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Acute Care NP Exam > Hem Onc > Flashcards

Hem Onc Flashcards

1
Q

Different types of white blood cells

A

Neutrophils - increased means infection - bands suggest bacterial infection

Lymphocytes: increased means viral infection

Eosinophils: parasites, allergic conditions

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2
Q

What diseases only have spherocytes on a peripheral blood smear?

A

Spherocytes are spheroid RBCs rather than bi-concave

Autoimmune hemolytic anemia - also has a positive direct Coombs test
—the spleen sees the spherocytes and identifies them as abnormal so it destroys them, therefore causing anemia

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3
Q

What are acanthocytes

A

RBCs that have a spiked cell membrane due to abnormal thorny projections.
“spur cell”

Usually caused by liver disease

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4
Q

What are schistocytes

A

RBC fragments as a result of mechanical destruction (fragmentation hemolysis) of a normal RBC.

Occurs when there is damage to a blood vessel and a clot begins to form

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5
Q

What are Howell-Jolly bodies

A

nuclear remnants in the cytoplasm

indicate splenic dysfunction

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6
Q

What do bands indicate?

A

These are immature white blood cells that are released when there is an infection

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7
Q

What might metamyelocytes suggest?

A

These are immature band cells

Indicate very immature WBC being sent out. Likely represents sepsis.

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8
Q

What do smudge cells indicate

A

remnants of cells that lack any identifiable cytoplasmic membrane or nuclear structure

Associated with chronic lymphocytic leukemia

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9
Q

What do blasts indicate if seen in the peripheral blood?

A

Usually indicates a leukemia or severe myelodysplastic syndrome

These are cancerous and should raise alarm

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10
Q

What are the three causes of anemia

A

-Problem with RBC production, usually in bone marrow
-Premature destruction of RBC (hemolysis) faster than new ones can be made
-Loss of blood

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11
Q

What are the three types of anemia

A

Microcytic: MCV <80

Normocytic: MCV 80-100

Macrocytic: MCV >100

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12
Q

Work up for microcytic anemia

A

Check iron levels
-If deficient (MOST LIKELY), work up for source of chronic blood loss
-if normal or elevated, consider anemia of chronic disease

Generally is caused by iron deficient anemia

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13
Q

Work up for normocytic anemia

A

Check a reticulocyte count (immature RBC)

-If low, anemia of chronic disease or bone marrow disease
-If elevated, blood loss or hemolysis

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14
Q

Work up for macrocytic anemia

A

Check B12/folate levels
-If low, vitamin B12 deficiency - Most likely - Pernicious anemia
-If normal, consider thyroid, ETOH, liver disease

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15
Q

Hemachromatosis: Causes, clinical presentation and treatment

A

Clinical syndrome of iron overload that is either caused by primary cause (gene mutation) or a secondary cause such as excessive blood transfusions or taking too many supplements.

Presents with interference of organ functions:
-Cirrhosis
-Bronzing of the skin
-CHF, arrythmias
-Endocrine problems

Treatment is phlebotomy to reduce ferritin
In primary gene mutation - can give Deferasirox (Exjade)

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16
Q

Lab findings in Thalassemia

A

Anemia with microcytosis and hypochromia

(low MCV and low MCHC)

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17
Q

Paroxysmal nocturnal hemoglobinuria - clinical presentation

A

-First morning urine is often dark or red (hgb)
-Prone to thrombosis especially in the skin (forms nodules), the hepatic and mesenteric veins
-Erectile dysfunction
-Esophageal spasm

Labs show thrombocytopenia, hemoglobinuria

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18
Q

What is autoimmune hemolytic anemia: Causes and presentation include labs

A

Increased RBC destruction
Intrinsic causes: spherocytes,
-hemoglobinopathies: thalessemia, sickle cell

Extrinsic - immune response, infx (malaria, babeiosis)

-All are caused by hyperbilirubinemia
—Could get GGT which will be normal because LFTs will all be elevated in hemolytic anemia and GGT only elevated in liver disease
-Positive Coombs test
-If you see shystocytes - autoimmune hemolytic anemia

Will present with rapid onset anemia, plus jaundice and splenomegaly

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19
Q

Treatment of autoimmune hemolytic anemia

A

Prednisone 1-2mg/kg/day
Plasmapheresis
Splenectomy
Transfuse as needed

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19
Q

Treatment of autoimmune hemolytic anemia

A

Prednisone 1-2mg/kg/day
Plasmapheresis
Splenectomy
Transfuse as needed

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20
Q

Polycythemia Vera - Cause and presentation

A

Mutation of the JAK2 gene results in the overproduction of all blood cells, causing an expanded blood volume and increased blood viscosity

Patients usually complain about pruritus, headache, dizziness, pulsatile tinnitus
Usually appear ruddy complexion and look swollen

Biggest complication is the blood viscosity and arterial thrombosis

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21
Q

Treatment of polycythemia vera

A

Regular phlebotomy to keep HCT <45

Hydroxyurea can be used as well if phlebotomy is not tolerate

Ruxolitinib is the only JAK2 inhibitor approved by the FDA

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22
Q

Disorders that cause thrombocytopenia

A

Immune thrombocytopenia purpura (ITP)
-Diagnosis of exclusion
-Sxs include spontaneous bruising, petechial rash, spontaneous bleeding from the nose, gums, vagina
-Platelet count will be very low
-Caused by decreased production due to destruction of the metakaryocytes
-Treatment can be supportive and it will resolve on its own or can give prednisone

Thrombotic Thrombocytopenic Purpura (TTP)
-Rare, hem emergency
-ITP plus hemolytic anemia
-blood clots form in small vessels throughout the body
-This causes low platelet count, low RBC count, and kidney, heart and brain dysfunction
-Presentation is fevers, AMS, thrombocytopenia, acute renal failure, hemolytic anemia
-Treatment is plasmapheresis and usually Rituximab
—Do not give platelets as this will only fuel the disease

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23
Q

Heparin-induced thrombocytopenia (HIT)

A

The immune system forms antibodies against heparin when it is bound to a protein called platelet factor 4

If you see platelet counts falling within 5 days of starting heparin, should stop heparin right away and start alternative anticoagulant
–bivalirudin, argatroban, fondaparinux
—This treats the clots that are formed because of the HIT
—Do not start Warfarin

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24
Disseminated Intravascular Coagulation (DIC)
Clotting cascade is activated either locally or systematically Condition is always secondary to something else -Sepsis -Retained products of conception -Malignancy, often acute leukemia -Starts with inappropriate activation of the clotting cascade and platelet activation -As it progresses, clotting factors and platelets are exhausted and spontaneous bleeding begins
25
Treatment of DIC
Treat the trigger Establish a baseline with lab parameters -Platelet count -PT, PTT -D-Dimer Transfuse blood products Follow the lab parameters every 4 hours If bleeding persists, consider heparin infusion if the platelets are >50 but contraindicated if the GI or CNS bleeding, placental abruption, need for operative management
26
Von Willebrand Disease: Cause and Presentation
The most common congenital disorder of coagulation -Deficiency in the quality or quantity of von Willebrand factor - a protein required for platelet adhesion Presentation ranges from mild bleeding that often goes undiagnosed because it is so small to severe bleeding with even minor trauma
27
Treatment of Von Willebrand Disease
For most patients it is DDAVP (Desmopressin) If more severe bleeding, can give Factor VIII
28
Hemophilia - Causes and complications
X-linked recessive disorder (therefore only occurs in males) Hemophilia A is a deficiency of Factor VIII Hemophilia B is a deficiency of Factor IX Diagnosis: Generally done by genetic counseling and diagnosed during pregnancy Complications: Deep internal bleeding from minor trauma Joint damage from hemarthrosis Spontaneous intracranial hemorrhage Treatment: DDAVP for mild cases Severe cases: regular administration of recombinant factors
29
Reversal of anticoagulation
Heparin and LMWH - Protamine Fonaparinux - cannot be reversed with Protamine Warfarin - Vit K, K centra DOACs - short half life so usually can just stop it --Pradaxa - Praxabind --Xarelto and Eliquis - Andexxa
30
Difference between acute and chronic leukemias
Acute: Rapid increase in the number of immature blood cells --Immediate treatment is needed because of the rapid progression and accumulation of blasts which can spill into blood stream and spread to other organs ---Usually easier to treat because the cells are so immature and differentiating so quickly that they are vulnerable Chronic: Excessive buildup of relatively mature, but still abnormal WBC --Usually seen in older patients ---Usually monitored for a bit to determine treatment course
31
Chronic Myeloid Leukemia (CML) - cause, presentation, treatment
-Caused by a chromosomal abnormality at the Philadelphia chromosome*** HALLMARK -Early stages are asymptomatic and usually picked up incidentally on routine lab studies -Can present in acute form - rapid progression, low survival rate - "blast crisis" ---spontaneous bleeding, fevers, petechia In chronic form, presents with fatigue, bone pain, splenomegaly Labs will show pronounced leukocytosis without obvious infection --Mature myeloid cell types predominate ---Bone marrow biopsy shows the bcr/abl genotype Treatment: -Since often found in the elderly, treatment may be deferred -If undertaken, usually treated with Tyrosine kinase inhibitors with good prognosis at 5 years --Curative with bone marrow transplant
32
Myelodysplastic Syndrome
Acquired clonal disorder of the hemotopoietic stem cell ---These cells are disorder and they make clones of themselves These cells stay in the marrow and do not leave Caused by radiation and chemotherapy Many patients had cancer before, were treated with chemotherapy, went into remission and then develop MDS because of the chemo. ---They then will progress to an Acute Myeloid Leukemia Treatment is supportive and blood products -Also hematopoietic growth factors Prognosis is months to years
33
Acute Myeloid Leukemia - Presentation and lab findings
More common in adults, specifically males Presentation is usually fatigue and spontaneous bleeding Labs: Leukocytosis, severe anemia, thrombocytopenia, blasts appear on the diff Malignant cell in AML is the myeloblast
34
Treatment of AML
High dose cytarabine and daunorubicin to stop the massive proliferation of myeloblasts Then consolidation of doses Then BMT
35
Acute Lymphocytic Leukemia - Causes and Presentation (including labs)
In ALL, the lyphoblast is the cancerous cell Usually presents in children -Often leptomeningeal spread to the CNS CBC shows atypical lymphocytes with pancytopenia ***HALLMARK
36
Chronic Lymphocytic Leukemia - causes, presentation, labs
CLL is a clonal malignancy of the B cell lymphocytes Usually very slow moving and is an accumulation of long-lived lymphocytes that do not work very well, therefore causing immunosuppression Presents similar to HIV More common in elderly patients CBC shows lymphocytosis - smudge cells present***HALLMARK
37
What is a Richter Transformation
In CLL, the disease can transform a lymph node into an aggressive large B-cell lymphoma
38
Hairy Cell leukemia
Similar to CLL however there is pancytopenia on CBC Treatment is focused on symptom burden and presence of opportunistic infections
39
Major difference between leukemias and lymphomas
In lymphomas - the CBC is usually normal
40
Burkitt's Lymphoma - causes, clinical presentation, treatment
Rapidly growing, invasive tumors of the lymph nodes and have a strong association with immune dysfunction (either post-viral or related to immunosuppression) Respond quickly to chemotherapy Spread quickly to the CNS and given that the patient is likely immunocompromised, can have high mortality rate
41
Hodgkin's Lymphoma
Presents as painful, tender lymph node, usually in one of the cervical chains B sxs often present - fatigue, malaise, weight loss Classic finding is a biopsy showing Reed-Sternberg cells Treatment is excision of the lymph node and chemotherapy
42
Plasma Cell Myeloma (formerly known as Multiple Myeloma) - Presentation, Diagnosis and treatment
Presents with CRABS: C: Hypercalcemia R: Renal failure A: Anemia B: Bony lesions - often moth eaten to long bones - pathologic fractures Diagnosis made by protein electrophoresis of the urine of blood to identify paraproteins (Bence-Jones Protein) Disease is incurable but the goal is to drive into remission and treat symptoms: Lenalidomide - immunomodulator Bortezomib - Proteasome inhibitor BMT Ortho intervention to treat pathologic fxs
43
Tumor Lysis Syndrome - When is it seen? Lab findings? Treatment
Most commonly seen following a treatment of a hematologic malignancy such as ALL or Burkett's Lymphoma Lab findings: -Hyperuricemia -Hyperkalemia -Hyperphosphatemia Acute renal failure develops shortly after Most effective treatment is prevention -Aggressive IVF before, during and after chemotherapy to keep urine output up and prevent the buildup of cellular materials from destroyed cancer cells Emergency hemodialysis might be needed in severe cases
44
What is the normal range for Total Iron binding capacity?
250-450
45
What is the normal range for serum iron
50-150
46
Normal range for mean corpuscular hemoglobin concentration (MCHC)
32-36 <32 is hypochromic >36 is hyperchromic
47
A higher Total iron binding capacity means the (greater/lower) the need for iron?
Greater need for iron
48
DDx for low MCV
Iron deficiency anemia (most common) or thalassemia
49
DDx for high MCV
B12 or folate deficiency, alcoholism, liver failure and drug effects Most likely is B12 or folic acid deficiency
50
What is megaloblastic anemia? Lab values?
B12 or folate deficiency High MCV
51
What is the DDx for normocytic anemia?
Anemia of chronic disease Sickle cell Renal failure Blood loss Hemolysis
52
Cause of iron deficiency anemia and what labs do we see?
Blood loss, inadequate iron intake, impaired absorption of iron Low H/H Microcytic, hypochromic Low serum iron Low serum ferritin - stores are low High TIBC - capacity is high High RDW
53
Pica is associated with what type of anemia
Iron deficiency anemia
54
What is the difference between thalassemia minor and thalassemia major
Thalassemia minor: Have only one copy of they beta thalassemia gene and have only mild anemia (may mimic iron-deficiency anemia) Thalassemia Major (Cooley's anemia): Have two genes for beta thalassemia --Anemia presents after a few months of life and becomes progressively severe ---FFT in a child ---Feeding difficulties (due to easy fatigue and lack of oxygen) ---Bouts of fever ---Diarrhea ---Hepatosplenomegaly and jaundice ---Maxillary enlargement
55
What are the labs associated with thalessemia
Decreased Hgb Microcytic, hypochromic Normal TIBC Normal ferritin Decreased alpha or beta Hgb chains
56
Which anemia is known to have decreased alpha or beta hemoglobin chains?
Thalassemia
57
Management of thalassemia
Usually no management is needed Might need RBC transfusion/splenectomy for more severe forms Iron is contraindicated as iron overload can occur Should consider prenatal testing
58
Folic Acid deficiency - what are the labs?
Macrocytic, normochromic HCT and RBC decreased Serum folate decreased
59
Symptoms of folic acid deficiency What is the difference in clinical presentation of folic acid deficiency and B12 deficiency
Folic acid Deficiency: -Fatigue -Dyspnea on exertion -Pallor -Headache -Tachycardia -Anorexia -Glossitis (Big beefy tongue) No neurologic signs are seen - this differentiates it from B12 deficiency
60
Pernicious Anemia - What are the labs?
Deficiency in B12 Macrocytic, normochromic Anti-IF (intrinsic factor) and anti-parietal cell antibody test H/H is also low Serum B12 <200
61
Clinical manifestations of pernicious anemia
Weakness Glossitis Palpitations Dizziness Anorexia BIG ONES: -PARESTHESIA -LOSS OF VIBRATORY SENSE -LOSS OF FINE MOTOR CONTROL -POSITIVE ROMBERG -POSITIVE BABINSKI Positive neuro findings with Pernicious anemia
62
Treatment for pernicious anemia
B12 (cyanocobalamin) 100mcg IM daily x1 week Then monthly for IM injections for life
63
What are the treatment priorities for sickle cell crisis
Fluids for dehydration (number 1 cause of crisis) Analgesics for pain Oxygen for hypoxemia
64
What is Von Willebrand Disease
A genetic disorder that results in the reduced ability to create blood clots Caused by mutation of deficiency in von Willebrand factor and clotting factor VIII
65
Management of von Willebrand Disease
Desmopressin (DDAVP)
66
What is a lab value that distinguishes Acute Lymphocytic Leukemia (ALL)
Pancytopenia with circulation blasts
67
What is the most common leukemia in adults?
Chronic Lymphocytic Leukemia (CLL)
68
What is the hallmark lab value for chronic lymphocytic leukemia
Lymphocytosis
69
Hallmark lab value of chronic myeloid leukemia (CML)
Philadelphia chromosome seen in leukemic cells
70
What is required to confirm diagnosis of leukemia?
Bone marrow aspiration
71
What is tumor lysis syndrome: Clinical presentation and management
Usually caused when chemotherapy starts to break down tumor cells and breaks them apart. This releases all of their toxins. Clinical presentation: Hyperuricemia - elevated uric acid in the blood Hyperkalemia Hyperphosphetemia Hypocalcemia Management is by allopurinol to reduce risk of tumor lysis syndrome
72
Staging of lymphomas:
Stage 1: Disease localized to single lymph node Stage 2: More than one lymph node, confined to one side of the diaphragm Stage 3: Lymph nodes and spleen involved, crossed diaphragm Stage 4: Live or bone marrow involved
73
Which disease is more virulent, Non-hodgkins or Hodgkins?
Non-Hodgkins is less predictable and advances quickly
74
Hodgkin's Disease is more common in men or women?
Men, average age is 32
75
How can we distinguish between Hodgkin's lymphoma and Non-Hodgkins?
Characteristic Reed-Sternberg cells are noted in Hodgkin's disease
76
Normal platelet counts
150,000-400,000
77
How do you confirm a diagnosis of idiopathic thrombocytopenia purpura?
Bone marrow analysis Low platelet count with other causes of thrombocytopenia ruled out May be a history of easy bruising or bleeding
78
Management of idiopathic thrombocytopenia purpura
May not be necessary until platelet count drops below 20,000 High dose corticosteroids or IV Gamma Globulin may help to elevate the platelet count within 2-3 days Platelet transfusions may be needed
79
What do you do if you think you might have Heparin-induced thrombocytopenia (HIT)
Immediately stop Heparin Can give Argatroban or Lepirudin which will reverse the HIT and offer some anticoagulation therapy
80
How do you differentiate between idiopathic thrombocytopenia purpura and SLE?
Need bone marrow analysis
81
What causes disseminated intravascular coagulation:
Acquired coagulation disorder which results from the activation of both the coagulation and fibrinolytic systems (thrombin and plasmin are activated) causing simultaneous thrombosis and hemorrhage
82
Lab results in DIC
Thrombocytopenia Hypofibrinogenemia (fibrinogen <170) Decreased RBC Increased FDP (Fibrin degradation products) Prolonged prothrombin time (>19 seconds) Prolonged PTT (>42 seconds) Elevated D-dimer
83
Management of DIC
Platelet transfusions, fresh frozen plasma (to replace clotting factors) and cryoprecipitate (to maintain fibrinogen levels)
84
If you are giving a lot of pRBC, what would be something to consider giving after a 4-6 units?
Fresh frozen plasma - need the clotting factors

Acute Care NP Exam (22 decks)

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