Anemia - Ch. 14 Flashcards

1
Q

Pale, weak, easily fatigued, exercise intolerance

A

Anemia

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2
Q

After 3-5 days…reticulocytosis, leukocytosis, thrombocytosis, erythroid precursor cells (BM) w/ blue-red cytoplasm, increased EPO

A

Anemia of acute blood loss

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3
Q

Anemia, splenomegaly, unconjugated jaundice, decreased haptoglobin

A

Extravascular hemolytic anemia

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4
Q

Anemia, hemoglobinemia, hemoglobinuria, hemosiderinuria, unconjugated jaundice, red-brown urine, decreased haptoglobin

A

Intravascular hemolytic anemia

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5
Q

BM - normoblasts (erythroid precursors)
PB - reticulocytosis, hemosiderosis
Labs - increased EPO, increased degradation products

A

Hemolytic anemia

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6
Q

RUQ abdominal pain, hemolytic anemia

Indicate what?

What else tends to happen in this setting?

A

Pigment gallstones

CHRONIC hemolytic anemia

Splenomegaly

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7
Q

Caucasian, anemia, splenomegaly, jaundice, episode of worsened anemia symptoms during an infection

A

Hereditary spherocytosis - complicated by aplastic crisis (parvovirus infection)

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8
Q

Osmotic lysis in hypotonic salt solutions

A

Hereditary spherocytosis

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9
Q

Heinz bodies, bite cells, spherocytes

A

G6PD deficiency (the Heinz bodies cause the formation of bite cells and spherocytes)

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10
Q

Episodic anemia, jaundice, weakness, pallor. Black or Mediterranean male. No splenomegaly or gallstones.

A

G6PD deficiency

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11
Q

Caucasian teenager, anemia, splenomegaly, jaundice, episode of cervical lymphadenopathy and swollen tonsils w/ decreased haptoglobin

A

Hereditary spherocytosis - complicated by hemolytic crisis (infectious mononucleosis)

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12
Q

Sickle cell, rapid splenic enlargement, hypovolemia, shock

A

Sequestration crisis

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13
Q

Crewcut X-Ray, enlarged cheekbones

A
  • Sickle cell disease

- Beta-thalassemia major

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14
Q

Beta-4 tetramers

A

Hemoglobin H - alpha-thalassemia - adolescents and adults

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15
Q

Gamma-4 tetramers

A

Hemoglobin Barts - alpha-thalassemia - young kids

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16
Q

Genetic differences in alpha vs beta thalassemias

A

Alpha - gene deletions

Beta - point mutations

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17
Q

Asians vs blacks - alpha-thalassemia genotypes

A

Asian - a/a -/-

Black - a/- a/-

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18
Q

HbH disease - explain

A

3 alpha-globin mutations = HbH formation = extreme tissue hypoxia, intracellular inclusions = red cell sequestration = moderate anemia

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19
Q

Hydrops fetalis - explain

Symptoms

A

4 beta-globin mutations = Hg barts formation + embryonic Hb tetramer formation

Pallor, genralized edema, massive HSM

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20
Q

Which thalassemias require regular blood transfusions?

A

Beta-major, hydrops fetalis

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21
Q

Intravascular hemolysis (anemia, jaundice, hemoglobinemia, hemoglobinuria, hemosiderin), autoimmune disease, venous thrombosis

Future consideration?

A

Paroxysmal nocturnal hemoglobinuria

Transform in AML or MDS (since its an HSC)

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22
Q

Immunohemolytic anemia - what is it?

Hemolysis type?

A

Premature destruction of RBCs due to antibodies or complement that attach

Extravascular (usually)

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23
Q

Causes of Warm Antibody Type immunohemolytic anemia

Antibody type? Against what?

A
  • Idiopathic
  • SLE
  • Drugs - penicillin, cephalosporins, alpha-methyldopa
  • Lymphoid neoplasms

IgG - anti-Rh

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24
Q

Warm Antibody immunohemolytic anemia - what happens?

A

IgG antibodies bind RBCs, causing (usually) extravascular hemolysis (loss of membrane –> spherocytes –> sequestration –> splenomegaly

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25
Q

Causes of Cold Agglutinin Type immunohemolytic anemia

Antibody type?

A
  • Acute = Mycoplasma, EBV (mono)
  • Chronic = idiopathic, lymphoid neoplasms

IgM (M = Mycoplasma)

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26
Q

Cold Agglutinin immunohemolytic anemia - what happens?

A

Child has self-limited infection OR chronic lymphoid neoplasm OR no identified cause –> RBCs circulate to COLD areas, IgM binds –> circulate to WARM areas, IgM releases –> C3b deposits cause extravascular hemolysis

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27
Q

Besides hemolytic anemia, what else is seen in Cold Agglutinin immunohemolytic anemia?

A

Vascular obstruction in cold extremities –> pallor, cyanosis, Raynaud phenomenon

28
Q

Cold Hemolysis immunohemolytic anemia - cause?

Antibody type? Against what?

A

Child after viral infection

IgG - binds to P blood group

29
Q

Cold Hemolysis immunohemolytic anemia - what happens?

A

Viral infection causes IgG autoantibodies –> RBCs circulate to COLD areas, IgG binds –> circulate to WARM areas, IgG causes complement-mediated lysis

30
Q

Causes of trauma to RBCs that lead to hemolytic anemia

A
  • Prosthetic cardiac valves

- Microangiopathies (DIC, TTP, HUS, malignant HTN, SLE, cancer)

31
Q

Schistocytes, burr cells, helmet cells, triangle cells

A

Trauma-induced hemolytic anemia

32
Q

Abnormally large erythroid precursors (promegaloblasts), giant metamyelocytes, and band forms in the BM

A

Megaloblastic anemia

33
Q

Abnormally large RBCs and hypersegmented neutrophils in peripheral blood

A

Megaloblastic anemia

34
Q

Vegans and vegetarians (B12 or folate)

A

B12 deficiency

35
Q

Fish tapeworm (B12 or folate)

A

B12 deficiency

36
Q

Chronic alcoholic (B12 or folate)

A

Folate deficiency

37
Q

Pregnancy, infancy, hemolytic anemia (B12 or folate)

A

Folate deficiency

38
Q

Hemodialysis (B12 or folate)

A

Folate deficiency

39
Q

Oral contraceptives (B12 or folate)

A

Folate deficiency

40
Q

Why the neuro symptoms in B12 deficiency?

A

Increased methylmalonate –> abnormal fatty acid accumulation in neuron lipids –> myelin breakdown

41
Q

Initiating event to autoimmune gastritis and pernicious anemia

A

Autoreactive T-cell response against gastric mucosa, causing autoantibody formation against intrinsic factor

42
Q

Pernicious anemia is associated w/ what else?

A

Thyroiditis, adrenalitis

43
Q

Non-pernicious causes of B12 deficiency

A
  • Achlorhydia (ex. patient taking HCl supplement)
  • Gastrectomy
  • Exocrine pancreas loss (can’t split B12-haptocorrin)
  • Ileal resection or disease
  • Fish tapeworm
  • Pregnancy, hyperthyroid, cancer, chronic infection (all increased requirement)
44
Q

Intestinalization, beefy glazed tongue, decreased HCl production, spastic paraparesis, paresthesias

A

Pernicious anemia

45
Q

Pernicious anemia…what to be cautious of?

A

Gastric carcinoma and atherosclerosis risks

46
Q

Elevated homocysteine, normal methylmalonate

A

Folate deficiency

47
Q

TMPRSS6 mutation

A

Elevated hepcidin –> microcytic iron-deficient anemia

48
Q

A patient is iron deficient, but has no dietary issues, no GI issues, no bleeding issues, and seems perfectly healthy. She does not respond to iron supplementation. Potential explanation?

A

TMPRSS6 mutation

49
Q

Abnormally low hepcidin…explanation?

A

Hemochromatosis (primary or secondary)

50
Q

Secondary hemochromatosis…major cause?

A

Ineffective hematopoiesis –> decreased hepcidin

51
Q

Decreased transferrin saturation, decreased serum ferritin

A

Iron deficiency

52
Q

Spooning of nails, hair loss, malabsorption, atrophic tongue

A

Iron deficiency

53
Q

Patient craving ice chips, soil, clay, or paper

A

Pica - iron deficiency

54
Q

Smooth glazed tongue, trouble swallowing foods, microcytic anemia

A

Plummer-Vinson syndrome

55
Q

Increased PIBC

A

Iron deficiency

56
Q

Low serum iron, reduced TIBC, increased hemosiderin

A

Anemia of chronic disease

57
Q

Describe anemia of chronic disease

A

Patient has source of chronic systemic inflammation, causing increased IL-6, which causes increased hepcidin, which causes iron-starved erythroblasts despite having plenty in marrow macrophages. Hepcidin also inhibits EPO production.

58
Q

Causes of ACD

A
  • Osteomyelitis, bacterial endocarditis, lung abscess
  • RA, regional enteritis
  • Carcinomas, Hodgkins lymphoma
59
Q

Baby with pancytopenia, kidney hypoplasia, spleen and bone anomalies…what is it? Cause?

A

Fanconi anemia - defective DNA repair

60
Q

Causes of aplastic anemia

A

Chemo, benzene, chloramphenicol, gold salts, viral infections, non-hepatitis hepatitis, irradiation, other

61
Q

How does chemo, radiation, etc. cause aplastic anemia?

A

Antigenic alteration of HSCs by the agent –> T-HELPER CELL suppression/destruction of HSCs via IFN-GAMMA and TNF

62
Q

Anemia, decreased Hb and Hct, normal WBCs and platelets, lack of erythroid progenitors in the BM

Associated with what?

A

Pure red cell aplasia

Thymoma, LGL leukemia, drugs, autoimmune disorders, parvovirus (aplastic crises)

63
Q

Myelophthisic anemia

Most common causes? (3)

A

BM failure due to space-occupying lesions that replace normal marrow components

Metastatic carcinomas, granulomatous disease, MPD spent phase

64
Q

Leukoerythroblastosis, dacrylocytic cells

A

Marrow replacement of some kind

65
Q

Effect of uremia on RBCs

A

Diminished EPO synthesis –> anemia

66
Q

Hypothyroidism + anemia…what kind?

A

Normochromic, normocytic

67
Q

Hepatocellular liver disease + anemia…why?

A

Lipid abnormalities –> RBC membranes acquire phospholipid and cholesterol –> destruction