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INPATIENT > Hematologic and oncologic diseases > Flashcards

Hematologic and oncologic diseases Flashcards

1
Q

Name 4 clinical manifestations of iron deficiency anemia.

A
  1. angular cheilosis
  2. atrophic glossitis
  3. pica
  4. koilonychia
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2
Q

Describe the 3 main etiologies of iron deficiency anemia.

A
  1. Chronic bleeding, e.g. GI, menstrual
  2. Decreased iron supply, e.g. malnutrition, celiac, Crohn’s, etc.
  3. Increased demand, e.g. pregnancy
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3
Q

What lab tests diagnose iron deficiency anemia?

A
  1. Decreased serum Fe
  2. Increased TIBC
  3. Decreased ferritin
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4
Q

Describe the main etiology of B12 deficiency anemia.

A

Decreased supply!

  1. malnutrition (alcoholics, vegans)
  2. malabsorption (lack of intrinsic factor, celiac, Crohn)
  3. increased competition (intestinal bacteria overgrowth, tapeworm)
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5
Q

What lab tests diagnose B12 deficiency anemia?

A

Decreased B12

Increased homocysteine AND methylmalonic acid

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6
Q

Describe the 3 main etiologies of folate deficiency anemia.

A
  1. Decreased supply (alcoholic malnutrion, elderly, celiac)
  2. Impaired metabolism (methotrexate, trimethoprim)
  3. Increased requirement (chronic hemolytic anemia, pregnancy, malignancy)
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7
Q

What lab tests are used to diagnose folate deficiency anemia?

A

Rule out B12 deficiency first, but:

Decreased folate

Increased homocysteine

NORMAL methylmalonic acid

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8
Q

Name 3 general causes of intrinsic hemolytic anemia and 3 general causes of extrinsic hemolytic anemia.

A

Intrinsic:

Enzyme deficiency - G6PD deficiency

Hemoglobinopathies - sickle cell

Membrane problems - hereditary spherocytosis, PNH

Extrinsic:

Immune-mediated

Infections, toxins

Entrapment - hypersplenism

purple book 5-4

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9
Q

What are the lab results for diagnosing a hemolytic anemia in general?

A

Increased reticulocyte count

Increased LDH

Decreased haptoglobin

Increased indirect bilirubin

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10
Q

What will the smear look like in G6PD deficiency?

A

Heinz bodies, bite cells

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11
Q

What lab test will be positive in an autoimmune hemolytic anemia?

A

Coombs test

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12
Q

What are some indications for bone marrow biopsy?

A
  • Unexplained anemia
  • Macrocytic anemia (to distinguish megaloblastic from normoblastic maturation)
  • Unexplained leukopenia
  • Unexplained thrombocytopenia
  • Pancytopenia
  • Presence of blasts on peripheral smear (investigation for possible leukemia)
  • Presence of teardrop red cells on peripheral smear (possible myelofibrosis)
  • Presence of hairy cells on peripheral smear (possible hairy cell leukemia)
  • Suspected multiple myeloma
  • Staging of non-Hodgkin’s lymphoma
  • Unexplained splenomegaly (possible lymphoma)
  • Fever of unknown origin
  • Confirmation of normal marrow in potential allogeneic donor
  • Work-up of amyloidosis (to detect clonal plasma cell disorder)

UpToDate

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13
Q

Where does erythropoeitin have its effects (where are receptors for it)?

What are the indications for exogenous EPO?

A
  • Affects colony forming cells and proerythrocytes in bone marrow
  • Indications:
    • CKD-related anemia
    • chemotherapy-related anemia
    • prep for surgery with high risk of blood loss

Medscape

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14
Q

There are 4 Black Box warnings associated with exogenous EPO. What are they?

(significant adverse effects)

A
  1. Erythropoiesis-stimulating agents (ESAs) increase the risk of death, myocardial infarction (MI), stroke, venous thromboembolism, thrombosis of vascular access.
  2. In controlled trials, CKD patients experienced greater risks of death, serious adverse cardiovascular reactions, and stroke when administered ESAs to target a hemoglobin level of greater than 11 g/dL.
  3. ESAs shortened overall survival and/or increased the risk of tumor progression or recurrence in some clinical studies in patients with breast, non–small cell lung, head and neck, lymphoid, and cervical cancers. Because of these risks, health care providers and hospitals must enroll in and comply with the ESA APPRISE Oncology Program to prescribe and/or dispense epoetin alfa to patients with cancer.
  4. Perisurgical: Due to increased risk of deep venous thrombosis (DVT), DVT prophylaxis is recommended.
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15
Q

Both iron deficiency and mild alpha thalassemia are a microcytic anemia with minimal, vague s/s. What lab tests can you use to differentiate between them?

Why is it so important to differentiate?

A
  1. Hemoglobin electrophoresis (abnormal in alpha thalassemia)
  2. Measure serum iron and ferritin (low in IDA)
  3. RDW likely to be low (not much size variation) in thalassemia; RDW likely to be high (lots of size variation) in IDA.

You really don’t want to treat thalassemia with iron - leads to hemochromatosis and end organ damage.

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16
Q

What are the indications for transfusion therapy in thalassemia?

A
  1. facial deformities (developing infants/children)
  2. growth impairment
  3. fractures/skeletal impairments
  4. extramedullary hematopoeisis/hepatosplenomegaly
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17
Q

What is the pathophysiology of sickle cell anemia?

A
  1. Autosomal recessive point mutation in gene for B-globin chain of hemoglobin
  2. Hemoglobin S molecules aggregate & polymerize into needle-like fibers when deoxygenated and RBCs assume a sickle shape.
  3. Microvascular occlusions lead to ischemic damage.
  4. Severe hemolytic anemia
  5. Painful vasoocclusive crises.
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18
Q

Describe the general approach to managing sickle cell pain crises.

A
  • Majority of symptoms are secondary to nociceptive pain and therapy should be directed to the treatment of nociceptive pain and not neuropathic pain.
  • Many health care providers perceive that patients with SCD are addicted to opioids and exhibit drug-seeking behavior - NOT TRUE.
  • Adults with SCD treated for pain should have an objective pain measurement to assess the impact of the treatment - the most common measurement for adults is the Visual Analog Scale (VAS), a continuous line, 100 mm in length, ranging from no pain to severe pain.
  • Given that individuals with SCD have most of their acute pain episodes at home, a standard care plan for treatment outside of the hospital is required, and pain treatment plans must be tailored to the individual.
  • Plans will range from treatment with non-opioid analgesics, such as NSAIDs or acetaminophen with codeine, to prompt presentation to a day hospital for intravenous opioids.
  • Successful management of pain in the hospital setting is typically achieved with scheduled opioid dosing or continuous infusion of opioids.
  • The most reasonable solution for breakthrough pain in hospitalized patients is the use of patient-controlled analgesia (PCA) that allows the individual to administer an immediate dose of pain medication without having to call the nurse.
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19
Q

List some common triggers for hospital admission in a patient with sickle cell anemia.

A

Number one reason for admission: pain crisis

infection

acute chest syndrome

aplastic crisis

sequestration crisis

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20
Q

What are the most common causes of thrombocytopenia?

A
  1. sepsis
  2. liver disease -> hypersplenism
  3. medications
  4. DIC
  5. infection
  6. massive transfusion
  7. alcoholism
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21
Q

What are the most common causes of reactive thrombocytosis?

A
  • Infection
  • Post-surgical status
  • Malignancy
  • Post-splenectomy state
  • Acute blood loss or iron deficiency

UpToDate

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22
Q

What are some causes of autonomous thrombocytopenia?

A

Chronic myeloid leukemia

Polycythemia vera

Myelodysplastic syndromes

Acute myeloid leukemia

23
Q

What are the steps of lab evaluation of thrombocytosis?

A
  1. CBC with smear (Howell-Jolly bodies, neutrophilia)
  2. Serum ferritin
  3. Acute phase reactants e.g. CRP

If the above tests don’t reveal a reactive cause of the thrombocytosis, then need a bone marrow biopsy to check for autonomous causes.

24
Q

What lab tests are used to work up thrombocytopenia?

A
  1. CBC with smear
  2. If asymptomatic/mild, repeat CBC in a month
  3. If symptomatic, test according to clinical picture for associated conditions e.g. liver, autoimmune, infection, etc.
25
Q

Review the ABO blood typing system.

A
26
Q

What is the initial management of a transfusion reaction?

A

Vigorous IV fluids, maintain urine output with diuretics or mannitol

27
Q

What are the s/s of a transfusion reaction?

A

Acute hemolytic fever
Hypotension
Flank pain
Renal failure

28
Q

Definition of neutropenic fever:

A

Fever: single oral temp > 101, or 100.4 for > 1 hr

101=38.3

100.4=38

Neutropenia: absolute neutrophil count < 500

purple book 5-36

29
Q

Treatment for neutropenic fever:

A

Low-risk patients: cipro + amoxicillin-clavulanate

IV abx: no clear winner

  • ceftazidime or cefepime or imipenem

OR

  • aminoglycoside + antipseudomonal B-lactam

purple book 5-36

30
Q

What are the clinical manifestations of vitamin K deficiency?

A
  • easy bruisability
  • mucosal bleeding
  • splinter hemorrhages
  • melena
  • hematuria

UTD

31
Q

What is vitamin K’s role in the coagulation process?

A
  • Vitamin K is essential for activity of several carboxylase enzymes within the hepatic cells, and therefore is necessary for the activation of coagulation factors VII, IX, X, and prothrombin.
  • The natural anticoagulants, proteins S and C also require vitamin K for their activity. Protein C, following its activation by thrombin, inactivates factors Va and VIIIa, thus inhibiting excess generation of thrombin. Protein S also helps prevent excessive coagulation through its action as a cofactor for activated protein C.

UTD

32
Q

Lab findings in vitamin K deficiency?

A
  • prolonged PT
  • elevated INR

UTD

33
Q

What are some causes of vitamin K deficiency?

A
  • Vitamin K deficiency in an otherwise healthy adult is rare.
  • Acquired deficiency can occur secondary to drugs such as antibiotics.
  • Patients on total parenteral nutrition are prone to develop vitamin K deficiency and require supplementation.
  • Vitamin K is a fat-soluble vitamin, thus any cause of fat malabsorption may result in vitamin K deficiency. Fat malabsorption may be caused by disorders of bile or pancreatic secretion, or by extensive disease or resection of the intestinal mucosa. E.g., CF, celiac, primary biliary cirrhosis

UTD

34
Q

Vitamin K deficiency is common in newborns.

T/F

A

True

Vitamin K deficiency is common in the newborn because of immature liver function and low transfer of vitamin K through the placenta and breast milk. If vitamin K is not replaced, the infant is at risk for vitamin K deficient bleeding (VKDB). This disorder is associated with cutaneous, gastrointestinal, and intracranial bleeding within the first week of life. To prevent VKDB, vitamin K1 is administered IM at birth.

UTD

35
Q

What is the pathophysiology of DIC?

A

Disseminated intravascular coagulation is a systemic process producing both thrombosis and hemorrhage. It is initiated by a number of defined disorders and consists of the following components:

  • Exposure of blood to procoagulants such as tissue factor and cancer procoagulant
  • Formation of fibrin within the circulation
  • Fibrinolysis
  • Depletion of clotting factors
  • End-organ damage

DIC is a complication of underlying illness occurring in approximately 1% of hospital admissions.

UTD

36
Q

What is the treatment for DIC?

A

Treatment is generally supportive with platelet and clotting factor replacement therapy. In selected conditions, judicious use of heparin may be of benefit. The key to management of DIC and a favorable prognosis is effective treatment of the underlying disease.

UTD

37
Q

What are the clinical manifestations of DIC?

A
  • Bleeding (64 percent)
  • Renal dysfunction (25 percent)
  • Hepatic dysfunction (19 percent)
  • Respiratory dysfunction (16 percent)
  • Shock (14 percent)
  • Thromboembolism (7 percent)
  • Central nervous system involvement (2 percent)

UTD

38
Q

What are the lab findings in DIC?

A

a. Coagulation abnormalities

  • increased PT and PTT
  • decreased serum fibrinogen

b. Platelet abnormalities

  • thrombocytopenia
  • increased bleeding time

c. Fibrinolysis abnormalities
* presence of Fibrin Degradation Products (FDPs) and D-dimers
d. Normocytic anemia due to:

  • extensive bleeding from skin and GI tract
  • mechanical damage to RBCs by fibrin thrombi causing a microangiopathic hemolytic anemia with schistocytes

Rapid Review Pathology, Goljan

39
Q

Describe the pathophysiology of the coagulopathy of liver disease.

A
  1. The fundamental problem underlying the coagulopathy in patients with liver disease is a lack of protein production by the poorly functioning liver.
  2. Because both procoagulant and anticoagulant proteins are diminished in unpredictable ratios, the predilection for either bleeding or clotting in an individual patient is not predictable with current testing paradigms.

Could be either:

  • Increased bleeding risk — Decreased production factors II, V, VII, IX, X, XI, XIII) is only one component of the coagulation process that disrupts hemostasis. Thrombocytopenia, altered platelet function, etc., all contribute to an increased bleeding risk.
  • Increased thrombotic risk — Decreased levels of the liver-synthesized natural anticoagulant proteins C and S, decreased antithrombin levels, decreased plasminogen, and elevated levels of endothelial cell-derived factor VIII and von Willebrand factor (vWF) favor thrombosis formation.

UTD

40
Q

Lab testing for coagulopathy of liver disease?

A

The following battery of tests is helpful in determining the coagulation status of the patient with liver disease.

  • Platelet count
  • Prothrombin time
  • Activated partial thromboplastin time
  • Thrombin time
  • Fibrinogen level
  • Fibrin D-dimer

UTD

41
Q

What are the treatments for the coagulopathy of liver disease?

A

Treatment of bleeding: depends on the specifics of what’s happening; could be vitamin K, FFP, antifibrinolytic agents

Prevention and treatment of thrombosis: maybe LMWH

UTD

42
Q

What are the pathogenic factors that contribute to venous thromboembolism?

A

Virchow’s triad

  1. Hypercoagulability, e.g. factor V Leiden, heparin-induced thrombocytopenia
  2. Stasis, e.g. prolonged bed rest
  3. Endothelial injury, e.g. CAD, DMII
43
Q

What are prophylactic treatment options for hospitalized patients at risk for VTE?

A
  • Low molecular weight heparin (enoxaparin)
  • Mechanical methods of thromboprophylaxis include intermittent pneumatic compression, graduated compression stockings, and venous foot pumps
44
Q

What patients are at higher risk of bleeding from thromboprophylaxis?

A

Risk factors include:

  • bacterial endocarditis
  • congenital or acquired bleeding disorders
  • active ulcerative or angiodysplastic GI diseases
  • severe uncontrolled hypertension
  • hemorrhagic stroke
  • use shortly after brain, spinal, or ophthalmic surgery
  • patients treated concomitantly with platelet inhibitors
  • recent GI bleeding or ulceration
  • renal dysfunction and hemorrhage
  • thrombocytopenia or platelet defects or history of heparin-induced thrombocytopenia
  • severe liver disease
  • hypertensive or diabetic retinopathy
  • patients undergoing invasive procedures
45
Q

What is the direct Coomb’s test assessing?

When is the direct Coomb’s test used and in what diseases might it be positive?

A
  • Used to detect antibodies already bound to erythrocytes
  • Provides definitive evidence of immune hemolysis
  • Can also be used to investigate possible blood transfusion reactions
  • Hemolytic disease of the newborn
  • SLE
  • Idiopathic cold hemagglutinin syndrome

Basic Skills in Interpreting Lab Data

46
Q

What is the indirect Coomb’s test detecting?

A
  • Used to detect antibodies in patient’s serum (not bound to erythrocytes)
  • Used to screen for antibodies in the preparation of blood for transfusion (cross-matching)
47
Q

What are some indications for transfusion of PRBCs?

A

Indications for PRBC transfusion include:

  • symptomatic anemia (causing shortness of breath, dizziness, congestive heart failure, and decreased exercise tolerance)
  • acute sickle cell crisis
  • acute blood loss of more than 30 percent of blood volume

AAFP

48
Q

What is an indication for transfusion of fresh frozen plasma?

A
  • reversal of anticoagulant effects

AAFP

49
Q

What is an indication for transfusion of platelets?

A
  • to prevent hemorrhage in patients with thrombocytopenia or platelet function defects

AAFP

50
Q

What is an indication for transfusion of cryoprecipitate?

A
  • in cases of hypofibrinogenemia, which most often occurs in the setting of massive hemorrhage or consumptive coagulopathy

AAFP

51
Q

What are some possible hazards of transfusion?

A

Noninfectious Serious Hazards of Transfusion

Acute

  • Acute hemolytic reaction, febrile nonhemolytic reaction
  • Allergic reaction, anaphylactic reaction, urticarial reaction
  • Metabolic derangements
  • Mistransfusion (transfusion of the incorrect product to the incorrect recipient)
  • Septic or bacterial contamination
  • Transfusion-associated circulatory overload

Delayed

  • Delayed hemolytic reaction
  • Iron overload
  • Overtransfusion or undertransfusion
  • Post-transfusion purpura
  • Transfusion-associated graft-versus-host disease

AAFP

52
Q

What are some potential infectious risks of transfusion?

A

Hep B, Hep C, HIV, CJD

53
Q

Which hospitalized patients are at risk for VTE?

A

INPATIENT (11 decks)

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