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hematology week 1 Flashcards

1
Q
  1. What are symptoms common to all anemias?
A

Pallor, fatigue, dyspnea, tachypnea – primary anemia sxs

Next step is to find out why

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2
Q
  1. Why might anemia accompany each of the following conditions:
    a. GI disease
    b. Kidney disease
    c. Heart valve disease
    d. Inflammatory disorders
A

a. GI disease – not absorbing req nutrients to make RBCs; GI cancer
b. Kidney disease – low EPO
c. Heart valve disease – can cause hemolysis
d. Inflammatory disorders – RA, lupus, etc….autoimmune Ab; anemia of chronic dz: body stops producing RBCs

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3
Q
  1. What dietary deficiencies might contribute to the development of anemia?
A

Fe (dietary deficiency is rare); B12, folate

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4
Q
  1. Why is it important to ask about the following lifestyle factors in a work-up for anemia?
    a. Alcohol use
    b. IV drug use
    c. Marathon running
    d. Toxic exposures
    i. Lead
    ii. Benzene
A

a. Alcohol use – bone marrow doesn’t like alcohol
b. IV drug use – heart valve issues; toxicity to blood cells
c. Marathon running – lots of running causes hemolysis
d. Toxic exposures – hard on blood cells
i. Lead
ii. Benzene

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5
Q
  1. What are the diagnostic criteria for anemia?
A

Labs – low Hb, Hct, and/or RBC number; peripheral smear

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6
Q
  1. What is the most common form of anemia?
A

Fe-def

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7
Q
  1. What is the most likely cause of iron deficiency in premenopausal women?
A

Excessive menstruation (too frequent, long, heavy)

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8
Q
  1. What is the most likely cause of iron deficiency in postmenopausal women and adult males?
A

Occult bleeding (in the GI)

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9
Q
  1. What signs and symptoms are more likely to be found with iron deficiency anemia than with other anemias?
A

Glossitis, cheilosis, koilonychias. Also pica – the desire to eat earth; restless legs, hair loss

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10
Q
  1. How will each of the following lab results be affected by Fe deficiency:
    a. MCV
    b. MCHC
    c. Ferritin
    d. TIBC
A

a. MCV – microcytic
b. MCHC – hypochromic
c. Ferritin – low
d. TIBC – high
CBC might look normal early but iron things will look off.

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11
Q
  1. What are some causes of acquired sideroblastic anemia?
A

Iron is sufficient but cannot make good heme: Alcoholism, lead poisoning, Cu deficiency, hypothermia.

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12
Q
  1. How will the labs for sideroblastic anemia be different than for Fe deficiency?
A

Stippled/target RBCs; high ferritin, low TIBC

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13
Q
  1. When might you suspect anemia of chronic disease?
A

They have a chronic inflammatory condition and possibly signs of anemia as well

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14
Q
  1. What lab result might suggest anemia due to kidney disease?
A

Low serum EPO

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15
Q
  1. What dietary deficiencies most commonly cause megaloblastic anemia?
A

B12 and/or folate
o B12 deficiency can be caused by vegan diet, gastric abnormalities (pernicious anemia, gastrectomy, gastritis), celiac disease and other malabsorption syndromes, pancreatitis, drugs (e.g. proton pump inhibitors).
o Folate deficiency is caused by poor dietary intake, malabsorption, drugs, alcohol

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16
Q
  1. What might be seen on physical exam with B12 deficiency?
A

Symmetric numbness of hands and feet (glove and stocking peripheral neuropathy), glossitis, diarrhea, muscle wasting.

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17
Q
  1. What will the following show with megaloblastic anemia?
    a. CBC
    b. Peripheral smear
    c. Bone marrow biopsy
A

a. CBC – high MCV
b. Peripheral smear – Howell-jolly bodies
c. Bone marrow biopsy – high levels of produced cells

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18
Q
  1. What else (besides B12/folate deficiency) can cause macrocytosis?
A

liver disease, alcoholism (independent of folate), aplastic anemia, and myelodysplasia

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19
Q
  1. What is aplastic anemia?
A

Some exposure poisoning the bone marrow (usually reversible) so blood cell precursors are gone.

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20
Q
  1. What are signs/symptoms of aplastic anemia?
A

Infections (low WBCs), bleeding (low platelets)

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21
Q
  1. What will the following show with aplastic anemia?
    a. CBC
    b. Bone marrow biopsy
A

a. CBC – low count of CBC, RBC, and platelets

b. Bone marrow biopsy – acellular

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22
Q
  1. Distinguish between the terms myelophthisic, myeloproliferative, myelodysplastic, and aplastic.
A

Myelophthisic anemia:
• Marrow is replaced by a tumor, granuloma, lipid storage disease, or fibrosis
• Extramedullary hematopoiesis or disruption of marrow causes release of immature cells.
Aplastic/Hypoplastic anemia:
• Anemia that results from loss of blood cell precursors in the bone marrow.
Myeloproliferative:
• Excessive cell production by the bone marrow
Myelodysplastic:
• Damaged stem cells in the bone marrow

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23
Q
  1. How might a hemolytic anemia present differently than an iron deficiency anemia in terms of:
    a. Signs and symptoms
    b. PE
    c. Labs
A

a. Signs and symptoms – jaundice, dark urine (bilirubin), gallstones made of bilirubin (pigmented)
b. PE – splenomegaly, jaundice, signs of anemia
c. Labs – increased reticulocytes (big demand for RBC), high serum bilirubin, high serum LDH (RBC energy source), low free haptoglobin (will be bound to the serum hemoglobin)

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24
Q
  1. What lab test is most useful to distinguish autoimmune hemolytic anemia from other types of anemia?
A

Coomb’s test – tells if you make Ab to RBCs

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25
Q
  1. What kinds of anemia are due to problems with the RBC membrane?
A

Hereditary spherocytosis and elliptocytosis; stomatocytosis.

RBCs end up not making it through the vessels efficiently due to shape.

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26
Q
  1. Why does G6PD deficiency cause hemolysis?
A

RBCs are unable to make enough energies to repair themselves from oxidative damage.

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27
Q
  1. What lab will distinguish G6PD deficiency from other hemolytic anemias?
A

G6PD assay.

Can also see Heinz bodies and ‘bite cells’ (where spleen takes out the Heinz body but leaves the rest of the cell

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28
Q
  1. What types of anemia are more common in Africans and African Americans?
A

Sickle cell, G6PD deficiency, thalassemia

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29
Q
  1. What are signs and symptoms of sickle cell anemia?
A

a. Severe anemia
b. Episodes of acute pain (which can occur anywhere in the body and last for several days), often accompanied by swelling and tenderness, along with systemic symptoms such as fever, tachypnea,  BP, nausea/vomiting.
c. Tissue damage: avascular necrosis of the femoral head, renal damage, punched out leg ulcers
d. Splenomegaly, splenic infarcts; reduced or absent splenic function leads to susceptibility to infection
e. Neurological disturbances, TIA, stroke
f. Developmental delays
g. Aplastic crisis (transient arrest in erythropoiesis) can occur with parvovirus B19 and other infections

30
Q
  1. What labs will distinguish sickle cell anemia from other types of anemia?
A

Hb electrophoresis

31
Q
  1. What are signs and symptoms of beta thalassemia major?
A

Trouble making hemoglobin (beta chain), but what is made is good.

  • S/Sx common to all hemolytic anemias
  • Bone marrow expansion occurs due to the need for increased erythropoiesis. This leads to skeletal deformities.
  • Hepatomegaly and splenomegaly occur, due to increased hemolysis and extramedullary erythropoiesis.
  • Iron overload from repeated transfusions causes liver damage and increases risk of diabetes and heart disease.
  • Bilirubin gallstones common
  • Growth retardation
  • Aplastic crisis with Parvovirus B19 (can stop RBC production)

Alpha thalassemia major is death after birth

32
Q
  1. What labs will distinguish thalassemias from other types of anemia?
A

Hb electrophoresis: absent or deficient alpha or beta globin chains, depending on type of thalassemia. Increased Hb F

33
Q
  1. What is neutropenia?
A

Decrease in neutrophil count (PMNs, granulocytes).

34
Q
  1. Why are chemotherapy patients at increased risk of infection?
A

Interferes with WBC production

35
Q
  1. What are some causes of lymphocytopenia?
A

a. Infectious disease- HIV, TB, SARS, hepatitis, sepsis
b. Dietary deficiency: protein, Zn, general malnutrition (may see with alcoholism)
c. Hematologic disease: aplastic anemia, leukemia, etc.
d. Autoimmune disease: SLE
e. Iatrogenic- immunosuppression, chemo, radiation
f. congenital

36
Q
  1. What types of infections are more likely to be seen with a patient with lymphocytopenia?
A

Recurrent viral, fungal, parasitic infections

37
Q
  1. What signs and symptoms suggest that a patient may have a bleeding disorder?
A

a. Unexplained epistaxis or gingival bleeding
b. Menorrhagia (excessive or prolonged menses) or metorrhagia (bleeding between periods)
c. Prolonged bleeding after minor cuts
d. Easy bruising (ecchymoses) without noticeable trauma
e. Petechiae: small capillary hemorrhages
f. Hematomas (bleeding into soft tissue)
g. Abnormal laboratory values that suggest a bleeding disorder or occult bleed (GI, GU)

38
Q
  1. How do bleeding disorders caused by platelet problems present differently than those due to clotting factor deficiencies?
A

Platelets: mucosal bleeding (mucous membranes, skin wounds) – superficial and immediate. Petechiae common.
Clotting factors: deep tissue bleeding (hemarthrosis and muscles hematoma) – deep and delayed

39
Q
  1. Why is vitamin K important in normal clotting? When might vitamin K be deficient?
A

It’s required for the synthesis of virtually all of the clotting factors.

40
Q
  1. Why are patients with liver disease at increased risk of bleeding?
A

All the factors are produced in the liver

41
Q
  1. What medications might be associated with bleeding disorders?
A

Warfarin – antagonist of vit K

42
Q
  1. What conditions will increase PT? PTT?
A

 PT/INR (extrinsic pathway) will be high with:
• Use of vitamin K antagonists (warfarin), and vitamin K deficiency
• Disseminated intravascular coagulation (DIC)
• Liver disease
• Deficiency of factors I (fibrinogen), II (prothrombin), V, VII, X.
• Antiphospholipid antibodies

 PTT (intrinsic) will be prolonged with:
• Use of heparin
• Liver disease (more severe disease is necessary to elevate PTT than PT)
• DIC
• Von Willebrand Disease (VWD) due to its function as carrier/stabilizer of factor VIII.
• Hemophilia A (factor VIII deficiency) or B (factor IX deficiency)
• Other factor deficiencies (XI, XII, X, V, II)
• Factor inhibitors (autoantibodies, usually to factor VIII)
• Antiphospholipid antibodies

43
Q
  1. What are some causes of thrombocytopenia that are due to reduced platelet production?
A

aplastic anemia, leukemia, myelodysplasias, B12/folate deficiency

44
Q
  1. What are some causes of thrombocytopenia that are due to increased platelet destruction or consumption?
A

ITP, TTP, HUS, DIC, SLE, infections, drugs

45
Q
  1. Why does splenomegaly cause thrombocytopenia?
A

Sequestration of platelets

46
Q
  1. What are signs and symptoms of thrombocytopenia?
A 
Mucosal bleeding
Petechiae
Menorrhagia
Small, numerous ecchymosis
Possible splenomegaly

Prolonged bleeding time
Normal PT/PTT

47
Q
  1. What is the underlying mechanism of ITP?
A

Autoimmune AB against platelets

48
Q
  1. How do you diagnose ITP?
A

Dx of exclusion. If everything looks normal except low platelets, think ITP. If there are other abnormalities, look for other causes.

49
Q
  1. How are TTP and HUS similar? How are they different?
A

TTP and HUS both result from the formation of platelet-rich micro thrombi in small vessels. The micro thrombi deplete and destroy platelets, damage RBCs, and cause tissue ischemia. They present exactly the same. Different etiologies and pathophysiologies.

TTP: protease malfunction allowing buildup of vWF polymers
HUS: toxin from E. coli infx

50
Q
  1. What are the 5 classic signs of TTP and HUS?
A

-Microangiopathic hemolytic anemia
-Thrombocytopenia
Possible: acute renal failure, neurological abnormalities, fever

51
Q
  1. How will the labs for ITP differ from TTP/HUS?
A

CBC: Low platelets AND anemia
Damaged RBCs and increased reticulocytes in the periphery
Increased LDH and bilirubin (looks like hemolytic anemia)
Increased bleeding time but normal PT/PTT

52
Q
  1. Why does aspirin cause increased bleeding?
A

Aspirin causes platelet dysfunction….numbers are still fine.

Causes irreversible binding unlike other drugs.

53
Q
  1. What is the underlying mechanism of von Willebrand’s disease?
A

w/o vWF (due to either decreased formation or formation of dysfunctional units) the platelets can’t attach to the endothelium to form an effective platelet plug.

54
Q
  1. What will a CBC with peripheral smear look like in a patient with VWD? What will coagulation studies show?
    CBC/PBS look normal.
A

Normal PT, possibly a slight increase to PTT (vWF stabilizes factor VIII)

55
Q
  1. Why does DIC cause both increased thrombosis and increased bleeding?
A

widespread activation of the clotting system and consumption of platelets and clotting factors

56
Q
  1. What are some causes of DIC?
A

Gm neg infx (meningococcal)
Malignancy
Obstetrical complication

57
Q
  1. How does DIC that develops slowly differ from acute DIC in terms of signs and symptoms? In terms of labs?
A

S/sx
Slow: Thrombosis more than bleeding (DVT, pulm. Embolism)
Acute: bleeding in all the small vessels can causes sepsis. Ischemic necrosis

Labs
Slow: mild thrombocytopenia, normal PT/PTT, normal fibrinogen, slightly elevated D-dimer
Acute: severe thrombocytopenia, prolonged PT/PTT, low fibrinogen, high D-dimer

Send acute cases to ER

58
Q
  1. How is DIC similar to TTP? How is it different?
A

?

59
Q
  1. Why are hemophilias only seen in males?
A

Sex-linked inheritance

60
Q
  1. What might be seen on physical exam with hemophilia?
A

Joint swelling, hematomas …… deep bleeding

61
Q
  1. What will the following labs look like in a hemophilia patient: CBC, PT, PTT. What coagulation factors might be low?
A

• CBC: normal
• Coagulation studies: bleeding time normal, PT normal, PTT prolonged
Factors VIII and IX

62
Q
  1. Which blood vessel conditions might lead to bleeding?
A

x

63
Q
  1. Which bleeding disorders are genetic?
A

x

64
Q
  1. Which bleeding disorders are caused by problems with platelets? Problems with clotting factors? Both?
A

x

65
Q
  1. What genetic conditions can place patients at higher risk of blood clots?
A

Factor V Leiden mutation, protein C and S deficiencies, antithrombin deficiency, prothrombin 20210 mutation, antithrombin deficiency

66
Q
  1. What acquired health conditions can place patients at higher risk of blood clots?
A

Atrial fibrillation, cancer, surgery/immobilization

67
Q
  1. What lifestyle factors place patients at a greater risk of blood clots?
A

Obesity (inflammatory state), smoking, pregnancy

68
Q
  1. Why should female patients with a clotting disorder be counseled about the use of birth control pills and hormone replacement therapy?
A

Estrogen increases blood clot risk

69
Q
  1. Why does Factor V Leiden mutation increase risk of blood clots?
A

The mutation of factor V makes it less susceptible to degradation by proteins C and S.

70
Q
  1. Why does protein C deficiency cause increased risk of blood clots?
A

Protein C helps breakdown factors V and VIII

Made in the liver and vit K dependent. Things that cause bleeding can also cause clotting.

71
Q
  1. Why does the anticoagulant medication warfarin cause blood clots in some patients, resulting in tissue necrosis?
A

Normally used to decrease clot formation. In the beginning it acts more quickly on protein C which can cause more clotting, not less.

72
Q
  1. If a female patient has a history of blood clots and miscarriages, what condition might you suspect?
A

Antiphospholipid antibody syndrome (lupus anticoagulant)

CPD (10 decks)

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