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PATH 375 > Hematolymphoid 2 > Flashcards

Hematolymphoid 2 Flashcards

1
Q

How is iron absorbed, transported, stored

A
  • Absorbed in small intestine → bound to transferrin and transported → incorporated into hemoglobin
  • Stored in ferritin (aggregates as hemosiderin)
  • Aging RBCs destroyed in the spleen and iron reutilized
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2
Q

Causes of iron deficiency anemia

A
  • Decreased intake
  • Decreased absorption
  • Increased loss
  • Increased requirements
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3
Q

Iron deficiency anemia lab results

A
  • Blood smear: hypochromic microcytic anemia
  • Hemoglobin and hematocrit low
  • Serum iron and ferritin low
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4
Q

Aplastic anemia

A

Characterized by loss of multipotent stem cell resulting in pancytopenia
- Decreased RBC = anemia
- Decreased WBC = infection prone
- Decreased platelets = bleeding

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5
Q

Aplastic anemia causes

A

Primary: Idiopathic

Secondary (related to BM suppression):
- Chemical agents (cytotoxic drugs)
- Radiation
- Viral infection
- Inherited

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6
Q

Megaloblastic anemia

A

Caused by deficiency of vitamin B12 or folic acid (essential for DNA synthesis and blood cell production)

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7
Q

Megaloblastic anemia pathogenesis

A
  • Deficiencies delay normal RBC maturation
  • RBC precursors do not mature and are transformed into megaloblasts
  • Megaloblasts are destroyed in BM or spleen
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8
Q

Megaloblastic anemia diagnosis

A

Diagnosis
- Peripheral blood smear: oval macrocytes, large segmented neutrophils
- BM biopsy: hypercellular with megaloblasts

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9
Q

Causes of Vitamin B12 deficiency

A
  • Decreased intake (uncommon)
  • Impaired absorption/increased loss (Pernicious anemia)
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10
Q

Pernicious anemia pathogenesis

A

Atrophic gastritis → results in decrease in gastric parietal cells → insufficient IF → B12 deficiency → megaloblastic anemia

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11
Q

Results of folate deficiency

A

Results in megaloblastic anemia (similar characteristics as B12 deficiency)

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12
Q

Causes of folate deficiency

A
  • Impaired absorption/increased loss (Disease of duodenum)
  • Decreased intake
  • Increased requirement
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13
Q

Thalassemias

A

Genetic defect in synthesis of normal Hb (no abnormal Hb is produced, defect is quantitiative)

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14
Q

Thalassemia classifications

A

Classified by type of chain affected
- a thalassemias → defecetive a chain synthesis
- b thalassemias → defecetive b chain synthesis

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15
Q

a thalassemia

What types?

A
  • Single gene deletion → silent carrier (asymptomatic)
  • 2 gene deletion → a thalassemia trait (mild anemia)
  • 3 gene deletion → Hemoglobin H disease (moderate to severe anemia; HbH tetramer of B globulins forms → poor O2 delivery → HbH sequestering/destruction in spleen)
  • 4 gene deletion → Hydrops fetalis (most severe; excess y chains form tetramers → poor O2 delivery → fetus death)
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16
Q

B thalassemia

What types?

A
  • Thalassemia minor (heterozygote) → mild, nonspecific symptoms
  • Thalassemia major (hommozygote) → severe, decreased RBC production and unpaired a chains prone to hemolysis/precipitation
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17
Q

Sickle cell disease

A

Group of inherited disorders of Hb due to defect in B globin gene
- In low O2 states, abnormal Hb polymerizes making RBCs sickle
- Results in chornic hemolytic anemia and small vessel occlusion

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18
Q

Cause of sickle cell disease

A
  • Point mutation in B globin gene → aa substitution → abnormal B chain
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19
Q

Sickle cell anemia

A

Homozygous for defective gene
- HbS < 40% → asymptomatic
- HbS 40-80% → mild to moderate
- HbS 80% → severe

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20
Q

Sickle cell trait

A

Heterozygous for defective gene
- <40% Hb is Hbs, thus cells do not sickle and patients are asymptomatic

21
Q

Hereditary spherocytosis

A

Group of genetic defect characterized by defect of structural proteins in RBC (most are autosomal dominant)
- Defective RBCs unable to maintain biconcave shape (spheres) and are removed by the spleen

22
Q

Clinical findings of hereditary spherocytosis

A

Anemia, splenomegaly, jaundice

23
Q

Polycythemia

A

(Erythrocytosis) → An increase in the number of RBCs

24
Q

Relative polycythemia causes

A

Hemoconcentration (dehydration)

25
Q

Absolute polycythemia causes

A

Primary (low erythropoietin):
- Polycythemia rubra vera (uncontrolled production of RBCs due to myleoproliferative disorder)

Secondary (high erythropoietin):
- Living at high altitude; chronic lung disease

26
Q

Polycythemia symptoms

A

Increased viscosity (sluggish blood flow and tendency to clot)

27
Q

Leukocytosis

A

Increased number of WBCs
- Typically benign
- Often associated with splenomegaly or lymphadenopathy

28
Q

Types of leukocytosis and effects

A

Neutrophilic leukocytosis (increased neutrophils) → acute bacterial infections

Eosinophilic leukocytosis (increased eosinophils) → parasites, allergies, drug reaction

Lymphocytosis (increased lymphocytes) → viral infections, chronic infections (e.x. TB)

29
Q

Leukopenia

A

Reduction in WBC count

30
Q

Types of leukopenia

A

Neutropenia and lymphopenia

31
Q

Neutropenia (Leukopenia)

A

Decreased number of neutrophils → susceptible to bacterial infection

32
Q

Neutropenia (Leukopenia) Causes

A
  • Ineffective granulopoiesis (e.x. aplastic anemia)
  • Accelerated removal or destruction of neutrophils (e.x. Ab destruction by SLE)
33
Q

Lymphopenia (Leukopenia)

A

Decreased number of lymphocytes (selective lymphopenia = decreased subset of lymphocytes)

34
Q

Lymphopenia (Leukopenia) causes

A
  • Ineffective hematopoeisis
  • Accelerated removal or destruction of lymphocytes
35
Q

Acute Lymphoblastic Leukemia

A
  • Prevelance: 20% (most common type in children)
  • BM infiltrated with immature lymphoid cells spill over into blood
  • Lethal without chemotherapy
36
Q

Acute Myelogenous Leukemia

A
  • Prevelance: 40% (most common type in adults)
  • BM infiltrated by immature myeloid cells spill over into blood
  • Classified by WBC linneages affected
  • Lethal without treatment (chemotherapy, radiotherapy, BM transplant)
37
Q

Chronic Myelogenous Leukemia

A
  • Prevelance: 15% (incidence increases with age)
  • BM infiltrated by myeloid cells
  • Characterized by Philadelphia chromosome
  • Slow insidious onset, asymptomatic
  • 3 phases: chronic phase → accelerated phase → blast crisis
38
Q

Chronic Lymphocytic Leukemia

A
  • Prevalence: 25% (Elderly, slow progression)
  • BM infiltrated by lymphoid cells, spills into blood
  • Involves LNs/spleen → small lymphocutic lymphoma
  • CLL cells grow slowly
39
Q

Hodgkin Lymphoma

A
  • Biomodal age distribution (25; 55)
  • 5 types
  • Staging is key for prognosis
  • Chemotherapy effective
40
Q

Hodgkin lymphoma types

A

Classical HL (90%) (presence of Reed Sternberg cell → malignant B cell):
- Nodular slcerosis HL (70%)
- Mixed cellularity HL (20%)
- Lymphocyte-rich HL (5%)
- Lymphocyte-depleted HL (5%)

Nodular lymphocyte predominant of HL (10%)

41
Q

Multiple myeloma age group

A

Middle age (>45)

42
Q

Multiple myeloma

A

Malignant disease of plasma cells
- Plasmacytoma = single lesion (can be of bone or extramedullary (soft tissue))

43
Q

Multiple Myeloma pathogenesis

A

Malignant transformation of single plasma cell → clonal expansion → monoclonal expansion of plasma cells → secrete monoclonal Ig’s

44
Q

Multiple myeloma clinical features

A

CRAB:
- C = Calcium (Hypercalcemia → calcium released from destroyed bones)
- R = Renal failure (Ig’s excreted damage renal tubes; hypercalcemia damages kidneys)
- A = Anemia (replacement of normal BM by tumor)
- B = Bone lesions (lytic bone lesions caused by plasma cells)

45
Q

Bleeding Disorders

A

Vascular disorders or Platelet disorders

46
Q

Vascular disorders (Bleeding disorders)

A
  • Common cause: mechanical trauma
  • Vessel wall fragility (old age, connective tissue disorder)
  • Immune damage (vasculitis)
47
Q

Types of platelet disorders (Bleeding disorders)

A

Qualitative or quantitative

48
Q

Quantitative platelet disorder (bleeding disorders)

A
  • Decreased production (aplastic anemia)
  • Increased destruction (autimmune disorders)
  • Increased utilization (disseminated intravascular coagulation)
49
Q

Qualitative platelet disorder (bleeding disorders)

A

Acquired: NSAIDs and aspirin

Congenital:
- Defect platelet adhesion (Benard-Souilver syndrome)
- Defective platelet aggregation (Glanzmann thrombasthenia)

PATH 375 (4 decks)

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