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Hematologic disorders Flashcards

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1
Q

What is erythropoiesis stimulated by?

A

Human RBC production (erythropoiesis) is stimulated by erythropoietin in the kidney

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2
Q

Where are RBCs produced?

A

Continuously produced in red bone marrow by committed stem cells

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3
Q

How long does it take for RBC formation to maturity

A

~7 days

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4
Q

How long is the lifespan of RBC?

A

120 days

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5
Q

Rate of RBC production

A

2 million cells/sec

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6
Q

What is the reticuloendothelial system (RES)?

A
  • Spleen, liver, bone marrow
  • Responsible for removing old or defective RBCs
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7
Q

What happens to the plasma membrane as RBC ages?

A

Plasma membrane undergoes changes increasing susceptibility to phagocytosis (eryptosis)

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8
Q

What is the rate of eryptosis equivalent to?

A

Rate of eryptosis = rate of erythropoiesis

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9
Q

Disorders of increased eryptosis

A
  • Sepsis
  • Malaria
  • Sickle cell anemia
  • Beta thalassemia
  • Glucose-6-phosphate dehydrogenase deficiency
  • Iron deficiency
  • Wilson disease
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10
Q

What is anemia?

A

Anemia is reduction of RBC volume, hemoglobin concentration below range or values that occur in healthy person (12-18g/100mL)

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11
Q

Acquired hypoproliferative anemia

A
  • Nutritional deficiency (iron, folate, vitamin B12 deficiency)
  • Acquired aplastic (pancytopenia)
  • Transient erythroblastopenia (may have viral cause)
  • Anemia of acute inflammation
  • Marrow replacement by malignancy (ex: leukemia)
  • Effects of drugs or toxins (ex: lead poisoning)
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12
Q

Congenital hypoproliferative anemia

A
  • Diamond Blackfan syndrome
  • Refractory sideroblastic anemia
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13
Q

Congenital hemolytic anemia

A
  • Inherited disorders of hemoglobin
  • Hemoglobinopathies (sickle cell disease, alpha and beta thalassemia)
  • Enzymopathies (ex: G6PD deficiency)
  • RBC membrane disorder (hereditary spherocytosis)
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14
Q

Acquired hemolytic anemia

A
  • Autoimmune hemolysis – body makes antibodies against own RBCs
  • Autoimmune disorders
    • Systemic lupus (SLE) rheumatoid arthritis, ulcerative colitis
  • Hemolysis related to infection
    • (CMV, Epstein Barr Virus, hepatitis) Rh/ABO incompatibilities
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15
Q

What possible hematological abnormality may be associated w/ oral ulcers?

A

Neutropenia

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16
Q

What possible hematological abnormality may be associated w/ glossitis?

A
  • Megaloblastic anemia
  • Iron deficiency anemia
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17
Q

What possible hematological abnormality may be associated w/ angular stomatitis?

A

Iron deficiency anemia

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18
Q

What possible hematological abnormality may be associated w/ candida?

A

Immunosuppression

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19
Q

What possible hematological abnormality may be associated w/ skin pallor?

A

Any anemia

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20
Q

What possible hematological abnormality may be associated w/ jaundice?

A

Hemolytic anemia

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21
Q

What possible hematological abnormality may be associated w/ excessive bruising?

A
  • Coagulation disorder
  • Thrombocytopenia
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22
Q

What possible hematological abnormality may be associated w/ purpuric/petechial rash?

A

Thrombocytopenia

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23
Q

Dental considerations for a low risk anemic patient

A

Cause of anemia known, cause corrected, normal hematocrit, on therapy, asymptomatic: treat as normal

24
Q

Dental considerations for a high risk anemic patient

A
  • Receiving repeated transfusions to prevent symptoms, abnormal pre-op screening hemogram, h/o ongoing hemorrhage, bleeding disorder + anemia:
  • Hematology consult – may require RBC transfusion
  • Defer elective tx until medical status is optimal
  • Tx goals aimed at minimizing stress
  • Deep sedation , GA + invasive surgical procedures may require hospitalization
25
Q

What is sickle cell disease characterized by?

A

Hemolysis, chronic organ damage, acute complication

26
Q

What causes sickle cell disease?

A

Variant of the beta globin gene causing the sickling of RBC

27
Q

Systemic manifestation of sickle cell disease

A
  • Predisposition to infections
  • Splenic sequestration (Hb levels <6 g/dL)
  • Acute vaso-occlusive pain
  • Avascular necrosis
  • Neurologic complications/stroke
  • Pulmonary disease (acute chest syndrome)
  • Renal disease
  • CV disorders (cardiomegaly or murmurs)
28
Q

Dental manifestation of sickle cell disease

A
  • Pale/jaundiced mucosa
  • Increased susceptibility to infection
  • Delayed eruption of permanent dentition
  • Step-ladder trabeculation pattern
29
Q

Sickle cell disease tx

A
  • Hydroxyurea (increases level of HbF)
  • Hematopoietic stem cell transplant
  • RBC transfusion
30
Q

Dental considerations for patients w/ sickle cell disease

A
  • Obtain detailed patient hx
  • Prescribe abx + pain medicine when appropriate to avoid crisis
  • No contraindications for LA w/ vasoconstrictor
  • Avoid hypoxia when using N2O or sedative agents
  • Monitor patients routinely for osteomyelitis
  • Risk of complications based on: type of sx planned, recent disease activity, h/o organ dysfunction, age, genetic haplotype
31
Q

Dental considerations for low risk SCD patients

A

Dental restorations + simple extractions can be performed on an outpatient

32
Q

Dental considerations for moderate + high risk patients

A
  • May require pre-sx + post-sx admission
  • Patient may need blood transfusion prior to sx
33
Q

Hemophilia A

A

Factor VIII deficiency

34
Q

Hemophilia B

A

Factor IX deficiency

35
Q

Von Willebrand disease

A

vW factor deficiency

36
Q

Hemophilia w/ inhibitor

A
  • Patients may develop an antibody to factor replacement routinely given prophylactically
  • Dental tx: No mandibular block injections
  • In younger children, this may be indication for dental rehab under GA to get all tx completed at once (usually oral intubation)
37
Q

Hereditary thrombophilia: Protein C, S, and Factor V Leiden

A

Increased tendency to form clots in veins

38
Q

Acquired clotting factor deficiencies

A
  • Hepatic disease - deficiency of proteins C and S
  • Malabsorption problems
  • Heparin therapy
  • Drug induced
  • Vitamin K deficiency → hypoprothrombinemia
    • Affects factors II, VII, IX, X
39
Q

How are platelets produced?

A

Via pluripotent stem cells in bone marrow

40
Q

What is the life cycle of platelets regulated by?

A

Thrombopoietin (produced by kidney + liver)

41
Q

How long does the entire process of platelets take?

A

~10 days

New platelets are stored in the spleen** for up to **3 days

42
Q

What is the life span of a platelet?

A

7-10 days

43
Q

What % of platelets are in circulation? Where are the remaining stored?

A

~60-75% of platelets are in circulation

Remainder are housed in the spleen

44
Q

What do platelets have membrane receptors for?

A
  • Collagen
  • ADP
  • Von Willebrand Factor
  • Fibrinogen
  • Thrombopoietin
  • Thrombin
  • Clotting factors: VIII, IX, Xa, XI
45
Q

Clotting cascade

A
46
Q

Platelet disorders – thrombocytopenia

A
  • Bone marrow failure
    • Aplastic anemia
    • Leukemia
    • Metastatic cancer
    • Folate deficiency
    • Vitamin B12 deficiency
    • Drug induced
47
Q

Peripheral platelet destruction – immune-mediate

A
  • ITP (immune thrombocytopenic purpura)
  • Post-transfusion
  • Drug induced
    • Furosemide
    • Gold
    • NSAIDs
    • PCN
    • Quinidine
    • Sulfonamides
    • Heparin
48
Q

Platelet destruction – non-immune mediated

A
  • TPP
  • Hemolytic uremic syndrome
  • Disseminated intra-vascular coagulation
  • Chemotherapy
  • Valproic acid (depakote for seizures)
49
Q

Abnormal distribution/hypersplenism

A
  • Partial HTN
  • Inflammatory disease
  • Cancer
50
Q

Drug-induced platelet dysfunction

A
  • Aspirin
    • Irreversible disruption of COX-1
    • Blocks ability of platelets to aggregate
    • Normal platelet function returns when affected platelets are replaced
  • Ibuprofen
    • Reversible inhibition of COX-1
    • Platelet function usually returns in 24 hrs
    • Co-administration of ibuprofen w/ aspirin may diminish aspirin’s effects
  • Naprosyn
51
Q

Congenital platelet dysfunction

A
  • Von Willebrand disease
  • Hereditary hemorrhagic telangiectasia (characterized by multiple small AVMs)
    • Management may include laser, iron supplements, or embolization
  • Glanzmann’s thrombastenia (failure of aggregation)
52
Q

Acquired platelet dysfunction

A
  • Henoch Schonlein Purpura (characterized by itchy purpuric rash)
    • Typically follows an infection
    • Spontaneous remission
  • Vasculitis of SLE
  • Chronic renal failures
53
Q

Disorders of connective tissue matrix of blood vessels

A
  • Marfan syndrome
  • Ehlers-Danlos syndrome
  • Scurvy (arr!)
54
Q

Dental considerations for platelet disorders

A
  • Health Hx
    • Frequent nosebleeds
    • Heavy menstrual cycles
    • Easy bruising
        • family h/o bleeding disorders
        • h/o excessive bleeding following sx
  • Physical findings
    • Petechiae
    • Ecchymosis
    • Generalized spontaneous gingival bleeding
  • Lab screening
    • Prothrombin time (PT) may be elevated due to warfarin, liver disease, vitamin K deficiency
    • Partial thromboplastic time (PTT) may be prolonged due to heparin, vW disease, liver disease
    • Platelet count
    • INR
  • Hematology consult: Mandatory in presence of significant historical, physical or lab findings
55
Q

Prothrombin time (PT)

A

Measures extrinsic clotting system + common pathway

56
Q

Partial thromboplastic time (PTT)

A

Measures intrinsic clotting system + common path

57
Q

INR - international normalized ratio

A
  • Based on a mathematical conversion of the PT to account for differences in lab assays
  • Normal INR = 1.0
  • Patients on Coumadin, targeted INR = 2-3

* (22 decks)

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