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Peds - Spring 2016 > Hematology/Oncology - Part 1 - Unit 4 > Flashcards

Hematology/Oncology - Part 1 - Unit 4 Flashcards

1
Q

Blood - has a plasma and cellular portion. T/F?

A

TRUE

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2
Q

Plasma - __% water, ___% solutes.

A

90% water, 10% solutes (albumin, electrolytes, proteins - clotting factors, globulins, circulating, antibodies, fibrinogen)

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3
Q

Cellular elements -
mature red blood cells =
White blood cells =
Platelets =

A

mature red blood cells = RBC/erythrocytes
White blood cells = WBC, leukocytes
Platelets = thrombocytes

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4
Q

where is blood formed?

A

Red bone marrow/lymphatic system.

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5
Q

What does the RBC do? Life span?

A

Transports hgb, which carries oxygen to the cells of the body. The lifespan = 120 days.

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6
Q

What does the WBC do? lifespan?

A

Function in the immune system, life span about 6-8 hours, composed of granulocytes (neutrophils, basophils, eosinophils) and agranulocytes (monocytes, lymphocytes)

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7
Q

What is the function of the platelets?

A

Function to start the process which will stop bleeding.

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8
Q

What is a granulocyte? Describe each of them.

A

Made in bone marrow.
Neutrophils - fight bacterial infections, aka segmented neutrophils or segs.
Bands - immature neutrophils.
Eosinophils - increased with allergies, parasitic infections, some cancers.
Basophils - increased with tissue damage.

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9
Q

Agranulocyte - made where? What are the parts?

A

Made in the bone marrow/lymph nodes, spleen, liver, and thymus.

Monocytes are involved in the early stage of inflammatory reaction and show evidence of chronic infections.
Lymphocytes are involved in development of antibodies and delayed hypersensitivity.

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10
Q

Where are the platelets made? Life span?

A

Made in bone marrow. Life span is 8-10 days, form plug when there is a bleed. Influence homeostasis by releasing serotonin which produces vascular spasm to decrease blood flow to the area of the injury.

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11
Q

What is anemia? Normal hgb level?

A

Decreased RBC in mass of cell and / or hgb. Caused by decreased production of RBC’s, increased destruction of the RBC’s, and loss of RBC’s. Normal = 11-5-14.5

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12
Q

What are some clinical manifestations of acute anemia? Chronic (compensated) ?

A

Headache, lightheadedness, irritability, decreased attention span, tachycardia, fatigue, muscle weakness.

Compensated - growth retardation, delayed sexual maturation, tachycardia, heart murmur.

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13
Q

What might cause a decreased production of RBC’s?

A

bone marrow is not working well (aplastic anemia), medication (chemo, anticonvulsants), kidney disease, decreased iron

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14
Q

What is hereditary spherocytosis?

A

Inflexible spheres that lead to hemolysis. Treated by IVIG and splenectomy

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15
Q

How does a child get sickle cell?

Should kids avoid extreme temp changes?

A

The gene is passed - the mother and father must BOTH have the defective gene for a child to be affected. If one parent has it, that means that the kid can have the trait and carry it but won’t have it. hmmm.

YES

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16
Q

Asians and Native Americans most commonly get sickle cell anemia. T/F?

What is percentage child could have disease?
Could have trait?
Could have neither trait nor disease?

A

FALSE - it’s usually african american, along with african, indian, caribbean, middle eastern, and the Mediterranean.

25%
50%
25%

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17
Q

Sickle cell anemia - def

A

normal adult hgb is partly or completely replaced by abnormal sickle hgb.

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18
Q

Sickle Cell C Disease - def

A

variant or SCA (Hgb SC)

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19
Q

What is sickle thalassemia disease?

A

Combination of sickle cell trait and b-thalassemia trait.

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20
Q

what is a vaso-occlusive crisis r/t sickle cell?

A

Non-life threatening, mild/moderate pain, localized, acute abdominal pain, priapism, arthralgia, dactylitis (fingers)

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21
Q

How do we treat a vaso-occlusive crisis?

A

Bedrest to decrease energy expenditure, hydration, oxygenation, electrolyte placement, pain management, blood replacement, antibiotic therapy.

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22
Q

What is a spleen sequestration crisis?

A

Causes decrease in blood volume and can ultimately lead to shock. Can be acute or chronic.

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23
Q

What is an aplastic crisis? what usually triggers it?

A

Decreased RBC reproduction - usually triggered by infection with a virus such as parovirus.

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24
Q

SCA - sickle cell changes form pliable disk shape to a crescent or sickle shape. T/F?

A

TRUE

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25
Q

What can initiate sickling?

A

dehydration, acidosis, hypoxia, temp changes.

26
Q

How can we reverse sickling?

A

Sometimes adequate O2 and hydration will do it

27
Q

How does SCA manifest?

A

sickle cells adhering to vessel walls, increasing RBC destruction. Cells live only 20 days of the normal 120 days. Spleen can become infarcted and the spleen is replaced by fibrotic tissue. Increased susceptibility to bacterial infection!

28
Q

How does SCA affect the liver? Kidney? CNS?

A

Liver - hepatomegaly, cirrhosis, intrahepatic cholestasis

Kidney - inability to concentrate urine, enuresis, progressive renal failure.

CNS - stroke, hemiparesis, seizures

29
Q

Which lab value tells us that the marrow is not making RBC’s? Values?

A

Reticulocyte count! Tells you what the marrow is doing.

typically 2-3 times higher. If it’s 0, IT IS AN EMERGENCY!

30
Q

What is a hyperhemolytic crisis?

A

Increased rate of RBC destruction, characterized by jaundice, anemia, and reticulocytosis.

31
Q

Stroke - sickle shaped cells block the major blood vessels in the brain leading to infarction, with an increase risk of having another one (70%) - T/F?

A

TRUE

32
Q

What is a transcranial doppler test?

A

Ultrasound of the major vessels of the brain. High blood flow = increased risk for stroke. Typically done at 1-2 years old, and then every 3-6 months as needed.

33
Q

What is acute chest syndrome? What is it typically treated with?

A

Sickling in the small blood vessels of the lungs that leads to occlusion. Looks like pneumonia! Signs = chest pain, fever, cough, wheezing, tachypnea, hypoxia, etc. Can be life threatening! Typically treated with a blood exchange!

34
Q

What is an infection related crisis?

A

Overwhelming infection as a result of defective splenic function! Fever is first sign of this in a child with SCD. So if they have a temp, TAKE THEM TO ER!

35
Q

What is some treatment for SCD?

A

Hydroxyuria (but can cause weight gain), hematopoetic stem cell transplant, folic acid, pen VK

36
Q

What is b-thalassemia?

A

Inherited blood disorders characterized by deficiencies in the rate of production of specific globulin chains in hgb.

37
Q

What are the 3 types b-thalassemia?

A

Minor, Intermedia, Major

38
Q

What is minor b-thalassemia?

A

Doesn’t cause issues, may have minor anemia.

39
Q

What is intermedia b-thalassemia?

A

Less severe than major, they may have anemia but it doesn’t usually require transfusions.

40
Q

What is major b-thalassemia?

A

SEVERE anemia which can be life threatening. The child presents with fussiness, paleness, poor appetite….requires regular blood transfusions.

41
Q

What is alpha thalassemia? 2 types?

A

Hemoglobin H (bone, overgrowth!) and Hydrops fetalis (severe form, still born :( )

42
Q

What is aplastic anemia?

A

Production of all cell lines are depressed. There is primary (congenital) and secondary (acquired, more common)

43
Q

Secondary Aplastic Anemia - what might cause it?

A

HPV, irradiation, drugs, household/industrial chemicals, diseases, idiopathic

44
Q

What is the treatment for aplastic anemia?

A

Aimed at restoring function to marrow - typically immunosuppressive therapy. Immune system can’t attack itself then. Cyclosporin A, ATG (Anti-thymocyte globulin) can be used.

45
Q

What is hemophilia?

A

Bleeding disorder resulting from congenital deficiency of specific coagulation proteins.

46
Q

What are the two most common hemophilia’s?

A

Factor 8 (Hemophilia A) and Factor 9 (hemophilia B)

47
Q

What are common bleeding sites for hemophilia? Where is the most common internal bleeding?

A

Subcutaneous/intramuscular are the sites, hemathrosis (joint bleeding) is the most common form of internal bleeding.

48
Q

how do we treat hemophilia?

A

Replacement of missing clotting factor. Prophylactic treatment helps decrease morbidity.

49
Q

What is von willebrand’s disease?

A

hereditary - deficiency/defect in protein (von willebrand) - results in prolonged bleeding time.

50
Q

How do we treat von willebrand’s disease?

A

DDAVP, Humate P

51
Q

What is idiopathic thrombocytopenic purpura? What does the platelet count do?

A

Acquireed hemorrhagic disordered - excessive platelet destruction/purpura/normal bone marrow. Most typically recover.
The body attacks the platelets as foreign - might go from 150,000 to 10,000

52
Q

thrombocytopenic purpura - platelet count typically less than _______.

Observe bruising when platelet count when less than _____>
Observe petechiae when platelet count less than ______.

A

Less than 20000.

Bruising when less than 50,000
Petechiae - less than 20,000

53
Q

thrombocytopenic purpura - children at risk for spontaneous bleeding when platelet count is less than ___

A

20,000

54
Q

What is IVIG treatment for thrombocytopenic purpura treatment?

A

ITP treatment, derived from blood plasma. Blocks body’s autoantibodies that cause destruction of platelets. Expensive and given over several hours.

55
Q

What is Win-Rho for thrombocytopenic purpura treatment?

A

Anti-D antibody - contains antibodies which coat RBC so spleen takes them out of circulation and leaves platelets alone.

56
Q

Win-Rho - only works if child is Rh __ and given over __ minutes.

A

Rh +

30 minutes.

57
Q

What are a few other thrombocytopenic purpura treatment options?

A

Prednisone (helps raise platelet count by decreasing body’s immune response), splenectomy (last resort!)

58
Q

what are some additional interventions for thrombocytopenic purpura?

A

Avoid trauma - no contact sports (it’s hard to keep a kid down, sooooo), provide safety measures, avoid injections, avoid aspirin which increases bleeding.

59
Q

what is DIC?

A

Secondary disorder of coagulation - clotting and clot breakdown occuring at same time. Uncontrolled bleeding is possible.

60
Q

How do we treat DIC?

A

Control underlying cause and administration of platelets and fresh frozen plasma.

61
Q

What is henoch-scholein purpura?

A

Referred to as allergic vasculitis - not related to platelet. They have arthritis, abdominal pain, nephritis, FOLLOWS URI, abrupt onset.

62
Q

Henoch-scholein purpura - rash often associated with maculopapular lesions, urticaria, and erythema, including marked edema of scalp, eyelids, lips, ears, dorsal, etc. Might also have GI or arthritic effects, possibly renal. T/F?

A

TRUE

Peds - Spring 2016 (29 decks)

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