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A - Step II Secrets > Hematology > Flashcards

Hematology Flashcards

1
Q

Define anemia

A

Hemoglobin

< 12 mg/dL in women

< 14 mg/dL in men

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2
Q

What are the symptoms and signs of anemia?

A

Symptoms: Fatigue, dyspnea on exertion, light-headedness, dizziness, syncope, palpitations, angina, and claudication.

Signs: Tachycardia, pallor (especially of the sclera and mucous membranes), systolic ejection murmurs (from high flow), and signs of the underlying cause (e.g., jaundice, pigment gallstones in hemolytic anemia, positive stool guaiac with a GI bleed).

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3
Q

What are the 5 important elements of the history when anemia is present?

A

Important points include:

  • medications
  • blood loss (e.g., trauma, surgery, melena, hematemesis, men- orrhagia)
  • chronic diseases (anemia of chronic disease)
  • family history (e.g., hemophilia, thalassemia, sickle cell disease, glucose-6-phosphatase deficiency)
  • alcoholism (iron, folate, B12 deficiencies, GI bleeds)
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4
Q

What medications can cause anemia? How?

A

Methyldopa, penicillins, sulfa drugs - cause RBC antibodies with subsequent hemolysis

chloroquine, sulfa drugs - cause hemolysis in patients with G6PD

phenytoin - causes megaloblastic anemia through interference with folate metabolism

chloramphenicol, cancer drugs, zidovudine - cause aplastic anemia and bone marrow suppression.

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5
Q

What test should be ordered first to help determine the cause of anemia?

A

CBC

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6
Q

After CBC indicates anemia, what is theoretically the next test that should be ordered?

A

peripheral blood smear, as there are many classic findings that can help make the diagnosis

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7
Q

What is this peripheral blood cell classic for?

A

Sickled cells (sickle cell disease)

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8
Q

What is this peripheral blood cell classic for?

A

Hypersegmented neutrophils (folate/B12 deficiency)

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9
Q

What is this peripheral blood cell classic for?

A

Hypochromic and microcytic RBCs (iron deficiency)

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10
Q

What is this peripheral blood cell classic for?

A

Basophilic stippling (lead poisoning)

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11
Q

What is this peripheral blood cell classic for?

A

Heinz bodies (glucose-6-phosphatase deficiency)

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12
Q

What is this peripheral blood cell classic for?

A

“Bite cells” (classically, glucose-6-phosphatase deficiency; other hemolytic anemias

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13
Q

What is this peripheral blood cell classic for?

A

Howell-Jolly bodies (asplenia)

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14
Q

What is this peripheral blood cell classic for?

A

Teardrop-shaped RBCs (myelofibrosis)

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15
Q

What is this peripheral blood cell classic for?

A

Schistocytes, helmet cells, and fragmented RBCs (intravascular hemolysis)

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16
Q

What is this peripheral blood cell classic for?

A

Spherocytes and elliptocytes (hereditary spherocytosis and elliptocytosis)

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17
Q

What is this peripheral blood cell classic for?

A

Acanthocytes and spur cells (abetalipoproteinemia)

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18
Q

What is this peripheral blood cell classic for?

A

Target cells (thalassemia, liver disease)

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19
Q

What is this peripheral blood cell classic for?

A

Echinocytes, including “burr” cells and acanthocytes (uremia)

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20
Q

What is this peripheral blood cell classic for?

A

Polychromasia (from reticulocytosis; should alert you to the possibility of hemolysis)

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21
Q

What is this peripheral blood cell classic for?

A

Rouleaux formation (multiple myeloma)

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22
Q

What is this peripheral blood cell classic for?

A

Parasites inside red blood cells (RBCs) (malaria)

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23
Q

What is this peripheral blood cell classic for?

A

Ringed sideroblasts seen in sideroblastic anemia.

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24
Q

What are reticulocytes?

What should high/low values in the setting of anemia indicate?

A

immature RBCs.

If abnormally decreased = marrow is not responding properly and is the problem

If high = the marrow is responding properly to something causing the anemia (hemolysis, blood loss)

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25
Q

What are the classic causes of microcytic, normocytic, and macrocytic anemia?

Which of these tends to have an inappropriately low reticulocyte count?

A
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26
Q

What clues point to hemolysis as the cause for anemia?

A
  • Elevated lactate dehydrogenase (LDH)
  • Elevated bilirubin (unconjugated + conjugated if the liver is functioning)
  • Jaundice
  • Low or absent haptoglobin (intravascular hemolysis only)
  • Urobilinogen, bilirubin, and hemoglobin in urine (only conjugated bilirubin shows up in the urine, and hemoglobin shows up in the urine only when haptoglobin has been saturated, as in brisk intravascular hemolysis)
  • Pigmented gallstones or history of cholecystectomy (usually at a young age)
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27
Q

What is the most common cause of anemia in the United States?

A

Iron deficiency anemia

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28
Q

Why do people get iron deficiency?

A

infants: if given cow’s milk before 1 year of age (due to GI bleed)

women of reproductive age: menstrual blood loss, pregnancy, lactation

patients > 40: colon cancer (causing chronic, asymptomatic blood loss)

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29
Q

What are the classic laboratory abnormalities in iron deficiency anemia?

What weird cravings may occur with iron deficiency?

A

low iron and low ferritin levels, elevated total iron-binding capacity (TIBC; also known as transferrin), and low TIBC saturation.

Rare patients may develop a craving for ice or dirt (pica)

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30
Q

What is Plummer-Vinson syndrome?

A

A triad: esophageal web resulting in dysphagia; iron deficiency anemia; and glossitis

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31
Q

How is iron deficiency treated?

A

First you must determine the cause.

  • In a menstruating woman, a presumptive diagnosis of menstrual blood loss is often made.
  • In patients older than 40 years, be sure to test the stool for occult blood and strongly consider colonoscopy to detect occult colon cancer.
  • Postmenopausal vaginal bleeding may also cause anemia and warrants screening for gynecologic cancer.

Treat with iron supplements for 3 to 6 months in uncomplicated cases to replete body iron stores.

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32
Q

What causes folate deficiency?

What do peripheral blood smears look like?

How should you treat this?

A
  • alcoholics (poor intake)
  • pregnant women (increased need)
  • poor diet (e.g., tea and toast)
  • methotrexate
  • prolonged therapy with trimethoprim-sulfamethoxazole
  • anticonvulsant therapy (especially phenytoin)
  • malabsorption

Peripheral blood smears

  • macrocytes
  • hypersegmented neutrophils with no neurologic symptoms or signs
  • low folate levels in serum or RBCs

Treat with oral folate.

33
Q

What is the most common cause of vitamin B12 deficiency?

What else may cause vitamin B12 deficiency?

A

Pernicious anemia - caused by antiparietal cell antibodies (most common)

  • Remember B12 absorption depends on intrinsic factor, which is secreted by parietal cells
  • B12 deficiency results in megaloblastic anemia
  • Achlorhydria is also present in pernicious anemia - remember that parietal cells secrete HCl as well

Others: Gastrectomy, terminal ileum resection or disease (e.g., Crohn disease), strict vegan diet, chronic pancreatitis, and Diphyllobothrium latum (fish tapeworm)

34
Q

How does B12 deficiency present?

How is it diagnosed?

A

patients have neurologic ∆s (loss of sensation and position sense, paresthesias, ataxia, spasticity, hyperreflexia, positive Babinski sign, dementia) due to degeneration of DCML

peripheral blood smear: macrocytes, hypersegmented neutrophils

Diagnosis: low serum B12 levels, (+) anti-intrinsic factor if pernicious anemia is the cause

35
Q

How is vitamin B12 deficiency treated?

A

Vitamin B12 supplements, usually given IM

PO doses may have erratic absorption, so it may be best utilized after levels have been normalized via the parenteral route. Supplementation may be required for life.

36
Q

How is thalassemia differentiated from iron deficiency? How are they the same?

A

iron levels are

  • low in iron deficiency anemia
  • normal in thalassemia

Both cause microcytic, hypochromic anemia

37
Q

How is alpha thalassemia different than beta thalassemia?

What diagnostic test confirms a diagnois of thalassemia?

How is it treated?

A

Patients with alpha thalassemia are symptomatic at birth or die in utero (fetal hydrops),

  • 4 gene loci for alpha chain

Patients with beta thalassemia are not symptomatic until 6 months of age.

  • 2 gene loci for beta chain
    dx: hemoglobin electrophoresis

trmt:

  • minor thalassemia: no treatment because these patients are often asymptomatic as they are used to living with a lower level of Hg
  • major thalassemia: transfusions, iron chelation therapy to prevent secondary hemochromatosis
38
Q

What two clues on the Step 2 examination often point to a diagnosis of sickle cell disease?

A

peripheral smear and African American race; usually have a high percentage of reticulocytes (8%-20%).

39
Q

What are the clinical manifestations and complications of sickle cell disease?

A
  • Aplastic crises (caused by parvovirus B19 infection)
  • Bone pain (due toinfarcts; the classic example is avascular necrosis of the femoral head)
  • Dactylitis (also known as hand-foot syndrome, seen in children)
  • Renal papillary necrosis
  • Splenic sequestration crisis
  • Autosplenectomy (increased infections with encapsulated bugs such as Pneumococcus, Haemophilus, and Neisseria species)
  • Acute chest syndrome (mimics pneumonia)
  • Pigment cholelithiasis
  • Priapism
  • Stroke
40
Q

How is sickle cell disease diagnosed and treated?

How is sickle cell crisis treated?

A

hemoglobin electrophoresis

Sickle cell trmt:

  • prophylactic penicillin until at least 5 years of age and perhaps longer, beginning as soon as the diagnosis is made.
  • Proper vaccinations: pneumococcal, meningococcal, and H. influenzae, yearly influenza vaccination.
  • folate supplementation
  • early treatment of infections
  • proper hydration

Sickle cell crisis

  • O2
  • IVF
  • analgesics
  • transfusions if symptoms/findings are severe
41
Q

What findings help you manage anemia in the setting of acute blood loss?

A

Remember that immediately after blood loss the hemoglobin may be normal; it takes at least 3 to 4 hours, often more, for reequilibration to occur.

Instead, look for signs of hypovolemic shock: obvious bleeding; pale, cold skin; tachycardia; and hypotension.

Consider internal hemorrhage in the setting of trauma and abdomi- nal aortic aneurysm in patients with a pulsatile abdominal mass.

Treatment: transfuse if indicated, even with a normal hemoglobin in the acute setting.

42
Q

What are the commonly tested causes of autoimmune hemolytic anemia?

A
  • Lupus erythematosus or medications that cause lupus-like syndromes (procainamide, hydralazine, and isoniazid)
  • Drugs (the classic example is methyldopa, but penicillins, cephalosporins, sulfa drugs, and quinidine also have been implicated)
  • Leukemia or lymphoma
  • Infection (the classic examples are mycoplasmosis, Epstein-Barr virus, and syphilis)
43
Q

What laboratory test is often positive in patients with autoimmune anemia?

A

Coombs test is positive in most autoimmune anemias.

You also may see spherocytes on peripheral smear because of incomplete macrophage destruction (extravascular hemolysis) of RBCs.

44
Q

What clues point to lead poisoning as a cause of anemia?

What are some symptoms that acute lead poisoning can cause? chronic?

A

clues:

  • basophilic stippling on peripheral smear
  • elevated free erythrocyte protoporphyrin or lead level
  • causes a hypochromic, microcytic anemia
  • almost always in a child that lives in an old, run down building

Acute symptoms: vomiting, ataxia, colicky abdominal pain, irritability (aggressive behavior, behavioral regression), and encephalopathy, cerebral edema, or seizures

45
Q

True or false: Children with risk factors should be screened for lead poisoning.

A

True.

Screening all asymptomatic children with a serum lead level at 1 - 2 years old, regardless of risk, is becoming controversial. However, screening should start at 6 months in children with risk factors, because chronic low-level exposure may lead to permanent neurologic sequelae.

risk factors: pica (especially paint chips and dust in old buildings that may have lead paint), residence in an old or neglected building, and/or residence near or family members who work at a lead-smelting or battery-recycling plant.

46
Q

How is lead poisoning treated?

A

decrease exposure to source (best strategy)

lead chelation therapy, if needed

  • succimer in children
  • dimercaprol in adults
  • in severe cases, use dimercaprol + EDTA for children or adults.
47
Q

How can sideroblastic anemia be recognized?

Should the presence of sideroblastic anemia raise concern about other conditions?

How should these patients be treated?

A

classic description: microcytic, hypochromic anemia with increased or normal iron, ferritin, and total iron-binding capacity (transferrin).

Look for polychromatophilic stippling and the classic “ringed sideroblast” in the bone marrow

Sideroblastic anemia may be related to myelodysplasia or blood dyscrasias.

Treatment: supportive; in rare cases, the anemia responds to pyridoxine/B6. Do not give iron.

48
Q

How do you recognize anemia of chronic disease?

What are the blood smear and lab findings?

Treatment?

A

First, look for the presence of a disease that causes chronic inflammation (e.g., rheumatoid arthritis, lupus erythematosus, cancer, tuberculosis).

Findings: normocytic (early) or microcytic (late) anemia

Labs: Low serum iron and total iron-binding capacity; therefore % saturation may be near normal. Elevated serum ferritin (ferritin is an acute-phase reactant)

Treatment: Treat underlying disorder. Do not give iron.

49
Q

Describe the hallmarks of spherocytosis.

Treatment?

A
  • Normochromic, normocytic anemia
  • spherocytes on peripheral smear
  • (+) family history (autosomal dominant)
  • splenomegaly
  • (+) osmotic fragility test
  • increased mean corpuscular hemoglobin concentration (the only occasion when this RBC index is useful for the Step 2 examination).

Treatment: splenectomy

50
Q

Why does anemia develop in patients with chronic renal disease?

How do you treat it?

A

Normocytic, normochromic anemia with decreased reticulocyte count develops in all patients with chronic renal failure because of decreased erythropoietin production.

Treatment: EPO, if necessary

51
Q

What clues in one’s history would point to a diagnosis of aplastic anemia?

What are some lab findnigs associated with aplastic anemia?

A

Although aplastic anemia may be idiopathic, on the Step 2 examination watch for

  • chemotherapy
  • radiation
  • malignancy affecting the bone marrow (especially leukemias)
  • benzene
  • implicated medications (chloramphenicol, carbamazepine, sulfa drugs, zidovudine, gold)

Labs: decreased WBC and platelets.

Treat:

  • first stop any possible causative meds
  • then try antithymocyte globulin, colony-stimulating factors (EPO, sargramostim, filgrastim, pegfilgrastim), or bone marrow transplant
52
Q

What is myelophthisic anemia caused by?

What clues on the peripheral smear suggest its presence?

How to make the diagnosis?

A

caused by a space-occupying lesion in the bone marrow (malignant invasion that destroys bone marrow, myelodysplasia, myelofibrosis)

Peripheral smear: marked anisocytosis (different size), poikilocytosis (different shape), nucleated RBCs, giant and/or bizarre-looking platelets, and teardrop-shaped RBCs.

Diagnosis: bone marrow biopsy may reveal no cells (“dry tap” if the marrow is fibrotic) or malignant-looking cells.

53
Q

How do you recognize glucose-6-phosphatase deficiency?

When does it usually manifest?

What does the peripheral blood smear usually show?

How is the diagnosis usually made?

A
  • X-linked recessive, affects males
  • most common in blacks + Mediterraneans
  • usually sudden hemolysis or anemia after exposure to fava beans or certain drugs (antimalarials, salicylates, sulfa drugs) or after infection
  • peripheral blood smear: Heinz bodies and “bite cells”
  • diagnosis: RBC enzyme assay, which should not be done immediately after hemolysis because of the potential for a false-negative result (all of the older RBCs have already been destroyed, and the younger RBCs are not affected in most patients)
  • Treat with avoidance of precipitating foods and medications; discon- tinue the triggering medication first.
54
Q

Name some other causes of anemia.

A
  • Endocrine failure (especially pituitary and thyroid; look for endocrine symptoms)
  • Mechanical heart valves (hemolyzed RBCs)
  • DIC, TTP, and HUS (schistocytes and RBC fragments on smear and other appropriate findings)
  • Hemoglobinopathies (hemoglobin C and E varieties are fairly common)
  • Paroxysmal nocturnal or cold hemoglobinuria
  • Clostridium perfringens infection, malaria, and babesiosis (cause intravascular hemolysis and fever)
  • Hypersplenism (associated with splenomegaly and often with low platelets and white blood cells)
55
Q

When is transfusion indicated for anemia (at what hemoglobin level)?

A

when Hg < 7 g/dL or if patient is symptomatic

56
Q

What are the indications for the use of these various blood products?

whole blood

packed red blood cells

washed red blood cells

platelets

granulocytes

fresh frozen plasma

cryoprecipitate

A
  • Whole blood: Used for rapid, massive blood loss or exchange transfusions (poisoning, thrombotic thrombocytopenic purpura).
  • Packed red blood cells: Used for routine transfusions.
  • Washed red blood cells: Free of traces of plasma, white cells, and platelets; good in IgA deficiency as well as for allergic or previously sensitized patients.
  • Platelets: Given for symptomatic thrombocytopenia (usually < 10,000/μL).
  • Granulocytes: Used on rare occasions for neutropenia.
  • Fresh frozen plasma: Contains all clotting factors; used for bleeding diathesis when vitamin K will take too long to take effect (e.g., DIC, severe warfarin poisoning) or when vitamin K will not work (liver failure).
  • Cryoprecipitate: Contains fibrinogen and factor VIII; used in hemophilia, von Willebrand disease, and DIC.
57
Q

What is the most common cause of a blood transfusion reaction?

What blood type can be given in an emergency to avoid a reaction?

A

laboratory error

Type O negative blood can be used to avoid a reaction when you cannot wait for blood typing or when the blood bank does not have the patient’s blood type.

58
Q

Describe the 4 signs and symptoms of a blood transfusion reaction.

A

Look for

  • febrile reaction (chills, fever, headache, back pain) from antibodies to WBC
  • hemolytic reaction (anxiety or discomfort, dyspnea, chest pain, shock, jaundice) from antibodies to RBCs
  • allergic reaction (e.g., urticaria, edema, dizziness, dyspnea, wheezing, anaphylaxis) to an unknown component in donor serum
  • Oliguria may be an associated finding
59
Q

What should you do if you suspect a transfusion reaction?

A

The first step is to stop the transfusion.

If oliguria is present, treat with IV fluids and diuresis (mannitol or furosemide).

60
Q

What are the 4 major risks of transfusion?

A
  • blood transfusion reaction (described in another card)
  • infection (usually viral such as hepatitis B and C, HIV, CMV)
  • hyperkalemia (from hemolysis)
  • bleeding diathesis may occur with large transfusions (> 5 U of packed RBCs) due to dilutional thrombocytopenia and citrate (a blood preservative and calcium chelator that prevents clotting). Look for oozing from puncture or IV sites.
61
Q

What are the most common causes of DIC?

A
  • pregnancy and obstetric complications (roughly 50% of cases)
  • malignancy (33%)
  • sepsis
  • trauma (especially head trauma, prostate surgery, and snake bites)
62
Q

How do you recognize and treat DIC in a classic at-risk patient?

A

DIC usually manifests with bleeding diathesis but may have thrombotic tendencies.

Look for

  • classic oozing or bleeding from puncture and IV sites
  • prolonged PT/PTT/BT
    • ​DIC is the only disorder on the Step 2 examination that prolongs all three tests.
  • (+) D-dimers
  • increased fibrin degradation products
  • thrombocytopenia
  • decreased fibrin
  • decreased clotting factors (including factor VIII, which is normal in hepatic necrosis).

Treat the underlying cause (evacuate the uterus, give antibiotics), fresh frozen plasma or, in rare cases, heparin (only if thrombosis occurs).

63
Q

With what conditions is eosinophilia associated?

A
  • Allergic or atopic diseases (allergic rhinitis, asthma, allergic bronchopulmonary aspergillosis, eczema, urticaria, atopic dermatitis, milk-protein allergy, drug reactions)
  • Parasitic infections
  • Fungal infections
  • HIV infection
  • Malignancies (lymphoma, leukemia, lung cancer, gastric cancer, pancreatic cancer, colon cancer, ovarian cancer)
  • Connective tissue/autoimmune diseases (Churg-Strauss vasculitis, rheumatoid arthritis, lupus, scleroderma, eosinophilic fasciitis, Dressler syndrome, IBD)
  • Granulomatous disorders (sarcoidosis)
  • Skin disorders (psoriasis, pemphigus)
  • Immune disorders (Wiskott-Aldrich syndrome, hyper-IgE syndrome, IgA deficiency, thymoma)
  • Adrenal insufficiency
  • Pulmonary eosinophilia (Löffler syndrome)
  • Cirrhosis
  • Atheroembolic disease
  • Familial eosinophilia
  • Eosinophilia-myalgia syndrome (from using L-tryptophan)
64
Q

With what conditions is basophilia associated?

A

Allergies or neoplasm/blood dyscrasia.

65
Q

True or false: The lupus anticoagulant causes a clotting tendency.

What are typical history or lab findings that would suggest lupus anticoagulant?

A

True.

Lupus anticoagulant may cause prolonged PTT, but patients have a tendency toward thrombosis.

Look for: associated lupus symptoms, (+) VDRL or (+) RPR,ora history of miscarriages

66
Q

What are genetic and acquired causes of an increased tendency toward clot-forming?

When should you consider these conditions?

How are these patients treated?

A

Genetic causes:

  • factor V Leiden mutation (or activated protein C resistance)
  • prothrombin G20210A mutation
  • hyperhomocysteinemia*
  • elevated factor VIII level
  • deficiencies in protein C, protein S, or antithrombin III

Acquired causes

  • antiphospholipid syndrome (lupus anticoagulant and anticardiolipin antibody)
  • hyperhomocysteinemia*
  • pregnancy
  • cancer
  • estrogen-containing medications

Note that hyperhomocysteinemia can be genetic or acquired.

Suspect these conditions when recurrent clots develop or when a clot develops in the absence of risk factors for clot development.

All are treated with anticoagulant therapy to prevent DVT and PEs.

67
Q

Which 3 clotting tests measure which portions of the coagulation cascade?

Which medications affect these tests?

A
  • PT measures the function of the extrinsic clotting pathway (prolonged by warfarin)
  • activated PTT measures the function of the intrinsic clotting pathway (prolonged by heparin)
  • BT measures platelet function (prolonged by aspirin).
68
Q

How does von Willebrand disease affect clotting tests in terms of:

PT

PTT

BT

Platelet Count

RBC count

A
69
Q

How does Hemophilia A/B affect clotting tests in terms of:

PT

PTT

BT

Platelet Count

RBC count

A
70
Q

How does DIC affect clotting tests in terms of:

PT

PTT

BT

Platelet Count

RBC count

A
70
Q

How does von Willebrand disease affect clotting tests in terms of:

PT

PTT

BT

Platelet Count

RBC count

A
71
Q

How does liver failure affect clotting tests in terms of:

PT

PTT

BT

Platelet Count

RBC count

A
72
Q

How does heparin affect clotting tests in terms of:

PT

PTT

BT

Platelet Count

RBC count

A
73
Q

How does warfarin affect clotting tests in terms of:

PT

PTT

BT

Platelet Count

RBC count

A
74
Q

How does ITP affect clotting tests in terms of:

PT

PTT

BT

Platelet Count

RBC count

A
75
Q

How does TTP affect clotting tests in terms of:

PT

PTT

BT

Platelet Count

RBC count

A
76
Q

How does scurvy affect clotting tests in terms of:

PT

PTT

BT

Platelet Count

RBC count

A
77
Q

What are the common causes of thrombocytopenia?

What kind of bleeding problems are caused by low platelet counts?

A

Common causes of thrombocytopenia include:

  • purpura (idiopathic or thrombotic)
  • hemolytic uremic syndrome
  • DIC
  • HIV
  • splenic sequestration
  • heparin (including heparin-induced thrombocytopenia; treat by first stopping heparin)
  • medications (quinidine and sulfa drugs)
  • autoimmune disease
  • alcohol

Bleeding from thrombocytopenia is in the form of petechiae, nose bleeds, and easy bruising.

78
Q

What are 4 potential causes petechiae or “platelet-type” bleeding in the setting of normal platelets?

A
  • Vitamin C deficiency (scurvy) causes bleeding similar to that seen with low platelets (splinter and gum hemorrhages, petechiae); perifollicular and subperiosteal hemorrhages are unique to scurvy. Patients have a poor dietary history (the classic example is hot dogs and soda or tea and toast), myalgias and arthralgias, and capillary fragility (bleeding is caused by collagen problems in the ves- sels).
    • Treat with oral vitamin C
  • Uremia (results in platelet dysfunction)
  • Inherited connective tissue disorders (Ehlers-Danlos syndrome, Marfan syndrome)
  • Chronic corticosteroid use (causes capillary fragility)

A - Step II Secrets (40 decks)

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