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RBC,, WBC, and Plt all come from a single cell type in the bone marrow. What is it??
- hematopoietic stem cell
- Most of these stem cells go on to differentiate to different cell types, some are retained in bone marrow as stem cells.
We don't need specifics of the RBC genesis but what happens in the stages (in general)?
- The nucleus in proerythroblast gets condensed to a small size and finally gets absorbed or extruded from the cell completely.
- At some later phases of this, some remnant material ER or Golgi apparatus or something (reticulocyte that cell that has some bluish material remaining)
- Reticulocyte stage, RBC goes from BM into blood (squeeze through pores of capillary membrane) and blue stuff disappears.
When would we see a high % of reticulocytes in a blood smear?
When you do see high % of reticulocytes in blood of in anemic patient, cells coming out of bone marrow earlier than normally would as a compensatory mechanism
What is the most important regulator of red cell production?!?!
- Tissue oxygenation
- **Test question**
we need enough RBC to carry enough oxygen but what happens if we have too many RBC?
if too many RBC (polycythemia) will impede blood flow because viscosity would increase.
What is the normal RBC value? (cells/microliter)
- Male: 4.7 to 6.1 million cells/mcL
- Female: 4.2 to 5.4 million cells/mcL
What is the formula and normal value for MCV?
What is the formula and normal value of MCH?
What is the formula and normal value of MCHC?
What does MCV stand for?
- mean capsular volume (MCV)
- anemias get defined according to erythrocyte size,
- typical RBC size
What does MCH stand for?
- Mean Corpuscular Hemoglobin
- (average amount of Hgb in a red cell).
What does MCHC stand for?
Mean capsular hgb concentration.
What type of anemia is it if the MCV is reduced?
What type of anemia is it if the MCV is increased? Give an example of this type of anemia
- macrocytic anemia
- (B12 and folate deficiencies are both nutritional anemias and a macrocytic anemia)
What type of anemia is it if the MCH is low?
TRUE or FALSE. If no erythropoietin, even in hypoxia, RBC production won’t be increased.
What will stimulate erythropoietin production (besides hypoxia)....think neuro/endocrine
Epinephrine, Norepinephrine, & Prostaglandins
What % of erythropoietin is made in the kidneys?
So 90% of erythropoietin is made in kidneys, another 10% made elsewhere (likely in the liver). If kidneys are non functional, the patient will become anemic because the remaining 10% made elsewhere is not enough to stimulate RBC production
What type of hormone is erythropoietin
What are the nutritional requirements of RBC production?
- Folic acid (folate)
a decrease in oxygen carrying capacity irrespective of cause of anemia.
What is the equation for concentration of O2 in the blood??
CaO2 (ml O2/dl blood= (SaO2 (as fraction) x Hgb gm/dl x 1.34 ml O2/gm hgb) + (0.003 O2 ml O2/dl blood/mmHg x PaO2 mmHg)
CaO2 = (O2Sat x Hb x 1.34) + (0.003 x PaO2)
Name two major functions of the RBC
- Transport HgB that then carries oxygen from the lungs to the tissues
- RBC also carry a large amount of the enzyme carbonic anhydrase
TRUE or FALSE. The RBC has a nucleus
What is the normal lifespan of a RBC?
Describe the shape of a RBC
Biconcave disk with a diameter of 7.8 microns
Why is the fact that the RBC carries a large amount of the enzyme carbonic anhydrase important?
- That catalyzes reaction of CO2 and water to form carbonic acid.
- It allows the blood to carry large amount of CO2 in the form of the bicarb ion from the tissues to the lungs, converted back to CO2 and then exhaled, gets rid of volatile acid
TRUE or FALSE. RBC is major buffer found in whole blood.
- TRUE !
- HgB is buffer in acid base. Protein is a really good buffer. RBC is major buffer found in whole blood.
Each gram of Hgb can carry about ____ml of oxygen
Average Hct & HgB for male is.....
45 & 15.
An individual can carry about __ml of oxygen for 100ml of blood
There are disorders that effect RBC metabolism. Describe the one example sue gave us
- One of those disorders is the G6PD deficiency (gluco-6-phosphate-dehydrogenase is an enzyme is glycocytic pathway) causes a chronic hemolytic anemia.
- Can also cause an acute episodic hemolytic anemia.
Is G6PD deficiency genetically transmitted?
What are the normal % of plasma, WBC & plt, and RBC in the blood?
- Plasma 54%
- Buffy (WBC & Plt) 1%
- RBC 45%
How is sickle cell inherited?
What is sickle cell (pathophys)
- Substitution of a valine for glutamic acid in beta-globin subunit (Hgb S)
- In the absence of oxygen, conformational change → hydrophobic region exposed
- Extreme de-O2 → these regions aggregate & life-span shortened
What kinds of things cause the HgB S to respond and change shape?
HgB S responds to hypoxemia (pa<40mmHg) or to acidosis, or to hyperthermia or dehydration
What is the difference between sickle cell trait and sickle cell disease?
- Trait: heterozygous
- Disease: homozygous
Describe the homozygous form of sickle cell anemia
- Presents early in life
- Severe hemolytic anemia
- Vaso-occlusive disease involving bone marrow, liver, spleen, kidney, CNS
How does sickle cell anemia effect the Oxygen hemoglobin dissociation curve?
- affects O2 dissociation curve to the right.
- P50 normal is 27mmHg, now it’s around 31 or so. (50% saturated is P50. PaO2 at which is hgb is 50% saturated)
What are the risk factors for peri-op M&M in sickle cell disease?
- Frequency of hosp/transfusions
- Prior Organ damage
- Current Infection
What should we know about sickle cell anemia and hip surgery?
Excess blood loss in 70% and sickling events in 19% of patients.
Are peri-op transfusions helpful in sickle cell patients?
Previous idea of aggressively transfusing patient to increased total amount of HgB but not shown to be beneficial. A lot of complications associated w/transfusion which would often outweigh the benefits
Where do we want the Hct and Hb for a sickle cell patient? Also specifically what % of Hb S and Hb A do we want?
- Transfuse to get a pre-op Hct of 30 (not push any higher). Hct around 30 and Hb around 10 is goal.
- Hb A concentration to be more than 50% and HgB S to be less than 40%.
What should we avoid in sickle cell patients?
- Hypotension & low flow situations
How can we ensure adequate hydration in sickle cell patients?
MIVF x1.5 for about 12hrs pre-op to ensure adequate hydration
What are some anesthesia considerations for sickle cell?
- Pre-oxygenate, watch sedation in pre-op so they don’t hypo ventilate.
- Pain can exacerbate the disease: treat aggressively.
- Acute chest syndrome can develop 2-3 days post-op. Aggressive look at oxygenation, pain management, possibly transfusion to improve oxygen carrying capacity.
- want to have patient fully reversed. Caution w/extubation. Don’t want them at risk for hypoxemia and acidosis.
- Post-op supplemental O2 for 12-18hrs.
Name the two types of anemia from ineffective erythropoiesis
- Macrocytic/megaloblastic anemia (Folate deficiency & Vitamin B-12 deficiency)
- Microcytic anemia (Iron deficiency)
Folate and B12 deficiency are main causes of macrocytic anemia in adults. Why are these two nutrients so important?
Vitamins needed for normal DNA synthesis. Deficiency in vitamin (one or the rather) the bone marrow is one of the 1st things effected.
Why is folate and B12 deficiency called megaloblastic?
Precursors to RBC in BM becomes large and can’t complete that process of cell division. These large red cells (precursors) get released into circulation
anesthetic considerations for macrocytic anemia can be influenced if the patient has some neurologic changes. what would we avoid?
N2O should be avoided for patient w/macrocytic anemia because it inhibits methionine synthestase. Even short periods can produce changes.
Defective globin chain production produces what???
- Microcytic anemia in both kids and adults
What is the geographic distribution of Thalassemias (microcytic anemia)??
- Predominates in Africa and Mediterranean.
- Beta: Africa
- Alpha: south east Asia and Mediterranean
What are the three types of Thalassemias?
- T. minor (Hb 10-14)
- T. intermedia
- T. major
What is the typical Hb in Thalassemia minor
How severe is Thalassemia major?
severe life threatening anemia during few months of life, patient need long term transfusion therapy to survive childhood.
What are the anesthesia implications for Thalassemia?
- Depends on continuum on where patient falls.
- T. Major: may already have splenomegaly, hepatomegaly. CHF. R sided HF. Cirrhosis and various endocrine pathies. So they can be sick.
What anemia is caused by decreased oxygen affinity
What is methemoglobinemia? Why is this important??
- Met Hb is when iron in HgB is oxidized from Fe2+ (ferrous) to Fe3+ (ferric) form.
- Shifts O2 dissociation curve to left and O2 is not being delivered to the tissues.
Normally RBC have about 1% of Methemoglobin. At what point does the MetHb become a problem?
- If level increases there is a shift to left.
- < 30% of total HgB no compromise in O2
- 30-50% patient will show s/s of compromised oxygenation and oxygen deprivation
- > 50% coma and death can result
A disorder of RBC production causing hypoproliferation causes what type of anemia?
Name two types (causes) of aplastic anemia
- Fanconi’s anemia
- Drug & radiation associated
What is Fanconi's anemia?
- constitutional aplastic anemia.
- Autosomal recessive disorder.
- Exhibits as pancytopenia. (involves all cell types)
TRUE or FALSE. If the aplastic anemia is d/t drug exposure, it's not usually irreversible damage to bone marrow and full recovery will usually occur.
Some causes of aplastic anemia cause pancytopenia. What are some concerns for this type of case?
- means reverse precautions.
- Low WBC and RBC count. Increased risk for infections.
- Often also stress steroids may be good idea for these patient.
- As well as antibiotics. Also, make sure all kinds of blood products are available. May not have enough platelets as well.
Tissue oxygenation is optimal at Hb of _________g/dl
If the Hb is higher than that which it often is, viscosity increases decreases flow and consequently oxygen delivery. At what Hct do we become concerned
- Up to a Hct of 50, fairly wide grace period, the effect is minor but then around that time, flow to key organs like brain is effected. May not see s/s at or below 50 but may see easy fatigue ability.
- Not enough O2 getting where it needs to go.
- After a Hct above 60%, increase in viscosity is life threatening because of decreased perfusion.
At what Hct is polycythemia life threatening?
What is Polycythemia vera
- Primary: (vera) is a stem cell disorder. At risk for both thrombosis and bleeding. Thrombosis is obvious. Bleeding is from acquired von willebrands disease.
- Secondary: is what happens to people living at high altitudes. Or d/t increased erythropoietin production. Might be an erythropoietin secreting tumor.
What are the anesthesia implications for polycythemia?
- Pre-op phlebotomy
- Oxygen therapy
- Aware of risk of thrombosis and bleeding.