Anemia Part 1&2 Flashcards
Anemia
Reduction in one or more of the major RBC measurements - lower ability for the blood to carry oxygen to body tissues
RBC Measurements (3)
- Hemoglobin concentration
- Hematocrit
- RBC count
Hemoglobin Count Men vs. Women
- Hgb <13 g/dL in men
- Hgb <12 g/dL in women
Symptoms of anemia
SOB, fatigue, light headedness, tachycardia, pounding heart beat, hypotension, pallor, exercise intolerance, irritability, headache, vertigo, angina pectoris.
Hgb, Hct, and RBC are all measurements based on…
Concentrations
- dependent on the red blood cell mass (RCM) as well as plasma volume
Will Hematocrit (Hct) over- or under- estimate blood loss?
Underestimate
- Patients with acute bleeding will often have normal values for Hgb and Hct.
A single RBC can carry _________ Hgb molecules.
250 million
Each Hgb can carry ____ oxygen molecules.
4
One RBC can carry as many as _________ molecules of oxygen.
One billion.
How long do RBCs live?
110-120 days
MCV
Mean corpuscular volume, the size of RBCs (microcytic or macrocytic)
MCHC
Mean corpuscular Hgb concentration
Elevated MCHC
Polychromasia
elevated in hereditary spherocytosis
MCH
Mean corpuscular Hgb, average mass of Hgb in RBCs
Decreased MCH
Hypo-chromic cells
Iron deficiency anemia
RDW
RBC distribution width
Normal = cells same size
Elevated = cells different sizes, called “poikilocytosis”
Hereditary spherocytosis appearance
They appear smaller and have no central pallor
Thalassemia appearance
Target cells (microcytic hypochromic anemia)
Define anisocytosis
Different sizes
Define poikilocytosis
Different shapes
Define schistocytes
RBC fragments (seen in microangiopathic disorders)
Define eliptocytes
Abnormally elongated RBCs
seen with both iron deficiency and megaloblastic anemia
Define helmet cells
Resembles a helmet (seen in microangiopathic anemia and TTP)
Where do you see target cells?
Seen in thalassemia, sickle cell disease, liver disease, s/p splenectomy.
Define sickle cells
Sharp edged, elongated, not pliable like normal, more rigid and sticky, shaped like sickles or crescent moons.
Define acanthocytes
Acantha means “thorn”
- Cell membrane has pointy edges
Define spherocytes
Sphere-shaped rather than bi-concave disk shaped.
seen in hemolytic anemias
RDW is high in…
Anisocytosis and iron deficiency anemia.
- note that it is normal in thalassemia
Basophilic stippling is seen in…
- precipitated RNA
- lead or heavy metal poisoning (microcytic)
- ETOH abuse (macrocytic)
- hemolytic anemia
What does reticulocyte count determine?
If bone marrow is functioning.
hypoproliferative anemias have low retic count
What is the kinetic approach to classifying anemia?
- production
- destruction
- loss
What is the morphologic approach to classifying anemias?
- microcytic
- normocytic
- macrocytic
Kinetic approach: production - reticulocyte and erythropoietin count interpretation
- Increased = bone marrow responding
2. Decreased = bone marrow not responding (nutritional deficiency or bone marrow failure
What tests would you run to look for destruction and would each marker be increased/decreased?
- increased LDH
- increased indirect bilirubin
- increased retic count
- decreased haptoglobin (binds free hgb)
- direct coombs (DAT) +/-
How would you interpret the destruction tests?
Hemolysis
What tests would you run to look for loss?
- history
- vital signs
- guaiac stool test
- colonoscopy
- EGD
Classification of anemia types (3)
- hypoproliferation
- RBC maturation problem
- hemolysis or hemorrhage
Hypoproliferation
defects in marrow production
RBC maturation
ineffective erythropoiesis
Hemolysis or hemorrhage
blood loss or destruction of RBCs
Decreased reticulocyte count
Think poor production (nutritional deficiency, bone marrow failure, or endocrine)
Increased reticulocyte count
Production is good, bone marrow is working - look for another cause of anemia (i.e. hemolysis)
Erythropoietin production in healthy kidneys
Anemia –> decreased oxygen –> increased Epo production –> correction of anemia
Acquired causes of hemolytic anemia
- immune mediated
- transfusion reaction
- infection
- physical/mechanical damage
- drugs/toxic agents
Hereditary causes of hemolytic anemia
- cell membrane defect
- enzyme defect
- hemoflobinopathy
What test would you use if you suspected immune-mediated?
Direct Coombs Test (DAT)
- if RBCs have auto-antibodies, they will agglutinate (+)
Positive Coombs Test (4)
- immune mediated hemolysis
- drugs/toxic agents
- transfusion reaction
- infection
Negative Coombs Test (4)
- inherited defects (hemoglobiopathies, sickle cell disease, G6-PD deficiency, pyruvate kinase)
- deficiency (spherocytosis)
- TTP
- DIC
Which anemia does lead poisoning cause?
- mild hemolytic anemia with basophilic stippling
Lead poisoning symptoms
- vague
- fatigue
- abdominal pain
- difficulty concentrating
- decreased libido
- muscle weakness
Lead poisoning treatment
chelating agents may be needed for those who are symptomatic or with very high levels
How are fragmented RBCs formed?
RBC is impaled on fibrin strand in microcirculation, the cell is ripped in two. The larger half becomes a helmet cell and the smaller half becomes a microspherocyte or mishapen fragmented cell.
Membrane disorders will produce what kind of anemia?
Hereditary spherocytosis
Enzyme disorders will produce what kind of anemia?
G6-PD deficiency
Hemoglobinopathies will produce what kind of anemia?
Sickle Cell anemia
What is the cause of hereditary spherocytosis?
Genetic mutation –> decreased spectrin and ankyrin –> defect in RBC membrane
Hereditary spherocytosis clinical pearls
-jaundice
-elevated bilirubin
-splenomegaly
-gallstones
+/- family history
Lab findings with hereditary spherocytosis
- normocytic anemia
- increased MCHC
- Heinz bodies
What is the most common inherited enzyme defect that leads to hemolytic anemia?
G6-PD
How was G6-PD discovered?
After giving anti-malarial drugs to African American soldiers, they developed hemolytic anemia.
(people with this deficiency have high relative resistance to lethal form of malaria)
What are Heinz bodies?
Inclusions within RBCs composed of denatured hemoglobin.
- occur as result of oxidative stress.
Steps in Heinz body formation.
- heme breaks away from globin
- globin oxidant attacks hemoglobin
- denatures and forms heinz bodies
- macrophages bite out heinz bodies leaving fragile deformed cell
- leads to hemolysis
G6-PD Oxidative Stressers include:
- foods (fava beans, broad beans)
- drugs (including anti-malarial, dapsone, sulfonamides)
- infections
G6-PD Clinical Pearls
- hemolytic anemia caused by stressor/trigger
- sx: malaise, weakness, abdominal or lumbar pain, followed by jaundice/dark urine
- can be abrupt
G6-PD Lab Findings
- normocytic anemia, normochromic, high LDH, elevated unconjugated bilirubin
- low/absent haptoglobin, peripheral smear shows anisocytosis, polychromasia
- spherocytes, and BIZARRE POIKILOCYTES with bite cells/blister cells
- presence of Heinz Bodies
What is the most common hemoglobinopathy?
Sickle Cell disease
What population is more likely to have sickle cell?
African Americans
Sickle cell inheritance pattern
Autosomal recessive
What are the steps to sickle cell anemia?
- mutation leads to abnormal amino acid
- abnormal beta globin chain
- unstable hemoglobin S
- polymerizes under stress
- sickled cells
- hemolysis
- anemia
In sickle cell, what replaced Hgb A?
Hgb S - result of mutated beta chain (only differs by one amino acid)
Sickle cell disease vs. trait
Disease = homozygous state for Hgb S Trait = heterozygous state for Hgb S
What is the lifespan of sickle cells?
10-20 days (note that 120 is normal for RBCs)
Sickle Cell characteristics
- HbS causes the characteristic sickle shape (less pliable & harder to traverse small capillaries)
- Sticky membranes (especially reticulocytes) that are abnormally adherent to the endothelium of small vessels, leads to occlusion
- Causes unpredictable episodes of microvascular occlusion AND premature RBC destruction (hemolytic anemia)
Clinical findings of Sickle Cell
- Episodes of pain esp. spine, long bones
- Jaundice
- Fever
- Hepatomegaly, splenomegaly
- Cardiomegaly
- Non-healing ulcers over lower tibia
What is sickle cell crisis?
Intermittent episodes of vasoocclusion leading to painful ischemia & acute pain/tenderness, fever, tachycardia and anxiety (Can last from a few hours to 2 weeks)
What is acute chest syndrome in sickle cell?
can mimic pneumonia, acute chest pain, hypoxemia, pulmonary infiltrates on CXR
Stressors/Triggers for sickle cell
- Infection
- Fever
- Excessive exercise
- Dehydration
- Abrupt change in temperature
- Hypoxia (going to the mountains)
Screening tests for sickle cell
- Sickle Solubility Test
- Hemoglobin Electrophoresis
- Peripheral Smear
True/False: there is a test to confirm sickle cell crisis.
FALSE - there is no test. Believe your patient when they tell you.
Sickle cell crisis treatment
- Vigorous Hydration
- Treatment of underlying cause such as infection
- Pain management (morphine, meperidine, ketorolac)
- Transfusion if needed
Acute chest syndrome in sickle cell treatment
- Medical emergency
- Vigorous O2 therapy
- Careful with IV fluids to avoid pulmonary edema
- Transfuse to keep hct >30
- Exchange transfusion may be needed
What is priapism in sickle cell?
Sustained, painful erection caused by infarction of penile venous overflow
Priapism in sickle cell treatment
- If lasts >3 hrs, is a urologic emergency.
- Risk of permanent impotence or necrosis.
- IV hydration and analgesia.
- If not improved in one hour, blood aspiration and irrigation of the corpus cavernosum with dilute phenylephrine may be needed.
- Simple exchange transfusions can be considered.
Define dactylitis
- Early complication of sickle cell disease
- Highest incidence 6 mo to 2 years
- Painful swelling of hands and feet
- Treatment involves fluids and pain medication
- Fevers treated as medical emergency
Anemia due to acute hemorrhage
A liter lost will decrease Hgb by ~1
Causes of anemia due to acute hemorrhage
- Heavy menses
- Trauma, surgery, childbirth
- GI bleed, colon cancer, gastric ulcer, esophageal varices
Work-up for anemia due to chronic blood loss.
- Slow loss over time, gradually depletes iron store, eventually causes iron deficiency anemia.
- In any NON-MENSTRUATING PERSON, look for colon cancer first!!
- ALWAYS get a stool guiac, in office per rectal exam, or send home a stool kit with patient.
- Stool FIT test localizes it to colon, regular hemoccult does not.
- Even if stool does not detect blood, still send for GI evaluation.
List the microcytic (MCV low) anemias
- iron deficiency
- thalassemia
- hereditary spherocytosis
- siderblastic
- anemia of chronic disease
- lead poisoning
List the normocytic (MCV normal) anemias
- acute blood loss
- hemoglobinopathies (sickle cell disease)
- hereditary spherocytosis
- acute hemolytic anemia
- chronic disease
List the macrocytic (MCV elecated) anemias
- B12 deficiency
- folate deficiency
- liver disease
- myelodysplastic syndrome
- ETOH abuse
- thyroiditis
What hormone should also be tested for with anemia?
TSH - thyroid stimulating hormone
What thyroid history is associated with macrocytic anemia?
Chronic autoimmune thyroiditis can be associated with pernicious anemia
What thyroid history is associated with microcytic anemia?
Hypothyroid women of childbearing age can become iron deficient from heavy menses
What thyroid history is associated with normocytic anemia?
Hypothyroidism can lead to decrease in red cell mass and a normochromic, normocytic hypo-proliferative anemia
Microcytic anemia due to production problems diff dx
RBC Maturation Problem/Cytoplasm Defect
- Sideroblastic Anemias
- Iron Deficiency Anemia
- Thalassemias
- Lead poisoning (rare)
What labs are associated with microcytic anemias?
Iron TIBC % saturation Ferritin Reticulocyte count TSH Soluble transferrin receptor Erythropoietin
Define sideroblastic anemia
The bone marrow produces ringed sideroblasts instead of healthy RBCs
-Can be acquired (bone marrow disease) or a congenital porphyria
Why is sideroblastic anemia considered an iron utilization anemia?
- Inadequate marrow utilization of iron for heme synthesis despite normal or even elevated iron levels
- Impairment of heme synthesis is due to an inability to incorporate iron into protoporphyrin
What will you see on peripheral smear for sideroblastic anemia?
Presence of polychromatophilia, and stippled RBCs (siderocytes)
Congenital Sideroblastic Anemia (3)
- X-linked inheritance (most common)
- Autosomal inheritance
- Causes Porphyrias
Acquired Sideroblastic Anemia
- Myelodysplastic syndrome (most common)
- Drugs
- Ethanol toxicity
- Lead toxicity
- Copper deficiency
- Pyridoxine deficiency (Vitamin B6)
Sideroblastic Anemia Treatment
- Elimination of toxin or drug
- Supplementation with copper or pyridoxine (B6)
- Treatment of underlying cause if myelodysplasia
- Congenital cases may respond to Pyridoxine 50mg PO TID, but usually incomplete response
Which anemia is the most common worldwide?
Iron deficiency anemia
What will you see on peripheral smear of iron deficiency anemia?
Microcytic
Hypochromic
High RDW
What is the earliest and best indication of iron deficiency anemia?
Ferritin is the earliest and best indication of Fe deficiency because it accurately reflects body iron stores
What are the implications of ferritin being an acute phase reactant?
In the presence of Liver disease or inflammation, Ferritin is an acute phase reactant and becomes elevated in the face of inflammation.
*Use Soluble Transferrin Receptor as a confirmatory test in these cases.
What lab findings do you expect with IDA?
Ferritin↓ Retic↓ TIBC↑
Soluble Transferrin Receptor↑ RDW↑
What ferritin level is confirmatory of IDA?
Ferritin <15 ng/mL is confirmatory for iron deficiency at ANY hemoglobin level (Microcytosis and low ferritin can happen before you see a drop in Hgb)
IDA is almost always due to…
BLEEDING
i.e. GI bleed (ulcer, cancer), Menorrhagia, Trauma, Surgery, Excessive phlebotomy, Hematuria, Paroxysmal Nocturnal, Hemoglobinuria, Hemodialysis
Which Iron deficient patient needs a GI work up
- All men
- All women without menorrhagia
- All women > 50 even with menorrhagia
- Women < 50 with menorrhagia: consider GI work up based on symptoms, or definitely if stool is positive for occult blood
Iron deficiency anemia due to inadequate iron
Didn’t Eat It: Decreased oral intake of iron; Dietary deficiency (limited meat, vegan)
Didn’t Absorb It
- Proton Pump inhibitors (low acid)
- H. pylori gastritis
- Inflammatory bowel disease
- Celiac Disease
- Atrophic Gastritis
- Partial Gastrectomy
- Gastric bypass
Iron deficiency anemia due to demand
i. e. used up all the stores
- Pregnancy
- Lactation
- Rapid growth in infancy or adolescence
- Erythropoeitin therapy
IDA symptoms
- Pica
- Pallor
- Glossitis
- Angular Cheilitis
- Koilonychias
IDA Treatment
See Pharm Notes
IDA Treatment Response
- Pica for ice disappears almost as soon as therapy starts
- Patient feels better in a few days
- Reticulocytosis occurs in 7-10 days
- Hemoglobin concentration starts to rise after 1-2 weeks. (The deficit should be halved in one month; Normal hgb usually occurs by 6-8 weeks)
- Re-evaluate patient in 2-4 weeks to check tolerance of oral iron and repeat hgb and retic
- Wait AT LEAST 4 weeks to re-check iron parameters; ~ after 3 months of therapy.
- Give Iron replacement until ferritin and transferrin saturation normalize
Thalassemia
The “other” microcytic hypochromic anemia
Thalassemia geographic origins
Found in Equatorial Africa, Mediterranean, Middle East, Arab Peninsula, Caribbean, India, Southeast Asia, South China
Thalassemia lab findings
Microcytic
Hypochromic
RDW normal (unlike iron deficiency)
Target cells
Thalassemia is a…
Hemiglobinopathy
Characteristics of Thalassemia
- Caused by an inherited defect in hemoglobin synthesis which causes a quantitative defect of hemoglobin (versus Sickle Cell anemia is also a defect in hemoglobin, but is a qualitative defect )
- Common in areas where malaria is endemic (1/200 worldwide; abnormal genes offer some protection against death from malaria)
How does Thalassemia occur?
Unbalanced synthesis of α and β chains –> intracellular accumulation of unmatched chains –> aggregates as INCLUSION BODIES –> injures RBC
Should you give pts with Thalassemia iron?
NO!
- Intramedullary hemolysis causes PERPETUAL HYPERFERREMIA in Thalassemia
- MCV is much lower in Thalassemia than in Fe+ deficiency
Alpha Thalassemia is due to…
Decrease in Alpha globin production
Alpha Thalassemia
Normally there are 4 copies of the Alpha globin gene (two copies on each chromatid of chromosome 16); this is why there are 4 forms of alpha thalassemia
How does alpha thalassemia occur?
-Decreased α globin production → a relative excess of β globins in adults and an excess of 𝝲 globins in newborns.
What are the types of Alpha Thalassemia?
-Homozygous Alpha thalassemia = Fetal Hydrops
-Heterozygous Alpha thalassemia = mild anemia
-Hemoglobin H = 4 beta chains; Thalassemia intermedia:
Moderately severe hypochromic microcytic anemia with hemolysis
Beta Thalassemia is due to…
Decreased β globin production
Beta Thalassemia
Normally there are 2 copies of the Beta globin genes (one copy on each chromatid of Chromosome 11)
What are the clinical features of β Thalassemia Minor or Trait?
- Hb α2β2 is mildly decreased.
- No accumulation of excess alpha chains.
- Hypochromia and microcytosis, but no significant anemia or hemolysis
What are the clinical features of β Thalassemia Major
or Cooley’s Anemia?
No β chain synthesis
No hgb A (α2β2 )
⬆︎⬆︎ α chains
Severe Hemolytic Anemia
Characteristics of β Thalassemia Major
or Cooley’s Anemia
- Manifestations occur in early childhood
- Medullary expansion due to overstimulation of bone marrow
- Marked splenomegaly and hepatomegaly
- Abdomen often protrudes because of spleen
- Cardiac enlargement
- Iron overload is common
Macrocytic anemias due to production problems
RBC Maturation Problems/Nuclear Defects
- B12 Deficiency
- Folate Deficiency
List the causes of macrocytic anemias
- B12 deficiency
- Folic Acid deficiency
- Chronic liver disease
- ETOH
- Endocrine (Hypothyroidism)
- Myelodysplasia or aplastic anemia
- Drugs that impair DNA synthesis: AZT, chemo, azathioprine Chloramphenicol, gold, sulfonamides,
B12 and folic acid deficiencies cause…
Megaloblastic anemia
- Both are needed for DNA synthesis
- If DNA synthesis is impaired, the maturation of the RBC nucleus is slowed while the cytoplasm and hemoglobinazation progresses are unimpaired.
- The resulting cell is macrocytic
Causes of B12 deficiency
- Most common cause = deficiency of intrinsic factor i.e. pernicious anemia
- Total Gastrectomy
- Fish Tapeworm
- Other defects in absorption
- Strict vegetarian diet
- Bacteria on plants may provide some B12
Causes of Folic Acid (B9) Deficiency
- Most common cause = inadequate oral intake (green leafy veggies)
- Pregnancy, Hemolytic anemias
- Malabsorption syndromes (Celiac dz, Tropical Sprue)
- Inadequate utilization: Ascorbic acid deficiency
- ETOH
What is the importance of intrinsic factor?
- Intrinsic factor is essential for absorption of B12 in the GI tract
- it is produced by parietal cells in the stomach
- if there is no intrinsic factor in stomach (pernicious anemia), then there will be no absorption in ileum
What groups of people is pernicious anemia most commonly found in?
Pernicious anemia is most frequently seen in individuals of Northern European descent and African Americans
-Average presenting age near 60, rare under age 30.
Megaloblastic Anemia lab findings
- MCV >100
- Retic Count Decreased
- Peripheral Smear: Hyper-segmented neutrophils, ovalocytes, anisocytosis, poikilocytosis, Howell-Jolly bodies
- Other Cells: Leukopenia and thrombocytopenia occurs commonly in pernicious anemia
B12 and Folate deficiencies also cause
abnormalities in the maturation of GRANULOCYTES
What system is only affected by B12 deficiency?
NEUROLOGIC
- Peripheral neuropathy (paresthesia, hyporeflexia)
- Spinal cord degeneration (gait instability, weakness, hyperreflexia, reduced vibratory and position sense)
- Dementia and disorientation
What systems are affected by both B12 and Folic Acid deficiency?
GI
Reproductive
Skin
B12 Supplementation
Cyanocobalamin 1000 mcg SC/IM Daily x 1 week then Weekly x 1 mo, then monthly
Folic Acid Supplementation
- Usual dose is 1mg/ day
- Pregnant women need to take Folic Acid
- All patients with hemolytic anemia need Folic Acid
Megaloblastic Anemia response to treatment
- Mental changes and tongue soreness improve almost immediately
- After 4-5 days, reticulocytosis appears, may elevate MCV further
- Soon thereafter, the hgb increases
- Neuropathic abnormalities improve slowly over several months, but may never disappear entirely if longstanding.
Normocytic anemias due to Production Problems
Bone Marrow Production Defects/Hypoproliferative:
Aplastic Anemia
Anemia of Chronic Disease/Chronic Inflammation
Myelofibrosis
Cancer
Chronic Renal Disease
Anemia of Chronic Disease
- Associated with proinflammatory cytokines (cytokines suppress erythropoiesis)
- One of the most common forms of anemia seen clinically
- Typically a mild anemia
- Differentiated from iron deficiency anemia by the elevated ferritin level
Anemia of chronic disease causes
COMMON CAUSES: inflammation, infection, tissue injury, or neoplastic disease
OTHER CAUSES: Severe Trauma, Diabetes, increased age, immune activation
Anemia of chronic disease lab findings
- Low reticulocyte count (hypoproliferative)
- Usually Normochromic, Normocytic
- Anemia is usually mild
- Ferritin will be high (NEVER low)
- Soluble Transferrin Receptor is normal
Anemia of chronic disease etiology
Chronic Inflammation
- ->increased cytokines
- -> increased release of HEPCIDIN
- -> iron RETENTION in cells (hepatocytes, enterocytes, macrophages)
- -> decreased release of iron
- -> normocytic anemia
Hepcidin
main iron regulating hormone in the liver
Hepcidin function
Binds and degrades ferroportin which decreases functional activity of ferroportin leading to decreased iron release into plasma
- Ferroportin = iron export protein located on cells, releases iron into plasma
- Hepcidin is an acute phase reactant, is upregulated by inflammatory cytokines
Hepcidin levels
- are low in iron deficiency and other anemias
- levels increase with infections and inflammation (is an acute phase reactant)
Aplastic anemia
- Most cases are idiopathic!
- Can be acquired or inherited
- Damage/Injury to bone marrow failure
- Hallmark is pancytopenia
- Can be abrupt onset or insidious
- Diagnosis confirmed with bone marrow biopsy
Aplastic anemia diagnosis
Combination of pancytopenia with a fatty empty bone marrow on biopsy
Aplastic anemia epidemiology
- Women and men equally affected
- Bi-phasic age distribution (teens & twenties, second rise in elderly)
Aplastic Anemia Biopsy
Abnormal bone marrow biopsy: Bone marrow hypocellularity
Causes of aplastic anemia (acquired vs. inherited)
ACQUIRED:
- Cytotoxic Chemotherapy
- Benzene (solvent)
- Radiation
- Viral (?) Hepatitis, HIV, EBV (rare), Parvovirus B19
- Pregnancy
- Immune disease
INHERITED
- Fanconi’s anemia
- Dyskeratosis congenita
- Shwachman Diamond syndrome
- Familial aplastic anemias
- Reticular dysgenesis
- Preleukemia
Aplastic anemia clinical presentation
- Bleeding is the most common early symptom
- Easy bruising, bleeding gums, nose bleeds, heavy menstrual flow
- Petechiae are sometimes noted
- SOB, weakness, pounding sensation in the ears
- Symptoms are typically restricted to the hematologic system
- Patients often feel and look well despite MARKEDLY low blood counts
- Infection is rarely a presenting symptom
Aplastic anemia treatment
- Can be fatal if untreated
- Bone marrow transplant (curative)
- Immunosuppression (combo): IV ATG (anti-thymocyte globulin) + Oral Cyclosporine
- -Side Effects of ATG: serum sickness
- -Side Effects: nephrotoxicity, seizures, HTN, opportunistic infection
- Transfusions to maintain RBCs and platelets
- Suppress menstruation in females
- Avoid ASA and NSAIDs, blood thinners
