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MED SURG > Anemia Handout > Flashcards

Anemia Handout Flashcards

1
Q

What are the usual causes of low RBC or HBG

A
  1. Blood loss
  2. Inadequate production
  3. Increased RBC destruction
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2
Q

Depending on the severity, anemia can affect what

A

All major organ systems

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3
Q

What is the pathophysiology of anemia

A

Altered HBG synthesis such as iron deficiency
Altered DNA synthesis such as vitamin B12 or folic acid deficiency
Bone marrow failure such as aplastic anemia ( stem cell dysfunction)
Increased RBC loss or destruction: acute or chronic blood loss: increased hemolysis such as sickle cell anemia, infection.

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4
Q

What are manifestations of anemia

A

Pallor of skin, mucous membranes, conjunctiva, nail beds
Increased heart and respiratory rates as body compensates
Angina, fatigue, dyspnea on exertion, night cramps
Increased erythropoietin activity may cause bone pain
Cerebral hypoxia, headache, dizziness, dim vision
Heart failure with severe anemia
Signs of circulatory shock with rapid blood loss
Systolic heart murmur with chronic blood loss due to decreased viscosity of blood.

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5
Q

What is the most common type of anemia

A

Iron deficiency anemia

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6
Q

What is iron deficiency anemia

A

An inadequate iron supply which in turn, the body cannot synthesize hemoglobin which results in fewer RBCs which are microcytic, hypochromic and malformed ( poikilocytosis).

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7
Q

What is poikilocytosis

A

Malformed RBCs

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8
Q

What is the cause of iron deficiency anemia

A

Inadequate dietary intake
Malabsorption
Increased iron needs as with pregnancy and lactation
Chronic bleeding, menstrual blood loss,
Chronic occult blood loss in older adults
Slowly bleeding tumors, GI inflammation, hemmorhoids
Cancer

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9
Q

What are additions manifestations of iron deficiency anemia

A

Brittle, spoon shaped nails
Cheilosis ( cracks at corner of mouth)
Smooth sore tongue,
Pica

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10
Q

What is pica

A

Craving unusual substances such as clay, starch.

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11
Q

What is cheilosis

A

Cracks at corner of mouth

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12
Q

What is sickle cell anemia

A

A hereditary, chronic hemolytic anemia
Characterized by episodes of suckling in which RBC becomes abnormally cresent shaped.
It has a autosomal genetic defect causing abnormal form of hemoglobin within RBCs.

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13
Q

Sickle cell anemia is more common in which race?

A

African descent

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14
Q

What is the pathophysiology of sickle cell anemia

A

HGB becomes deoxygenated under hypoxemia and red blood cells deform into cresent or sickle shaped
The sickled cells clump together and obstruct capillary blood flow leading to ischemia and possible infarction of surrounding tissue. Under normal oxygen tension, sickled RBCs regain normal shape and u sickle. Repeated episodes weakens RBC and they are hemolyzed: RBC has a shortened life span.

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15
Q

What are general manifestations of sickle cell anemia

A 
Pallor
Fatigue
Jaundice
Irritability
With vaso-occlusive crisis (4-6 days); painful swelling of hands, feet, large joints, priapism, abdominal pain, stroke.
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16
Q

What is priapism

A

Persistent, painful erection

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17
Q

What is aplastic anemia

A

Due to shortened life span of RBC and compromised erythropoesis

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18
Q

What is sequestration crisis

A

Pooling of large amounts of blood in liver and spleen occurring more in children

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19
Q

What is treatment of sickle cell anemia

A 
Largely supportive: rest, oxygen, pain management, adequate hydration, 
Treat precipitating factors 
Folic acid supplementation
Blood transfusions 
Genetic counseling
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20
Q

What is aplastic anemia

A

BONE MARROW FAILURE, resulting in pantocytopenia ( low levels of RBC, WBC, platelets)
Marrow is replaced by fat

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21
Q

What are causes of aplastic anemia

A

Causes as idiopathic,
Viral infection, stem cell damage from radiation, exposure to chemicals, certain antibiotics ( chloramphenicol), chemotherapeutic drugs

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22
Q

What are manifestations of aplastic anemia

A

Fatigue, pallor, headache, exertional dyspnea, tachycardia, heart failure
Bleeding due to low platelet levels
Fever, increased infection risk due to low WBC

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23
Q

What is treatment for aplastic anemia

A

Removal of causative agent
Blood transfusions
Bone marrow transplant

*Ensure adequate tissue oxygenation
Treatment determined by underlying cause

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24
Q

What are diagnostic tests for aplastic anemia

A

CBC, blood cell count, hemoglobin, hematocrit, RBC indices.
Iron levels and total iron-binding capacity ( TIBC): deficits occur with iron deficiency anemia
Serum ferritin
Sickle cell test
Hemoglobin electrophoresis
Shilling test
Bone marrow examination quantative assay of G6PD

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25
Q

What is serum ferritin

A

It is low with depletion of total iron stores

Ferritin is iron storage protein produced by the liver, spleen, and bone marrow.

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26
Q

What is hemoglobin electrophoresis

A

Separation of normal from abnormal forms of hemoglobin

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27
Q

What is the shilling test

A
  1. Measures vitamin B12absorption before and after intrinsic factor administration
  2. Includes 24 hour urine test
  3. Used to differentiate between pernicious anemia and intestinal malabsorption
28
Q

What does a bone marrow examination do

A

Diagnosis aplastic anemia

29
Q

What is a quantitative assay of G6PD

A

Diagnosis of aplastic anemia thru diagnosis of G6PD deficiency

30
Q

What are meds for aplastic anemia

A

Iron supplements, oral or parenteral
Vitamin B12 parenterally
Folic acid for pregnant woman, clients with sickle cell disease, folic acid deficiency.
Hydroxyurea: promotes fetal hemoglobin production and reduces crisis for clients with sickle cell disease
Immunosuppressive therapy for clients with aplastic anemia

31
Q

What are complimentary therapies of aplastic anemia

A

The use of specific plant enzymes

32
Q

What is nursing mgmt of aplastic anemia

A

Prevention by teaching clients good dietary habits

Concurrent use of vitamin C with iron enhances iron absorption

33
Q

What are nursing diagnosis for anemia

A

Activity intolerance
Impaired oral mucous membranes
Risk for decreased cardiac output
Self care deficit

34
Q

What is the definition of anemia

A

Abnormally low number of circulating Red blood cells, hemoglobin concentration or both.

35
Q

What are the types of polycythemia

A

Primary ( polycythemia-Vera-PV

Secondary

36
Q

Who acquires polycythemia

A

It is uncommon affecting males of European Jewish ancestry aged 40-70

37
Q

What is myeloproliferative disorder

A

It is a type of primary polycythemia

RBC are produced in absence of erythropoietin

38
Q

What are manifestations of myeloproliferative disorder

A

Initially a symptomatic
Hypertension in common
Plethora, ruddy coloration of face, hands,feet, mucous membranes; painful pruritis of fingers and toes
Hyper metabolism: thrombosis, hemmorhage

39
Q

What is secondary polycythemia

A

Response to elevated erythropoietin levels occurring as compensation to hypoxia ( living in high altitudes, smoking, chronic lung disease)

  • RBC COUNT IS NORMAL BUT FLUID LOSS INCREASES THEIR CONCENTRATION
40
Q

What is treatment for polycythemia

A
  1. Treat the underlying cause; smoking cessation
  2. Periodic phlebotomy, removing 300-500 ml of blood
  3. Primary polycythemia may be treated with medications hydroxyurea: to suppress bone marrow function
  4. Antihistsmines for pruritis
  5. Aspirin to decrease risk of thrombosis
41
Q

What is thrombocytopenia

A

Platelet count less than 100,000 {abnormal bleeding}
Platelet count less than 20,000 { spontaneous bleeding and hemmorhage from minor trauma}
Platelet count less than 10,000 { serious or fatal bleeding can occur}

42
Q

What type of bleeding occurs with thrombocytopenia

A

Usually bleeding occurs in small vessels resulting in
PETECHIAE- very small red or purple spots on skin
PURPURA- purple bruising
Areas prone to bleeding include mucous membranes of nose, mouth, GI tract, vagina.

43
Q

What are mechanisms leading to thrombocytopenia

A

Decreased production
Increased sequestration in spleen
Accelerated destruction

44
Q

What is primary thrombocytopenia

A

Immune thrombocytopenia purpura (ITP) or idiopathic thrombocytopenic purpura
It is a autoimmune disorder with accelerated platelet destruction

45
Q

Who does immune thrombocytopenia purpura typically occur in

A

Chronic form affects adults aged 20-40 mostly females

Acute form lasts 1-2 months

46
Q

What is the pathophysiology of immune thrombocytopenia purpura

A

Platelets stimulate antibody production igG

Functions normally but destroyed by spleen after 1-3 days of circulation

47
Q

What are manifestations of immune thrombocytopenia

A

Petechaie and purpura on chest, arms, neck, oral mucous membranes, epistaxis,excessive menstrual bleeding, bleeding gums, hematuria

48
Q

What is thrombotic thrombocytopenia purpura ( TTP)

A
  1. Rate disorder in which thrombi occlude arterioles and capillaries of microcirculation and the client develops hemolytic anemia.
49
Q

What are manifestations of thrombic thrombocytopenia purpura (TTP)

A

Purpura
PETECHIAE
Neurological symptoms

  • can be fatal without treatment
50
Q

What are diagnostic tests for primary thrombocytopenias

A

CBC
PLATELET COUNT: decreased
Antinuclear antibodies (ANA): assess antibodies
Serologic studies for hepatitis viruses, cytomegalovirus, Epstein- Barr virus, toxoplasma, HIV
bone marrow examination

51
Q

What are medications for thrombocytopenia

A

Immunosuppressive meds including glucocorticoids, azathioprine, cyclophosphamide, cyclosporine

52
Q

What are treatments for thrombocytopenia

A

Platelet transfusions for acute bleeding { expected increase is 10,000 ml per unit transfused
Plasmapheresis for acute TTP

53
Q

What surgery is may be needed for thrombocytopenia

A

Splenectomy is the treatment of choice for ITP, which relapsed after glucocorticoids were stopped

54
Q

What is the function of erythrocytes

A

Transport oxygen and some carbon dioxide

55
Q

What is the function of leukocytes

A

Part of the body’s defense against disease

56
Q

What is the role of neutrophils

A

Phagocytosis

57
Q

What is the role of eosinophils

A

Counteracts histamine in allergic reactions

Destroys parasitic worms

58
Q

What is the role of basophils

A

Release histamine and the anticoagulant heparin; called mast cells in the tissues

59
Q

What are lymphocytes

A

Produce antibodies: functions in immunity

60
Q

What is the role of monocytes

A

Phagocytosis: engulf relatively large particles called macrophages in the tissues

61
Q

What is the role of thrombocytes

A

Helps control blood loss by forming a platelet plug and releasing factors necessary for blood clotting.

62
Q

Hydroxyurea

A

Prevents RBC from sickling

63
Q

Sequestration crisis

A

Pooling of large amounts of blood in liver and spleen, most commonly seen in children

64
Q

What is aplastic anemia

A

Bone marrow failure resulting in pantocytopenia

The marrow is replaced by fat

65
Q

What is serum ferritin

A

Iron storage protein produced by the liver, spleen, bone marrow

66
Q

What type of therapy is recommended for aplastic anemia

A

Immunosuppressive therapy

67
Q

What is polycythemia

A

Excess of RBC with HCT above 55%

MED SURG (15 decks)

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