be used to evaluate qualitative Plt function
- Ivy bleeding time
- Clot retraction
Does Plt aggrenometry provide qual or quant info?
What info can a thromboelastogram (TEG) provide?
Quantitative info about clot retraction
What parameters does a TEG assess?
- R- rxn time, how long it takes for a clot to begin to form (thrombin required)
- K- clot formation time, time after R for clot to reach 20 mm width
- Alpha angle- speed of clot formation
- F- rate of fibrinolysis
- MA- max amplitude, strength of fully formed clot
If thrombin were decreased what might be seen on TEG?
- Increased K
- Decreased alpha angle
- Due to increased clot formation time
Do aPTT, TT, ACT, and PT measure primary or secondary hemostasis
T or F, factors must be decreased by 30% before PT or PTT is prolonged
PT is most sensitive to a decrease in what factor?
What about PTT?
With heparin therapy, the ___ will be prolonged
With coumadin therapy, the ___ will be prolonged
PT or INR
What does TT (thrombin time) measure?
Ability of thrombin to convert fibrinogen to fibrin
Which is more common, hemophilia A or B?
Hemophelia A is a deficiency in factor ___.
Hemophelia B is a deficiency in factor ___.
What are the 2 parts to factor 8?
Coagulant factor 8 and VWF
T or F, hemophelia is sex linked and occurs mostly in males?
Pts with hemophilia A usually have normal amounts of ___ and decreased levels of ____.
Hemophelia A tx
- factor 8
- -replaced to 25% if pt is bleeding
- -replaced to 50-100% of normal for elective surgery
What's the difference (clinically) in the presentation of hemophilia A and B?
Infusion guidelines of factor 8c for hemophilia A pts
- Initial infusion: 50-60U/ kg
- Then: 25-30U/kg q 8-12 hours
Factor 8c halflife
- 12 hours
- (decreased to ~6 hours in peds)
For each U / kg of factor 8 given, plasma factor 8 concentration increases by _____.
How long is factor 8 replacement therapy continued post-op to prevent bleeding that would interfere with wound healing?
What about with bone and joint surgery?
- 2 weeks
- Bone and joint: 4-6 weeks
Peri-op, what should be avoided with hemophilia pts?
- Nasal intubations
- IM injections
- Regional anesthesia