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Family Medicine EOR > Hematology > Flashcards

Hematology Flashcards

1
Q

What is iron deficiency anemia?

A

-decrease MCV (microcystic), decrease MCH (hypo chromic), increase TIBC, decrease Ferritin (best test, low iron stores) target cells, pica, and nail spooning

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2
Q

What are the characteristics of iron deficiency anemia?

A
  • MC cause of anemia and usually from blood loss
  • in men: chronic occult bleeding; women = menses
  • always consider GI bleed
  • s/sx: fatigue, palpitations, SOB, weakness, HA, tinnitus, (nail), atrophic glossitis (tongue), angular cheilitis
  • associated with pica and nail spooning (koilonychia)
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3
Q

How is iron deficiency anemia dx?

A
  • microcytic/hypochromic anemia
  • CBC: low reticulocyte count, high RDW
  • iron studies: decreased serum iron, transferrin saturation; increase TIBV, decrease ferritin (Best test, low iron stores) < 15 diagnostic
  • H&H: <13.5 & 39 for men, <12 and 37 for women
  • peripheral smear: poikilocytes; rarely bone marrow examination; hemoccult if indicated
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4
Q

What is the tx for iron deficiency anemia?

A

FeSO4 325 mg TID

  • ferrous sulfate 3 mg/kg once or twice daily between meals with juice (not milk)
  • ferrous fumarate 100-200 mg/day in 2-3 doses; ferrous gluconate 3-6 mg/kg/day in 3 doses
  • s/e: gray staining/teeth (liquid preps); GI upset/constipation
  • six weeks to correct; six months to replete iron stores; rechecked blood counts every 3 months x 1 year
  • packed red cells when Hgb < 8
  • other causes decreased MCV: lead poisoning, sideroblastic anemia, basophilic stippling, thalassemia
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5
Q

What is anemia of chronic disease?

A

normal or decrease MCV, decrease TIBC, increase Ferritin (high iron stores), decrease serum erythropoietin

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6
Q

What are the dx studies for anemia of chronic disease?

A

normochromic/normocytic anemia initally

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7
Q

What is the tx for anemia of chronic disease?

A

erythropoietin and treat the underlying disease

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8
Q

What is aplastic anemia?

A

the only anemia where all three cell lines are decreased: decrease WBC, decrease RBC, decrease platelets - will have normal MCV and decrease Retic
-loss of blood cell precursors = hypoplasia of bone marrow, RBCs, WBCs, and platelets without reticulocytosis

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9
Q

What are the causes of aplastic anemia?

A

chemicals, drugs, radiation (ACE-I, sulfonamides, phenytoin, chemo, radiation)

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10
Q

What are the signs and symptoms of aplastic anemia?

A

severe pallor, weakness, petechiae, ecchymosis, mucosal bleeding, severe infection

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11
Q

What are the dx studies for aplastic anemia?

A

pancytopenia = decreased WBC, RBC, platelets; most accurate = bone marrow biopsy

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12
Q

What is the tx of aplastic anemia?

A

stop causative agent, RBC transfusion, bone marrow transplant, immunosuppressive agents

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13
Q

What is folate deficiency?

A

decrease folate, increase MCV (macro cystic anemia) - looks like B12 but no neurologic symptoms

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14
Q

What population does folate deficiency occur to?

A

alcoholics

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15
Q

What are the diagnostic studies for folate deficiency?

A
  • megalobalstic anemia
  • serum folic acid: low
  • macro-ovalocytes and hypersegmented PMNs (pathognomonic)
  • elevated homocysteine, normal MMA
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16
Q

What is the tx for folate deficiency?

A
  • PO folic acid 1-5 mg/d (first line)
  • Avoid ETOH and folic acid antagonists (Bactrim, phenytoin, sulfasalazine)
  • green leafy vegetables, yeast, legumes, fruits, animal proteins
  • prophylatic folic acid - pregnant/lactating women, contemplating pregnancy, sickle cell patient
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17
Q

What is G6PD deficiency?

A

after infection or medication (oxidative stress) in an African American male (x-linked) + Heinz bodies and bite cells on smear (damaged hemoglobin - G6PD protects RBC membrane

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18
Q

What are the characteristics of G6PD?

A
  • hemolytic anemia
  • african, middle eastern, S. asian population
  • flare triggers: fava beans, antimalarials, sulfonamides
  • diagnostic studies: Heinz bodies and bite cells on smear
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19
Q

What is the tx for G6PD?

A
  • avoid potentially harmful drugs, monitor infection

- acute - blood transfusion

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20
Q

What is hemolytic anemia?

A

a disorder in which red blood cells are destroyed faster than they can be made
-the destruction of red blood cells is called hemolysis

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21
Q

What are the hemolytic anemias?

A
  • autoimmune hemolytic anemia (+ direct Coombs test) - increase retic, increase LDH, decrease haptoglobin, and increase bilirubin (indirect)
  • hereditary spherocytosis (+) osmotic fragility test, increase retic, increase LDH, decrease haptoglobin, and increase bilirubin (indirect) and the presence of spherocytes
  • G6PD deficiency after infection or medication (oxidate stress) in an African American male (x-linked) + Heinz bodies and bite cells on a smear (damaged hemoglobin - G6PD protects RBC membrane)
  • sickle cell anemia (very increase retic count + pain in African American male, hemoglobin electrophoresis: hemoglobin S, blood smear: sickled RBCs, Howell-Jolly bodies, target cells)
  • thalassemia very decrease MCV (microcytic and hypo chromic) with a normal TIBC and ferritin, elevated iron and family history of blood cell disorder
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22
Q

What is sickle cell anemia?

A

African American, pain, family history of blood disorder, hemoglobin electrophoresis: Hemoglobin S, blood smear: sickled RBCs, Howell-jolly bodies, target cells

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23
Q

What are characteristics of sickle cell anemia?

A
  • population: African American, presents in the 1st year of life
  • hemolysis, jaundice, splenomegaly, priapism, poor healing, pain/swelling hands and feet, acute chest syndrome, pigmented gallstones
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24
Q

How is sickle cell anemia dx?

A

hemoglobin electrophoresis: hemoglobin S

-blood smear: sickled RBCs, Howell-Jolly bodies, target cells

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25
Q

What is the tx of sickle cell anemia?

A

hydroxyurea

-Vaccine: meningococcal, pneumococcal, H. influenzae, influenza

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26
Q

What is thalassemia?

A

family history of blood cell disorder, microcytic hypo chromic, elevated iron

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27
Q

What is beta thalassemia major?

A
  • most severe, mediterranean descent, failure to thrive
  • hemoglobin electrophoresis: hemoglobin A2 and F
  • treatment: transfusion dependent, iron chelation (deferoxamine)
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28
Q

What is beta thalassemia trait?

A
  • mild anemia, often misdiagnosed as iron deficient

- hemoglobin electrophoreis: Hemoglobin A2

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29
Q

What is alpha thalassemia?

A
  • chinese and southeast Asians

- hemoglobin electrophoresis: hemoglobin H (H disease), hemoglobin Bart’s (hydros fetalis), hemoglobin A (trait)

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30
Q

What is Vitamin B12 deficiency?

A

increase MCV > 100 (macrocytic anemia), hyper segmented neutrophils and normal folate, decreased vibratory and position sense

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31
Q

What is the etiology of Vitamin B12?

A 
pernicious anemia (antibody  to intrinsic factor), gastrectomy, vegans 
-glossitis: smooth beefy, sore tongue, neurologic symptoms (poor balance, low proprioception)
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32
Q

What are the diagnostic studies for Vitamin B12 deficiency?

A
  • megaloblastic anemia (MCV >100), hyperhsegmented neutrophils
  • elevated serum MMA, elevated homocysteine
33
Q

What is pernicious anemia?

A

schilling test (less than 10% radiolabled vitamin B12 in the urine, normal results when repeated with the administration of intrinsic factor)

34
Q

What is the tx of Vitamin B12 deficiency?

A
  • lifelong IM B12: 1-3 ug/d (animal products, fortified cereal) for pernicious anemia
  • IV cyanocobalamin 1 mg IM daily x 7 d, then weekly x 4 weeks, then monthly for life
  • PO B12 1-2 mg PO daily for vegans and bariatric surgery
  • years to deplete stores
35
Q

What are clotting factors?

A

proteins that interact to help the blood clot, stopping the bleeding,

36
Q

What is von Willebrand disease?

A

found in plasma, platelets, and the walls of the blood vessels

  • when the factor is missing or defective, platelets cannot adhere to the vessel wall at the site of an injury
  • as a result, bleeding does not stop as quickly as it should
37
Q

What are the characteristics of von Willebrand disease?

A
  • most common genetic bleeding disorder, autosomal dominant
  • decrease von Willebrand’s factor (vWF) and decrease Factor VIII
  • patient may present with excessive bleeding after a cut or increased menstrual bleeding
  • you can differentiate this from hemophilia by lack of Hemarthrosis, small amount of superficial bleeding, common to have bleeding with minor injury and petechiae
38
Q

What is the tx of von Willebrand disease?

A

DDAVP (desmopressin) or in cases of excessive bleeding a transfusion of concentrated blood clotting factors containing von Willebrand factor

39
Q

What is hemophilia?

A

a hereditary bleeding disorder caused by a deficiency in one of two blood clotting factors: Factor VIII (A) or factor IX (B)

40
Q

What is hemophilia A?

A

which accounts for 80% of all cases, is a deficiency in clothing Factor VIII (“aight”)

41
Q

What is hemophilia B?

A

a deficiency in clotting factor IX (Christmas disease)

42
Q

What are the characteristics of hemophilia?

A
  • hemophilia A = “aight” and B comes after A which if factor NINE
  • x-linked recessive so will affect males (most of the time)
  • hemarthrosis, bruising and bleeding
  • increase PTT, normal PT and platelets, with decrease Factor VIII or decrease factor IX on assay
43
Q

What is tx of hemophilia?

A

involves the replacement of Factor VIII or IX

44
Q

What is acute lymphocytic leukemia?

A
  • child + lymphadenopathy + bone pain + bleeding + fever in Child, bone marrow > 20% blasts in bone marrow
  • population: children - most common childhood malignancy peak age 3-7
  • highly responsive to chemotherapy (remission > 90%)
45
Q

What is chronic lymphocytic leukemia?

A
  • middle age patient, often asymptomatic (seen on blood tests), fatigue, lymphadenopathy, splenomegaly
  • population: adults - most common form of leukemia in adults - peak age 50 y/o
  • diagnostic studies: SMUDGE cels on peripheral smear, mature lymphocytes
  • treatment with observation, if lymphocytes are >100,000 or symptomatic, treat with chemotherapy
46
Q

What is acute myeloid leukemia?

A

BLASTS + AUER RODS in Adult patient

  • population: adults (80%) majority of patients >50 y/o
  • anemia, thrombocytopenia, neutropenia, splenomegaly, gingival hyperplasia and leukostatis (WBC >100,000)
  • auer rods and >20% blasts seen in bone marrow
47
Q

What is chronic myeloid leukemia?

A

strikingly increased WBC count >100,000 + hyperuricemia + adult patient (usually >50 years old)

  • 70% asymptomatic until the patient has a blastic crisis (acute leukemia)
  • diagnostic studies: philadelphia chromosome (translocation of chromosome 9 and 22) - Philadelphia CreaM cheese”), splenomegaly
48
Q

What is the age of Hodgkin’s disease of lymphoma?

A

bimodal peaks in 20’s then in 50’s

49
Q

What is the cell type for Hodgkin’s disease of lymphoma?

A

Reed-Sternberg cells are pathognomic - B cell proliferation with bilobed or multilobed nucleus - “owl eyes”

50
Q

What is the lymph node involvement for Hodgkin’s disease of lymphoma?

A
  • painless lymphadenopathy: upper body lymph nodes: neck, axilla, shoulder, chest (mediastinum)
  • contigous spread to local lymph nodes: usually localized single group of nodes
51
Q

What are B symptoms for Hodgkin’s disease of lymphoma?

A

B symptoms are common - fever, weight loss, night sweats

52
Q

What is the EBV association with Hodgkin’s disease of lymphoma?

A

associated with EBV (40% of patients)

53
Q

What is the dx of Hodgkin’s disease of lymphoma?

A

CXR to check for mediastinal adenopathy

54
Q

What is the tx for Hodgkin’s disease of lymphoma?

A

chemo, radiation, highly curable

-excellent 5-year cure rate (60%)

55
Q

What is the age of Non Hodgkin’s lymphoma?

A

> 50 years old, increased risk with immunosuppression (ex HIV)

56
Q

What are the cell type of Non Hodgkin’s lymphoma?

A

B cell: diffuse large B cell

T cell, natural killer cells

57
Q

What is lymph node involvement for Non Hodgkin’s lymphoma?

A
  • peripheral, multiple lymph nodes: axially, abdominal, pelvic inguinal, femoral
  • non contiguous, extranodla spread: GI and skin most common
58
Q

Are B symptoms common with Non Hodgkin’s lymphoma?

A

B symptoms not common

59
Q

Is there EBV assocaition with Non Hodgkin’s lymphoma?

60
Q

What are the s/sx with Non Hodgkin’s lymphoma?

A

SOB, intussusecption, bowel obstruction, abdominal masses

61
Q

What is the tx of Non Hodgkin’s lymphoma?

A

rituximab, chemo, variable course

-variable cure rate

62
Q

What is polycythemia?

A
  • primary polycythemia due to factors intrinsic to red cell precursors
  • polycythemia vera is a malignancy of the bone marrow that results in overproduction of red blood cells (primarily) but also can affect platelets, and white blood cells
63
Q

What are the symptoms of polycythemia vera?

A
  • classic symptoms include pruritus after hot baths, as well as swelling, burning pain, and rubber of the hands and feet (erythromelalgia)
  • patients may also have gout due to increased cell turnover leading to hyperuricemia
64
Q

What are the 4 H’s of polycythemia?

A

hypervolemia (increase RBC), Histaminemia (increase histamine due to release from mast cells), hyperviscoisty (increase hematocrit = increased viscosity), and hyperuricemia (increase uric acid)

  • elevated RBC count, hemoglobin hematocrit (usually > 50)
  • thrombocytosis, leukocytosis may be present
  • serum erythropoietin levels are reduced
  • elevated vitamin B12 level
  • hyperuricemia is common
  • increase histamine - proposed mechanism for intense pruritus associated with this disorder
  • postive Jak2 tyrosine kinase mutation
  • bone marrow biopsy confirms the diagnosise
65
Q

What is the tx of polycythemia?

A

treatment consists of repeated phlebotomy to lower hematocrit to <42%

  • older patients (>60 year old) and those with prior thrombosis should be treated with a myelosuprressive agent, most commonly hydroxyura with or without aspirin
  • anagrelide may be used to decrease platelet count
66
Q

What is secondary polycythemia?

A

caused by either a natural or artificial increases in the production of erythropoieint
-altitude related, hypoxic disease-associated (COPD, sleep apnea), bloodletting, genetic, neoplasms, (i.e pheochromocytoma, liver tumors)

67
Q

What is DIC?

A

abnormal activation of the coagulation sequence, leading to the formation of micro thrombi throughout the microcircualtion

  • this causes the consumption of platelets, fibrin, and coagulation factors
  • fibrinolytic mechanisms are activated, leading to hemorrhage, therefore bleeding and thrombosis occur stimulaneously
  • infection, obstetric complications, trauma, malignancy, shock
  • decrease platelets, increase bleeding time, increase PT, increase PTT, (+) d-dimer
68
Q

What is the tx for DIC?

A

cryoprecipitate, FFP, platelet transfusion (if <30,000), heparin, treat cause

69
Q

What is idiopathic thrombocytopenia purpura?

A

autoimmune reaction to platelets usually after a viral illness (ITP is insidious and chronic)

  • diagnosis of exclusion
  • associated with HIV, HCV, SLE, CLL
  • CBC normal expect low platelets (+ direct Coombs test)
70
Q

What is the tx of ITP?

A
  • children supportive care (IVIG for refractory casesO

- adults treat with prednisone

71
Q

What are the differences of TTP vs ITP?

A

different from ITP (ITP is insidious and chronic) from TTP which is an acute febrile disease with multi-organ thrombosis (hence the name “thrombotic” thrombocytopenia)

72
Q

What is thrombotic thrombocytopenia (TTP)?

A

decrease platelets + anemia + schistocytes (RBC fragments) on smear

73
Q

What is the cause of TTP?

A
  • after drugs: quinidine, cyclosporine and pregnancy

- inhibition of ADAMTS13

74
Q

What is the presentation of TTP?

A
  • adults

- purpura and “FAT RN” - fever, anemia, thrombocytopenia, renal failure, neurological symptoms

75
Q

How is TTP dx?

A

CBC normal expect low platelets, schistocytes (RBC fragments) on smear, (-) Coombs test

76
Q

What is the tx of TTP?

A

steroids, plasmapheresis

77
Q

What is Hemolytic uremic syndrome (HUS)?

A

decrease platelets + anemia + renal failure (associated with E. coli O157:H7 and diarrheal illness in a child)

78
Q

What is the presentation of HUS?

A
  • post-infection: E.coli or shigella
  • children
  • severe kidney problems

Family Medicine EOR (14 decks)

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