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week 9- heme 1 Flashcards

1
Q

• What causes EPO production?

A

o Decreased O2 and increased androgens

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2
Q

• What is needed for RBC production?

A

o EPO, Fe, B12, folate, and more…

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3
Q

• What are the 4 main mechanisms of anemia?

A

o Blood loss, acute or chronic
o Decreased absorption
o Def erythropoiesis
o Excessive hemolysis

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4
Q

• What risk factors for anemia should you ask about?

A

o dietary assessment (look for def), menstruation, GI assessment (including gastric ulcer and color of stools), pregnancy, lactation, hemoglobinopathies, alcoholism, prescription drugs, CA, rheumatic d/os, chronic inflammatory dz, COPD, CHF, heart dz heart valve, marathon running

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5
Q

what should you ask about family hx for anemia?

A

o bleeding d/o (eg, von Willebrand dz, hereditary hemorrhagic telangiectasia, sickle-cell anemia), colonic malignancy (eg, hereditary non-polyposis colon CA)

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6
Q

what are general sxs of anemia?

A

o most occur only if anemia is severe.
o Weakness, fatigue, seeing spots, drowsiness, syncope, angina, SOB, DOE.
o Mb: vertigo, HA, tinnitus, pica, restless leg syndrome, amenorrhea or menorrhagia, loss of libido, and GI complaints.
o Personal or family hx of bleeding d/os or events
o compensate over time, so anemia not always obvious

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7
Q

• What are anemia sxs due to blood loss? Decreased absorprion?

A

o Blood loss: melena, epistaxis, hematochezia, melena hematemesis, menorrhagia, hematuria, blood donation, excessive blood draws
o Decreased absorption: generalized malabsorption, hypo/achlorhydria, medications, Celiac, H. Pylori.
o Factors that dec absorption: phytates, polyphenols, calcium, soy protein.
o inc absorption: ascorbic acid, heme Fe

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8
Q

• Anemia sxs due to hemolysis, CA, sickle cell, B12/folate def?

A

o Hemolysis: jaundice, pruritis, dark urine
o CA: weight loss, pain
o Sickle cell: severe bone or chest pain
o B12/folate def: stocking/glove paresthesias

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9
Q

• What PE is done for anemia?

A

o BP: supine, seated and standing (orthostatic)
o Inspect conjunctiva, lines of palms, mucus membranes, skin color
o Inspect nails for blueness, ridges, spooning, poor nutrition
o Cardiovascular exam

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10
Q

• What are clinical signs of anemia?

A 
o	Orthostatic hypotension  
o	Pallor (skin, palmar creases, nail beds, mucus membranes, conjunctiva) 
o	Inc HR
o	Indication of causes: SM, peripheral neuropathy, abdominal distention, petechiae, fever/heart murmurs, heart failure
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11
Q

• What testing should be done for anemia?

A

o Stool occult blood test
o CBC with smear to help differentiate def RBC production from excessive RBC destruction
o Fe, ferritin, TIBC if CBC or sxs warrant
o TSH, free T4 (fatigue, menstrual complaints)
o Serum bilirubin, LDH (elevated in hemolysis); if anemia is present

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12
Q

• What are dx criteria for anemia?

A

o Adult male: RBC < 4.5 million/uL; or Hb < 14.0 g/dL; or Hct < 42%
o adult female: RBC < 4.0 million/uL; or Hb < 12.0 g/dL; or Hct < 37%
o values lower in pregnancy and vary during childhood, with lower values after infancy.

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13
Q

• What is microcytic anemia?

A

o MCV < 80 fL
o Altered heme or globin synthesis
o IDA, thalassemia, and Hb-synthesis defects, Cu def, Zn poisoning, lead poisoning, alcohol.
o MB seen in ACD

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14
Q

• What is macrocytic anemia?

A

o MCV > 95 fL
o Impaired DNA synthesis
o B12, folate def, chemotherapeutic agents, alcoholism, HIV anti-retroviral agents, MDS

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15
Q

• What causes normocytic anemia? What is RDW?

A 
o	Normocytic: def EPO, hemorrhage
o	RDW (degree of RBC size variation): if elevated, could mean simultaneous micro and macrocytosis, RBC fragments
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16
Q

• What are the 2 groups of Hb anemias?

A

o Hypochromic: MCH < 30% (concentration/RBC)
o Normochromic: normal levels of MCH and MCHC
o **hypochromic doesn’t exist

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17
Q

• What can reticulocyte count tell you in anemia?

A

o Hi: excessive RBC destruction

o Lo: decreased RBC production

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18
Q

• What are the classes of RBCs based on size and shape?

A

o RBC injury – RBC fragments, ovalocytes, schistocytes
o Anisocytosis: RBCs of excessive variation in size
o Poikilocytosis: RBCs of excessive variation in shape

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19
Q

• When would you do a BM aspiration and biopsy?

A 
o	Unexplained anemias
o	Other cytopenias
o	Unexplained leukocytosis
o	Thrombocytosis
o	Suspected leukemia, multiple myeloma, or myelophthisis
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20
Q

• What are the anemias causes by def erythropoiesis?

A 
o	IDA
o	Fe-utilization/Sideroblastic anemias
o	ACD/inflammation
o	Hypoproliferative anemias
o	Aplastic/hypoplastic anemia
o	Myelophthisic anemia
o	Macrocytic anemias
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21
Q

• What evidence tells you it’s anemia caused by def erythropoiesis?

A

o Reticulocytopenia
o MCV:
o Microcytic: defective heme or globin synthesis; test for Fe stores; IDA, Fe-transport def anemias, Fe-utilization anemias, and thalassemias
o Normocytic: BM failure
o Macrocytic: defective DNA synthesis; B12, folate def

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22
Q

• What is the most common anemia?

A

o IDA; in all age groups

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23
Q

• What are the non-specific sxs of IDA, seen more when severe?

A

o Fatigue, headaches, irritability, loss of stamina, increased pallor, difficult concentration
o Severe def – pica, glossitis, cheilosis, concave nails, increased heart rate, dyspnea, restless leg syndrome, glossal pain, reduced salivary flow leading to dry mouth, atrophy of tongue papillae, cheilosis, and occasionally, alopecia

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24
Q

• Describe the absorption of Fe?

A

o Stomach, duodenum and upper jejunum
o Determined by type of Fe molecule and substances ingested with it
o Absorbed best as heme Fe (meat products)
o Non-heme Fe must be reduced and unbound from other food molecules (gastric secretions)
o Ascorbic acid increases non-heme Fe absorption
o Adults absorb 1 mg of 15 mg Fe ingested per day
o Reduced by antacids, plant phytates (wheat, cereals), tannins (black tea), lead
o Reduced by malabsorption d/os such as achlohydria, atrophic gastritis, Helicobacter pylori gastritis, SIBO, gastric bypass, and celiac dz

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25
Q

• What are the 2 storage forms of Fe?

A

o Ferritin – liver, bone marrow, spleen, RBCs, and serum

o Hemosiderin – Liver, marrow

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26
Q

• What is the daily requirement of Fe?

A

o 25 mg/day.

o Reabsorption/recycling of Fe provides 97% of this requirement

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27
Q

• What are the common etiologies of Fe-def anemia in adults?

A

o Men: often chronic bleed (colon cancer, colitis, PUD, ASA use)
o Pre-menopausal Women: menstruation; Repeated pregnancy (Women lose ~1g of Fe per pregnancy/lactation cycle)
o Chronic intravascular hemolysis
o Post gastrectomy
o Malabsorption
o Under-nutrition

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28
Q

• Common cause of IDA in infants/kids?

A

o Growth spurts

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29
Q

• What hx should you get for IDA?

A 
o	complete diet and drug history
o	Menstrual/pregnancy/lactation history
o	Evidence of gastric bleeding/history of ulcer
o	Exercise levels
o	Blood donation history
o	All past dzs and possible chronic dzs
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30
Q

• What labs are done for IDA? Results?

A

o Suspect in microcytic anemia and chronic blood loss
o Stool Occult blood (Men, post-menopausal women, or normal menses)
o Fe absorption test: fasting serum Fe level is compared to that at 1-4 hours after oral 325 mg Fe sulfate (Fe content 65 mg) and water. Should increase at least 100 ug/dL if absorption is normal
o CBC with smear, serum Fe, Fe-binding capacity, serum ferritin
o Serum Fe and/or ferritin low, TIBC high
o Any of the following: Low Hb, Hct, Red cell count, MCV, and high RDW

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31
Q

• What are Fe-utilization/Sideroblastic anemias?

A

o Inadequate or abnormal utilization of marrow Fe, despite adequate stores
o Polychromatophilic, stippled, targeted RBCs (siderocytes)
o Usu part of MDS, hereditary or 2nd to drugs or other toxins. Reversibly if dt alcoholism, Cu def (Zn excess), drugs or hypothermia
o Also may occur in Hb-opathies, esp thalassemia

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32
Q

• How is sideroblastic anemia diagnosed?

A

o microcytic anemia or high RDW, inc ferritin, Fe and transferrin saturation
o CBC with smear, Fe, ferritin, bone marrow bx (refer), Erythrocyte protoporphyrin, molecular genetics studies mb lead screen
o microcytic and hypochromic (but mb normochromic), high RDW
o marked anisocytosis; siderocytes in smear.
o high serum Fe, transferrin and ferritin
o ringed sideroblasts, erythroid hyperplasia in the bone marrow (refer, necessary for diagnosis)
o Check serum lead concentration if cause is unknown

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33
Q

• What causes ACD/inflammation? Ssx?

A

o Causes: infectious, inflammatory, neoplastic dz, severe trauma, heart failure, diabetes mellitus, anemia of the elderly, and acute or chronic immune activation
o Bone marrow responsiveness to erythropoietin is mediated by inflammatory cytokines, IL-6, esp IL-1 beta and TNF-alpha
–high WBC production -> lower RBCs, even if enough EPO
o Ssx: Those of the underlying dz
o Suspect in microcytic/marginal normocytic anemia with chronic infection, cancer or inflammation (chronic leukocytosis)

34
Q

• What are lab results for sideroblastic anemia?

A

o CBC with smear, Serum , transferrin, transferrin receptor, and serum ferritin, ESR and CRP if underlying cause is unknown
o Mild-moderate anemia -hb concentration of 10 to 11 g/dL, usu no less then 8.0g/mL
o Initially normochromic, normocytic
o As progresses: microcytic/marginal normocytic, hypochromic
o RDW normal in early stages
o low serum Fe and low TIBC if Fe def is also present
o Recognizing coexisting Fe def in pts with ACD is challenging- use response to oral Fe to help
o Measure of EPO. CA, RA, or AIDS who have EPO levels <500 mU/mL should be given Epogen

35
Q

• What are hypoproliferative anemias?

A

o Low marrow activity due to lack of EPO or inability of marrow to respond to it.
o 6 different patterns- should be evaluated by hematologist
o Renal dz dt low EPO
o Hypo metabolic/endocrine def states: hypothyroidism, hyperthyroidism, panhypopituitarism, and primary or 2nd hyperparathyroidism
o protein malnutrition- severe

36
Q

• how are hypoproliferative anemias diagnosed?

A

o Labs: Renal function (EPO falls when creatinine clearance drops below 30 mL/min), TSH, CBC with smear, bone marrow biopsy
o Dx: Based on labs, made by hematologist

37
Q

• What is aplastic/hypoplastic anemia?

A

o Pancytopenia of all cell lines, or pure RBC aplasia. Both are uncommon (2-4/1,000,000).

38
Q

• What is etio of aplastic anemia?

A

o genetic or acquired.
o Chemical exposure: drugs, pesticides, industrial chemicals, benzenes, anti-cancer agents (unknown mechanisms)
o Infections such as Parvo-B19, HIV, HepC and EBV
o Genetic inability to clear toxicity via glutathione S-transferase

39
Q

• What is fanconi’s anemia?

A

o rare type of inherited aplastic anemia
o genetic abnormalities, anemia, bone abnormalities, microcephaly, hypopigmented spots and café-au-lait spots, abnormality of thumbs, hypogonadism
o usu dx in childhood

40
Q

• what is pure red cell aplasia?

A

o Type of aplastic anemia?

o infections, thymomas, immune system injury, fertilizer exposure, B2 def, CLL

41
Q

• what are ssx of aplastic anemia?

A

o insidious onset or very acute and sudden
o Anemia: pallor, tachycardia, fatigue, dizziness
o Thrombocytopenia: petechiae, ecchymosis, bleeding from gums, ocular fundi, other tissues
o Agranulocytosis: life-threatening infections
o Suspect in (particularly young) pts with pancytopenia (WBCs <50,000/µL)

42
Q

• How is aplastic anemia diagnosed?

A 
o	CBC with smear, Fe, reticulocytes, bone marrow bx (refer to hematologist)
o	Low RBCs
o	low WBC
o	low platelets
o	low reticulocytes
o	elevated serum Fe
o	acellular bone marrow (diagnostic)
43
Q

• what is myelophthisic anemia? Ssx?

A

o BM is replaced by tumor, granuloma, lipid storage dzs, or fibrosis (MF)
o Ssx: of the underlying dz; May see SM

44
Q

• How is myelophthisic anemia diagnosed?

A 
o	CBC with smear, marrow bx
o	marked anisocytosis and poikilocytosis
o	nRBCs in the blood
o	Immature myeloid cells in the blood
o	Bone marrow bx is definitive (refer)
45
Q

• What causes macrocytic anemias?

A

o Due to defective DNA synthesis
o Alcoholism, B12 or folate def are the most common causes, along with cytotoxic drugs, hypothyroid, liver dz
o When dt B12/folate def - Megaloblastic anemia

46
Q

• What are ssx of macrocytic anemia?

A

o Usu no sxs until severe
o Neurological signs (stocking/glove neuropathy, dementia)
o Glossitis, diarrhea, muscle wasting

47
Q

• How is macrocytic anemia diagnosed?

A

o CBC with smear, B12, folate
o MCV > 95-100
o Aniso, poik, high RDW
o Howell-Jolly bodies (fragments of nucleus)
o Hypersegmented PMNs initially, neutropenia later
o Determine cause: Vitamin B12 and folate levels are required

48
Q

• What are the anemias caused by hemolysis?

A 
o	AIHA
o	hereditary spherocytosis and elliptocytosis
o	stomatocytosis and hypophosphatemia
o	G-6-P def
o	Sickle cell anemia
o	Hb C dz
o	Thalassemia
49
Q

• What are the general causes of hemolytic anemia?

A 
o	Intrinsic: abn RBC membranes; RBC metabolism d/os; Hb-opathies
o	Extrinsic (RBCs are normal): Hypersplenism-acts as a trap; Toxic exposures- oxidants; Autoimmune dz- abs against RBC membrane; Mechanical injury- prosthetic valves, DIC, TTP; Infectious agents- malaria, C. perferingens
50
Q

• How is hemolytic anemia different from other causes of anemia?

A

o mb acute, chronic, or episodic
o Ssx:
o Acute/severe hemolytic crisis (uncommon): fever, chills, back and abdominal pain, prostration, and shock
o Severe hemolysis: jaundice and splenomegaly
o Splenomegaly, jaundice, and cholelithiasis mb present from the hemolysis.

51
Q

• How is hemolytic anemia diagnosed?

A 
o	Suspect in pts with anemia and hi retic, esp with SM or other probable causes
o	smear (see table 131-2, pg 1047) – Spherocytosis
o	Bilirubin (elevated), LDH (elevated), ALT (normal)
o	2nd: Urinary hemosiderin (present), Hb (present), serum Hp (if decreased, indicates intravascular hemolysis)
o	Identify cause: Consider risk factors; Examine for splenomegaly; Coombs' test (auto-immunity), smear
o	Others: Hb electrophoresis, RBC enzyme assays, flow cytometry, cold agglutinins, osmotic fragility, acid hemolysis, sucrose lysis
52
Q

• What is AIHA?

A

o The body makes abs to its own RBCs, resulting in hemolysis; mb severe and fatal
o Mb warm ab hemolytic anemia (> 37 C) or cold ab (< 37 C)

53
Q

• What is warm AIHA?

A

o most common, more in women
o abs react: Spontaneously or viral infections, immune def, drugs, SLE, lymphoma, CLL
o Occurs primarily in spleen
o Ssx: Anemia, mild splenomegaly; If severe, fever, chest pain, syncope, heart failure

54
Q

• What is cold AIHA?

A

o Infections (mycoplasma pneumonia) – acute
o Lymphoproliferative states
o ½ are idiopathic – chronic
o Hemolysis is primarily in the liver, with mild anemia
o May see acrocyanosis, Raynaud’s, levido reticularis, scleral icterus and an enlarged spleen

55
Q

• How is AIHA diagnosed?

A

o Direct antiglobulin test (Coombs’) – ab patterns determine warm versus cold ab dz

56
Q

• What is hereditary spherocytosis and elliptocytosis?

A 
o	Congenital RBC membrane defects
o	Spherocytosis (chronic familial icterus, congenital hemolytic jaundice): AD; Hemolysis of spheroidal RBCs and anemia
o	Elliptocytosis (Ovalocytosis): Rare, AD; Oval or elliptical RBCs
57
Q

• What are ssx of spherocytosis

A

o Moderate jaundice and anemia sxs if severe
o May see hepatomegaly
o Splenomegaly
o Cholelithiasis

58
Q

• How is spherocytosis diagnosed?

A

o Spheroidal or oval RBCs
o Prominent anisocytosis
o Normal or low MCV
o Elevated MCHC
o Reticulocytosis and leukocytosis is common
o RBC osmotic fragility is abnormal
o Inc LDH, inc unconjugated bilirubin, and dec serum Hp

59
Q

• What is stomatocytosis?

A

o Rare, congenital or acquired RBC membrane d/os
o RBC membrane fragility is increased
o Congenital form is very severe, presenting early
o Acquired form due to recent excessive alcohol ingestion (will normalize after 2 weeks off EtOH)
o Sxs are those of anemia
o RBCs have straight or rectangular area of central pallor

60
Q

• What is hypophosphatemia?

A

o Low phosphate depletes RBC ATP, resulting in rigid RBCs, more susceptible to injury
o Results in small, spheroid RBCs

61
Q

• What is G-6-P def?

A

o Reduces energy available to maintain integrity of RBC membrane
o Due to abnormal enzymes, genetic polymorphism, drug sensitivity
o X-linked d/o fully expressed in 12% of African-American males, variable in females. Also seen in people of Mediterranean descent
o Hemolysis in cells exposed to peroxide or other oxidants: primaquine, salicylates, sulfonamides, nitrofuran, Vit. K derivatives and many others (fava beans)
o Hemolysis can be precipitated by stress, fever, acute infection, diabetes
o usu self limited; More severe in African Americans

62
Q

• What are ssx of G-6-P def? Labs?

A

o anemia, sudden onset jaundice, pallor, and dark urine, w/ or w/o abd and back pain
o may lead to renal failure
o anemia, reticulocytosis, sometimes Heinz bodies (particles of dead cytoplasm), bite cells
o G6PD assay

63
Q

• What is sickle cell anemia?

A

o Chronic hemolytic anemia, occurring almost exclusively in Africans and African Americans
o Lifespan is increasing constantly – now > 50 yrs
o Cause: Homozygous inheritance of the Hb S gene
o Sickle cell trait occurs in heterozygous people (no anemia), with varying expression

64
Q

• What are ssx of sickle cell anemia? Trait?

A

o painful bony crises, renal damage, punched out leg ulcers
o splenic infarcts, aplastic crises
o anemia usu severe
o developmental delays
o avascular necrosis of the femoral head
o severe abdominal pain with vomiting
o neurological disturbances
o splenomegaly
o Usu results in death by middle age due to infection, pulmonary emboli, vessel occlusion.
o Sickle cell trait S/SX: myalgias, hematuria (during hypoxia)

65
Q

• What are lab results for sickle cell anemia?

A 
o	Low RBCs, Hct, Hb
o	normal white cells, or high
o	normocytic anemia
o	elevated bilirubin
o	nRBCs in blood and sickle cells seen
o	high plasma Hb
o	Hb electrophoresis differentiates hetero (more Hb A than Hb S) from homozygotic (only Hb S, variable Hb F)
66
Q

• What is HbC dz? Ssx?

A

o Genetic Hb-opathy, more common in African descent and mb assoc with sickle cell dz
o anemia mb severe but condition is highly variable
o Ssx: bone pain; large spleen; mild jaundice; anemia

67
Q

• What are lab findings for Hb C dz?

A

o normochromic anemia
o with 30-100% target cells, spherocytes
o May see nucleated red cells
o no anemia in the heterozygote

68
Q

• what is thalassemia?

A

o Inherited defects in synthesis of globin chains
o Ineffective/Lo RBC production
o Most common in Mediterraneans, Africans, SE Asians, South Pacific Islanders
o Mb concurrent with sickle cell anemia
o Prenatal diagnosis is the goal
o Thalassemia major: homozygous, with beta thalassemia major being the most serious (autosomal dominant)
o Thalassemia minor: heterozygous, milder dz
o Inheritance patterns can be complex, esp with alpha thalassemia
o Some heterozygotes are free of dz, and homozygotes usu die

69
Q

• What are ssx of thalassemia?

A

o heart failure, failure to thrive, splenomegaly; with jaundice, leg ulcers, and gallstones common
o thick malar eminences and cranial bones

70
Q

• what are lab results for thalassemia?

A 
o	microcytic, hypochromic anemia
o	Target cells, basophilic stippling (precipitated ribosomes and mitochondria), nucleated red cells
o	Marked aniso and poik
o	Abnormal Hb electrophoresis
o	Normal or elevated Fe
o	Elevated ferritin and bilirubin
o	Thalassemia major see Hb < 6g%
71
Q

• What is thalassemia px?

A

o rare to live long with thalassemia major and most die by their teens
o Normal life expectancy with most thalassemia minors

72
Q

• What is leukopenia?

A

o absolute decrease in the number of WBCs circulating and mb pancytopenic, or just one type
o Definition: <4,000 cells/mm3

73
Q

• What is neutropenia? Severities?

A

o decrease in neutrophil count (PMNs, granulocytes).
o = main defense against bacterial and fungal infections
o When reduced, inflammatory response to infections is ineffective
o More than 1200/mm3 in blacks and 1500/mm in whites results in normal resistance
o 1000-1500/mm3 - mild risk of infection
o 500-1000/mm3 - moderate risk
o <200/mm3 – rapidly fatal infections
o Skin, mucosal and vascular integrity, nutritional status ( i.e. “terrain”) all influence the risk of infection

74
Q

• What are ssx of neutropenia?

A

o Signs depend on degree of decrease in white cells
o Symptoms only occur with infection:
o Fever mb only sign
o Most frequent infections in profound neutropenia are cellulitis, liver abscesses, furunculosis, pneumonia, and septicemia
o If drug induced, may also have rash, LAD

75
Q

• What are the 2 types of neutropenia?

A

o Intrinsic and 2nd

76
Q

• What are causes of intrinsic neutropenia?

A

o dt defects in myeloid cells or precursors. All types are rare
o Congenital causes
o Chronic idiopathic and benign neutropenias – other cell lines unaffected.

77
Q

• What causes 2nd neutropenia?

A 
o	Drugs may induce – usu idiosyncratic and unpredictable; Sometimes dose- dependent, as in chemotherapy
o	BM infiltration  - CA, MF
o	Hypersplenism
o	Infections, sepsis: Common childhood viral infections; HIV
o	Alcoholism
o	Autoimmune- esp SLE
o	Folate, B12 def
o	Leukemias
o	Transfusions
78
Q

• How is neutropenia diagnosed?

A

o CBC
o Priority is to determine presence of infection, signs of which mb subtle
o PE of mucosal surfaces, lungs, abdomen, urinary tract, skin/nails, venipuncture sites, catheter sites
o If acute, do bacterial and fungal blood cultures if pt is febrile
o Skin lesions are aspirated or biopsied for culture
o Urinalysis, urine culture for all pts
o CXR for all pts
o Radiography of sinuses if signs of sinusitis are present
o Determine mechanism and cause:
o Good hx of meds or toxins ingested
o PE looks for underlying dz and splenomegaly
o Ultimately, bone marrow examination mb necessary

79
Q

• What is lymphocytopenia?

A

o reduction in lymphocytes
o Defined as < 3000/mm3 in children <2 yo
o Lymphocytes include T cells (75%) and B cells (25%)
o 65% of T Cells are CD4
o Lymphocytes account for 20-40% of total WBC count

80
Q

• What causes lymphocytopenia?

A

o Inherited or acquired
o Infectious dz- TB, HIV, SARS, hepatitis, EBV, CMV
o Dietary def
o Iatrogenic- immunosuppression, chemo, radiation
o Systemic dzs with autoimmune features- SLE, RA, Sarcoid, Cushing’s
o Other- EtOH, Zn def, malnutrition, others

81
Q

• What are ssx of lymphocytopenia?

A

o none specific to the reduction in cells
o Will see signs of the primary illness
o May see absent or diminished tonsils or LNs
o If tumors are the cause, there mb palpable LA
o Hematologic dz: jaundice, pallor, petechiae, splenomegaly
o Recurrent viral, fungal, parasitic infections

CPD 1 (10 decks)

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