Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Emergency Medicine EOR > Hematology > Flashcards

Hematology Flashcards

You may prefer our related Brainscape-certified flashcards:
Royal College: Emergency Medicine flashcards
1
Q

What is acute lymphocytic leukemia (ALL)?

A

CHILD + lymphadenopathy + bone pain + bleeding + fever in a CHILD, bone marrow> 20% blasts in bone marrow

  • population:children - most common childhood malignancy peak age 3-7
  • highly responsive to chemotherapy (remission>90%)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is chronic lymphocytic leukemia (CLL)?

A

middle age patient, often asymptomatic (seen on blood tests), fatigue, lymphadenopathy, splenomegaly

  • population: adults - most common from of leukemia in adults - peak age 50 y/o
  • diagnostic studies: SMUDGE CELLS on peripheral smear, mature lymphocytes
  • treatment with observation, if lymphocytes are >100,000 or symptomatic, treat with chemotherapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is acute myeloid leukemia (AML)?

A

BLASTS + AUER RODS in ADULT PATIENT

  • population: adults (80%) majority of patients >50 y/o
  • anemia, thrombocytopenia, neutropenia, splenomegaly, gingival hyperplasia and Leukostasis (WBC >100,000)
  • Aur Rods and >20% blasts seen in bone marrow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is chronic myeloid leukemia (CML)?

A

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

  • population: adults - patient usually >50 y/o
  • 70% asymptomatic until the patient has a plastic crisis (acute leukemia)
  • diagnostic studies: Philadelphia chromosome (translocation of chromosome 9 and 22) “Philadelphia CreaM cheese”, splenomegaly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is anemia of chronic disease?

A

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

  • diagnostic studies: normochromic/normocytic anemia initially
  • treatment: erythropoietin and treat the underlying disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is aplastic anemia?

A

the only anemia where all three cell lines are decreased, decrease WBC, decreased RBC, decreased platelets - will have normal MCV and decreased retic
-diagnostic studies: pancytopenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is folate deficiency?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the population and diagnsotic studies for folate deficiency?

A 
population: Alcoholics 
Diagnostic studies:
-megaloblastic anemia
-serum folic acid: low
-Macro-ovalocytes and hypersegmented PMNs (pathognomonic) 
-elevated homocysteine, normal MMA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
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
  • prophylactic folate acid - pregnant/lactating women, contemplating pregnancy, sickle cell patient
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is G6PD deficiency?

A

after infection or medciation (oxidative stress) in a African American male (x-linked) + Heinz Bodies and Bite Cells on a smear (damaged hemoglobin - G6PD protects RBC membrane)

  • hemolytic anemia
  • African, middle eastern, S. Asian populations
  • flare triggers: fava beans, antimalarials, sulfonamides
  • Diagnostic studies: Heinz Bodies and Bite Cells on smear
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the tx for G6PD deficiency?

A
  • avoid potentially harmful drugs, monitor infection

- acute - blood transfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is hemolytic anemia?

A

Caused by the premature breakdown of RBCs

  • autoimmune hemolytic anemia (+Direct Coombs test) - increase retic, increased LDH, decreased haptoglobin, and increased 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 (oxidative 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 decreased MCV (microcytis and hypochromic) with a normal TIBC and ferritin, elevated iron and family hisotyr of blood cell disorder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is iron deficiency?

A

decrease MCV (microcytic), decrease MCH (hypo chromic), increase TIBC, decreased ferritin (best test, low iron stores), target cells, pica and nail spooning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the characteristics of iron deficiency?

A
  • most common anemia in the US
  • always consider GI bleed
  • associated with pica and nail spooning
  • Diagnostic studies:
  • microcytic hypothermic anemia
  • low ferritin (best test)/Fe, high TI
  • target cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the tx for iron deficiency?

A

FeSO$ 325 mg TID

-packed red blood cells when Hgb <8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is hemolytic anemia?

A
  • Population: African Americans, presents in the 1st year of life
  • Hemolysis, jaundice, splenomegaly, priapism, poor healing, pain/swelling hands and feet, acute chest syndrome, pigmented gallstones
  • diagnosis: hemoglobin electrophoresis: Hemoglobin S
  • blood smear: sickled RBCs, Howell-Jolly bodies, target cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the tx of sickle cell anemia?

A

Hydroxyurea

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is thalassemia?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is beta thalassemia trait?

A
  • mild anemia, often misdiagnosed as iron deficient

- hemoglobin electrophoresis: hemoglobin A2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is alpha thalassemia?

A
  • Chinese and Southeast Asians

- hemoglobin elctrophoresis: Hemoglobin H (H disease), hemoglobin Bart’s (hydrops fetalis), Hemoglobin A (trait)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is Vitamin B12 deficiency?

A

increase MCV >100 (macrocytic anemia), hyperhsegmented neurophils and normal folate, decreased vibratory and position sense

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the characteristics of Vitamin B12 deficiency?

A
  • etiology: pernicious anemia (antibody to intrinsic factor), gastrectomy, vegans
  • glossitis: smooth beefy, sore tongue, neurologic symptoms (poor balance, low proprioception)
  • Diagnostic studies:
  • megaloblastic anemia (MCV>100), hyperhsegmented neutrophils
  • elevated serum MMA, elevated homocysteine
  • pernicious anemia: Schilling test (less than 10% radio labeled vitamin B12 in the urine, normal results when repeated with the administration of intrinsic factor)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the tx for 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 wk, then monthly for life
  • PO B12 1-2 mg PO daily for vegans and bariatric surgery
  • years to deplete stores
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is aplastic anemia?

A

the only anemia where all three cell lines are decreased, decreased WBC, decreased RBC, decreased platelets - will have normal MCV and decreased retic

  • loss of blood cell precursors = hyperplasia of bone marrow, RBCs, WBCs, and platelets without reticulocytosis
  • causes: chemicals, drugs, radiation (ACE-I, sulfonamides, phenytoin, chemo, radiation)
  • s/sx: severe pallor, weakness, petechiae, ecchymosis, mucosal bleeding, severe infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How is aplastic anemia dx?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the tx for aplastic anemia?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is Von Willebrand Disease (vWD)?

A

the Von Willebrand factor is 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the characteristics of Von Willebrand Disease?

A
  • most common genetic bleeding disorder, autosomal dominant
  • decrease von Willebrand’s factor (vWF) and decreased 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 amounts of superficial bleeding, common to have bleeding with minor injury and petechiae
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the treatment for Von Willebrand Disease?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
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_

33
Q

What are the two forms of hemophilia?

A
  • hemophilia A, which accounts for about 80% of all cases, is a deficiency in clotting factors VIII (“aight”)
  • hemophilia B is a deficiency in clotting factor IX (Christmas disease)

Remember: Hemophila A =”aight” and b comes after A which is factor NINE

34
Q

What are the characteristics of hemophilia?

A
  • X-linked recessive so will affect males (most of the time)
  • hemarthrosis, bruising, and bleeding
  • Increased PTT, normal PT and platelets, with decrease Factor VIII or decrease factor IX on assay
35
Q

What is the tx for hemophilia?

A

treatment involves the replacement of Factor VIII or IX

36
Q

What is the presentation of easy bruising?

A

when a patient presents with easy bruising the major workup should be looking for platelet dysfunction or some type of coagulation deficiency or medication

37
Q

What are the causes of easy bruising?

A
  • medications (aspirin, coumadin, Xarelto, Eliquis, NSAIDs)

- genetics (hemophilia A, B, C, Von Willebrand’s, idiopathic thrombocytopenic purpura)

38
Q

What is the initial workup of easy bruising?

A
  • CBC with platelet count
  • peripheral blood smear
  • promthrombin time (PT) and partial thromboplastin time(PTT)
39
Q

How is easy bruising dx?

A
  • prolongation of PT or PTT may reflect clotting factor deficiency
  • presence of an inhibitor of a component of the coagulation pathway (including the presence in the circulation of direct oral anticoagulants inhibiting thrombin or factor Xa)
40
Q

What are the pearls of easy bruising?

A
  • mild platelet dysfunction can be causes by aspirin, P2Y12 inhibitors, or NSAIDs and is very common
  • easy bruising with no other clinical manifestations and normal laboratory test results is probably benign
41
Q

What are the ddx for hypercoagulable state?

A

The differential diagnosis can be remembered with the mnemonic PVCS:

  • platelets: too many (usually more than 1 million/uL) or overactive (TTP, Heparin-induced thrombocytopenis (HIT), HUS, and HELLP)
  • vascular injury: from plaques, trauma, or burns
  • clotting factors: anti-clotting factors protein C, protein S, or antithrombin III deficient or not working
  • Stasis and surgery
42
Q

What is Virchow triad?

A

blood stasis, hypercoagulable state, and vascular injury

  • genetic causes include antithrombin III deficiency, factor V Leiden (activated protein C resistance), protein C deficiency, protein S deficiency, dysfibrinogenemia, and abnormal plasminogen
  • acquired hypercoagulable states: malignancy, pregnancy, nephrotic syndrome, ingestion of meds (estrogen), immobilization, myeloproliferative DZ, US/Crohn’s. Behcet’s syndrome, polycythemia vera, intravascular devices, DIC, hyperlipidemia, antiphospholipid syndrome
  • Heparin can cause HIT, causing decrease platelets followed by platelet activation causing clotting and infarction
  • Lupus anticoagulants: IgM and IgG immunoglobulin is seen in 5-10% of pt with SLE but MC without lupus or in those taking phenothiazines
43
Q

What is Factor V Leiden?

A

(MC): procoagulant clotting factor - amplifies the production to thrombin a clot formation

  • mutated factor V resistant to breakdown by activated protein C = hypercoagulability
  • increased DVT and PE especially in young patients
  • Dx: activated protein C resistance assay; normal PT/PTT
  • Tx: LMWH bridge to warfarin; long term antithrombotic therapy not recommended
44
Q

What is Protein C Deficiency?

A

vitamin K dependent anticoagulant liver protein that stimulates fibrinolysis and clot lysis (inactivates factor V and VIII) - potentiated by protein S

  • increased risk recurrent DVT/PE; may have family hx
  • Dx: protein C/S functional assay: decreased protein C/S activity levels
  • at risk for skin necrosis on warfarin
  • Tx: heparin and oral anticoagulation for life
45
Q

What is Protein S Deficiency?

A

vitamin K dependent that is cofactor for activated protein C, which inactivates procoagulant factors Va and VIIIa = reducing thrombin generation

  • VTE = risk
  • Dx: protein C or S functional assay: decreased protein C or S activity levels
  • Tx: heparin/oral anticoagulation for life
46
Q

What is Antithrombin III Deficiency?

A

recurrent venous thrombosis and PE, repetitive intrauterine fetal death (IUFD)

  • Antithrombin III = natural anticoagulant; inhibits thrombin (IIa), Xa and other proteases; potentiated by Heparin
  • associated with VTE; first episode 20 to 30 yo
  • asymptomatic pt requires anticoagulation only before surgical procedures
  • Pt with thrombotic events require high dose IV heparin then oral anticoagulation indefinitely
47
Q

What is Antiphospholipid Antibody Syndrome?

A

autoimmune; often associated with SLE; characterized by thromboses and recurrent spontaneous abortions

  • autoantibodies react against platelet membranes, activating endothelial cells and platelets = complement-mediated thrombosis
  • Dx: lupus anticoagulant, anticardiolipin, DRVVT test, prolonged PTT
  • Tx: high dose IV heparin with thrombotic events then oral anticoagulation indefinitely
48
Q

What is Hodgkin’s Lymphoma?

A

painless lymphadenopathy + bimodal age distribution (15-35) and (>60)

  • fever, chills, and nigh sweats for >1 month
  • painless enlarged posterior cervical and supraclavicular lymph nodes Virchow’s node
  • CXR - mediastinal adenopathy
  • Excisional biopsy of the lymph node shows Reed-Sternberg cells
49
Q

What is Non-Hodgkin Lymphoma?

A

look for an immunocompromised (HIV) patient with GI symptoms and painless peripheral lymphadenopathy

50
Q

What is the age of patients with Hodgkin’s Disease Lymphoma?

A

bimodal peaks in 20’s then in 50’s

51
Q

What is the age of patients with Non Hodgkin’s Lymphoma?

A

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

52
Q

What is the cell type with Hodgkin’s Disease Lymphoma?

A

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

53
Q

What is the cell type with Non Hodgkin’s Lymphoma?

A

B cell: diffuse large B cell

T cell, natural killer cells

54
Q

What is the lymph node involvement with Hodgkin’s Disease Lymphoma?

A

painless lymphadenopathy: upper body lymph nodes: neck, axilla, shoulder, chest (mediastinum)
-contiguous spread to local lymph nodes: usually localized single group of nodes

55
Q

What is the lymph node involvement with Non Hodgkin’s Lymphoma?

A

peripheral, multiple lymph nodes: axillary, abdominal, pelvic inguinal, femoral
-non contiguous, extranodal spread: GI and skin most comon

56
Q

What are the B symptoms with Hodgkin’s Disease Lymphoma?

A

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

57
Q

What are the B symptoms with Non Hodgkin’s Lymphoma?

A

B symptoms not common

58
Q

What is the EBV Association with Hodgkin’s Disease Lymphoma?

A

associate with EBV (40% of patients)

59
Q

What is the EBV Association with Non Hodgkin’s Lymphoma?

A

rare

60
Q

What is the management with Hodgkin’s Disease Lymphoma?

A

excellent 5-year cure rate (60%)

61
Q

What is the management with Non Hodgkin’s Lymphoma?

A

variable cure rate

62
Q

What is primary polycythemia?

A

due to factors intrinsic to red cell precursors

63
Q

What is polycythemia vera?

A

a malignancy of the bone marrow that results in the overproduction of red blood cells (primarily), but also can affect platelets, and white blood cells

64
Q

What are the classic symptoms of polycythemia vera?

A

pruritus after hot baths, as well as swelling, burning pain, and rubor of the hands and feet (erythromelaigia)
-patients may also have gout due to increased cell turnover leading to hyperuricemia

65
Q

What are the 4 H’s of polycythemia?

A

Hypervolemia (increase RBC), histaminemia (increase histamine due to release from mast cells), hyperviscosity (increased hematocrit = increased viscosity), and hyperuricema (increased uric acid)

  • elevated RBC count. hemoglobin, hematocrit (usually > 50)
  • elevated RBC count, hemoglobin, hematocrit (usually > 50)
  • thrombocytosis, leukocytosis may be present
  • serum erythropoietin levels are reduced
  • elevated vitamin B12 level
  • hyperuricemia is common
  • increased histamine - proposed mechanism for intense pruritus associated with this disorder
  • positive Jak2 tyrosine kinase mutation
  • bone marrow biopsy confirms the diagnosis
66
Q

What is the tx for polycythemia?

A

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

  • older patients (>60 years old) and those with prior thrombosis should be treated with a myelosuppressive agent, most commonly hydroxyurea with or without aspirin
  • anagrelide may be used to decrease the platelet count
67
Q

What is secondary polycythemia?

A

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

68
Q

What is idiopathic thrombocytopenic purpura (ITP)?

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 except low platelets (+ Direct Coombs Test)
69
Q

What is the tx for ITP?

A
  • children supportive care (IVIG for refractory cases)

- adults treat with prednisone

70
Q

What is thrombotic thrombocytopenic purpura 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)

71
Q

What is thrombotic thrombocytopenia (TTP)?

A

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

72
Q

What is the cause of TTP?

A
  • after drugs: quinidine, cyclosporine, and pregnancy

- inhibition of ADAMTS13

73
Q

What is the presentation of TTP?

A
  • adults

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

74
Q

What is the dx and tx for TTP?

A

dx: CBC normal expect low platelets, schistocytes (RBC fragments) on the smear, (-) coombs test
- tx: steroids, plasmapheresis

75
Q

What is hemolytic uremic syndrome (HUS)?

A

decreased platelets + anemia + renal failure (associated with E. coli 0157:H7 and diarrheal illness in a child)

76
Q

What is the presentation of HUS?

A
  • post-infection: E. coli or Shigella
  • children
  • severe kidney problems
77
Q

What is DIC?

A

abnormal activation of the coagulation sequence, leading to the formation of microthrombi throughout the microcirculation
-the causes the consumption of platelets, fibrin, and coagulation factors

78
Q

What are the characteristics of DIC?

A
  • fibrinolytic mechanisms are activated, leading to hemorrhage
  • therefore, bleeding and thrombosis occur simultaneously
  • infection, obstetric complications, trauma, malignancy, shock
  • decreased platelets, increased bleeding time, increased PT, increased PTT, (+) D-dimer
79
Q

What is the tx for DIC?

A

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

Emergency Medicine EOR (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions