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Adult I > Hematologic problems > Flashcards

Hematologic problems Flashcards

1
Q

Name the five hematologic problems that are caused by a decrease in RBC production.

A
  1. ) Iron deficiency anemia
  2. ) Thalassemia
  3. ) Megaloblastic anemias- Cobalamin (vit b12) and Folic acid deficiency
  4. ) Chronic disease
  5. ) Aplastic
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2
Q

Blood loss is a type of anemia that can either be _____ or ______.

A

Acute- ex: trauma, ruptured aortic aneurysm, GI bleeding.

Chronic- ex: bleeding duodenal ulcer, colorectal cancer, liver disease

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3
Q

Name the hematologic problems that are caused by a increase in RBC destruction.

A
  1. ) Sickle cell disease
  2. ) Hemolytic
  3. ) Acquired hemolytic
  4. ) Hemochromatosis
  5. ) Polycythemia
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4
Q

What are three bleeding problems that are caused by problems with hemostasis?

A
  1. ) Thrombocytopenia
  2. ) Hemophilia and Von Willebrand Disease
  3. ) Disseminated Intravascular Coagulation (DIC)
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5
Q

Name one resistance problem that is caused by decreased WBCs?

A

Neutropenia

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6
Q

Anemia is not a specific disease, but a deficiency in the number of ________ (RBCs), quantity of _______ (Hgb), or volume of packed RBCs (_______).

A

Erythrocytes, hemoglobin, hematocrit

*Leads to tissue hypoxia, which accounts for many of the signs and symptoms of anemia.

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7
Q

Significant diagnostic studies in the evaluation of anemia include:

  1. ) Hemoglobin: ___-___ (female); __-__ (male)
  2. ) Hematocrit: ___-___ (F); __-___(M)
  3. ) RBC count: __-__ (F); ___-__ (M)
  4. ) WBC: _____-_____ (differential), shows sign of infection
  5. ) Platelets: ______-______ (tells ability to clot)
A
  1. ) 12-16, 13-18
  2. ) 38-47%, 40-54%
  3. ) 4-5, 4.5-6
  4. ) 4,000-11,000
  5. ) 150,000-400,000
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8
Q

______ is the measurement of degree of RBC Hemolysis.

A

Bilirubin

* Yellow color shows up in sclera, urine, (Jaundice)

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9
Q

This test differentiates among types of hemolytic anemia, detects immune bodies and Rh factor.

A

Coombs test

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10
Q

Erythropoietin is produced in the ______ and it produces RBCs

A

kidneys

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11
Q

The Erythrocyte Sedimentation rate (ESR) indirectly measures the degree of _________ present in the body.

A

inflammation

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12
Q

This test separates normal Hgb from abnormal and used to detect thalassemia and sickle cell disease.

A

hemoglobin electrophoresis

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13
Q

What test is used to differentiate between malabsorption and pernicious anemia?

A

Schillings test
*Uses radioactive Vit. b12 and measures in urine…if there is a lot of cobalamin, the body is not absorbing b12 properly.

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14
Q

What is ferritin?

A

A major iron storage protein in RBCs

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15
Q

Folic acid is needed for ____ production.

A

RBC

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16
Q

What is serum iron?

A

reflects amount of iron combined with proteins in blood

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17
Q

What is total iron binding capacity (TIBC)?

A

Measures all proteins available for binding iron

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18
Q

What is the reticulocyte count?

A

Immature RBCs

*This may be elevated if anemic, the body is trying to compensate for loss.

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19
Q

What test is done if all of the other anemic tests are inconclusive?

A

Bone marrow aspiration (marrow is where RBC are produced)

  • This provides info about hematopoiesis, hematocytology, and chromosomal abnormalities
  • done at bedside
  • nurse assist physician with sterile procedure
  • done at post. iliac crest
  • apply site pressure for 5-10 min
  • assess vital signs frequently
  • position on side done for 30-60 mins to decrease any bleeding
  • monitor for signs of bleeding for 24 hrs as well as signs of infection
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20
Q

What is the hemoglobin (hgb) level of mild anemia?

A

10-14

*may not have any symptoms

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21
Q

What is the hgb level of moderate anemia?

A

6-10

*may have cardio-pulmonary symptoms (arrhythmia’s, bounding pulse, dyspnea (SOB)

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22
Q

What is the hgb level of severe anemia?

A

<6
*may exhibit pallor, jaundice, pruritus (from increase in bilirubin), glossitis, tachycardia, increase pulse pressure, systolic murmurs, intermittent claudication, heart attack, disorientation, dysphagia, sensitive to cold.

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23
Q

What are some additional assessment findings of anemia that are not listed from severe anemia?

A

palpitations, diaphoresis, bounding pulse, roaring in the ears, glossitis, cheilitis, anorexia, abdominal pain, impaired thought process, neuromuscular manifestations-paresthesias, abnormal lab values- depends on which values as to which anemia they have.

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24
Q

The etiology of iron-deficiency anemia includes 1.) _____ _____, 2.) hemolysis (RBC breakdown) and 3.) _______.

A

1.) Blood loss- 2 mL whole blood contain 1 mg iron, major cause of iron deficiency in adults, chronic blood loss most common through GI and GU systems.

  1. ) Pregnancy
    * normal menstruation is 45 mL- my friend has iron def. anemia and blood loss, so they put her on birth control to control bleeding

**iron def. can also be from poor diets (alcoholism)

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25
Q

What are clinical manifestations of Iron-Deficicency anemia?

A
  • General symptoms of anemia listed before, but vary depending on severity.
  • Pallor is the most common finding
  • Glossitis is the second most common finding
  • Cheilitis (lips)
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26
Q

Iron-Deficiency anemia has what type of collaborative care?

A

-Goal is to treat underlying disease causing reduced intake or absorption of iron

  • Efforts are aimed at replacing iron
    1. ) Nutritional therapy (need iron, vit. b12, folic acid, amino acids, vit c) -liver, muscle meat, eggs, dried fruits, legumes, green leaf. veggies, whole grains, cereal, pasta. Iron is best absorbed in acidic environ. (give with OJ), dilute liquid iron and give with straw (may stain teeth)
    2. ) Oral or occasional parenteral iron supplements
    3. ) Transfusion of packed RBCs
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27
Q

What is drug therapy of Iron-Def. anemia?

A
  1. Oral iron (inexpensive- daily dose is 150-200mg)
  2. ) Paraenteral
    * IV- give a test dose before entire dose
    * IM- use needle to fill syringe, and a separate needle to inject pt. Z-track method, never give more than 2mL.
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28
Q

What is the etiology of Thalassemia?

A
  • A group of diseases involving inadequate production of normal hemoglobin
  • Therefore decreased erythrocyte production
  • Common in ethnic groups from Mediterranean sea area
  • Major and Minor cases
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29
Q

Thalassemia minor is characterized by having one gene of the disease, is ________ frequently, has _______ anemia (6-10), and the body adapts to reduction in Hgb- thus no treatment is indicated.

A

Asymptomatic, moderate

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30
Q

Thalassemia major is determined by __ genes. As the bone marrow responds to the deficit of O2- carrying capacity of the blood, RBC production is stimulated, and marrow becomes paced with ______ erythroid precursors that die.

A

2, immature

  • Also characterized by chronic bone marrow hyperplasia (ex: enlarged cranium from increased bone production)
  • Major is a life threatening disease, causes mental retardation, physical problems, enlarged liver and spleen, jaundice, overactive erythropoesis
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31
Q

What is collaborative care for Thalassemia?

A
  • No specific drug or diet is effective in treating this
  • Thalassemia major: blood transfusions or exchange transfusions with chelating agents that bind to iron to reduce iron overloading, splenectomy.
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32
Q

__________ anemias are a group of disorders caused by impaired DNA synthesis, or presence of abnormally large, immature RBCs. The majority result from deficiency in ________ (Vit. b12) or ______ acid.

A

megaloblastic, cobalamin, folic

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33
Q

_______ anemia is a type of cobalamin deficiency. The inability to absorb Vit. B12, because of the lack of ______ factor.

A

pernicious, intrinsic

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34
Q

Intrinsic factor is secreted by the parietal cells of the gastric mucosa. IF is required for cobalamin absorption in the _____ _____, if IF is not secreted, cobalamin will not be absorbed.

A

distal ilium

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35
Q

Cobalamin deficiency can also occur in the following situations: ___ surgery (wont produce intrinsic factor), chronic _____ of the GI tract, chronic ______ (lack of b12), long term users of H2-______ receptor blockers and proton pump inhibitors.

A

GI, diseases, alcoholics, histamine

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36
Q

What are the general symptoms of pernicious anemia?

A
  • symptoms of anemia related to tissue hypoxia
  • GI manifestations: sore mouth, anorexia, nausea, vomiting, abdominal pain
  • Neuromuscular: weakness, paresthesias of feet and hands, reduced vibratory and positions senses, ataxia (uncoordinated mvmt) , impaired though processes, muscle weakness
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37
Q

What are some diagnostic studies for pernicious anemia?

A
  • RBC’s appear macrosytic and have abnormal shapes
  • Serum cobalamin levels are decreased
  • Serum folate levels may be normal
  • Because these patients at higher risk or gastric cancer, gastroscopy and biopsy of gastric mucosa may be done.
  • Schillings test: radioactive cobalamin administered with amount secreted in urine measured- inability to absorb results in low level secreted in urine.
  • parenteral (nasally) administration of intrinsic factor may also be used; this is followed by increased secretion of cobalamin in urine
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38
Q

What is the management of pernicious anemia?

A
  • Increasing dietary cobalamin ingestion is non effective unless deficit is due strictly to inadequate dietary intake (vegetarians, vegans at risk)
  • Instruct pt on principles of good nutrition
  • Administer parenteral (cyanocobalamin) or hydroxocobalamin- typical 1000 mg daily for two weeks, followed by weekly until hct is normal then monthly for life.
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39
Q

Cobalamin deficiency that is NOT related to intrinsic factor is lack of ______ intake (strict vegetarians)

A

dietary

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40
Q

The collaborative care of cobalamin deficiency includes parenteral or _______ administration of Vit. B12 is the treatment of choice.

A

intranasal

  • Patient can die within 1-3 yrs without treatment
  • This anemia can be reversed with ongoing treatment but long-standing neuromuscular complications can not be reversed.
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41
Q

Another cause of megaloblastic anemia is ____ acid deficiency.

A

folic

  • This acid is required for DNA synthesis (RBC formation and maturation)
  • Clinical symptoms are similar to those of cobalamin, but absence of neurologic problems differentiates them.
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42
Q

What are some common causes of folic acid deficiency?

A
  1. ) Dietary deficiency- increase green leafy veggies, liver, meat, fish, whole grains, citrus fruits
  2. ) Malabsorption syndromes- ex: small bowel problem
  3. ) Drugs- ex: Phenobarbital (anticonvulsant)
  4. ) Increased requirement
  5. ) Alcohol abuse and anorexia
    6) Loss during hemodialysis (filters blood through machine-it can break down RBCs)
43
Q

In folic acid deficiency, serum _____ is low. Serum cobalamin level is normal.

A

folate

  • normal is 3-25 mg/ml (7-57 mol/L)
  • treatment by replacement therapy (usual dose is 1mg orally per day.
  • encourage patients to eat foods with large amounts of folic acid.
44
Q

Anemia of chronic disease is caused by chronic ________, autoimmune and infectious disease (HIV, hepatitis, malaria), ____ failure, malignant diseases, ______ episodes

A

inflammation, heart, bleeding

*Cytokines are produced by these issues and cause RBC to be stored in body and not circulated.

45
Q

Anemia of inflammation is associated with __________ of RBCs, mild shortening of RBC survival (normocytic, normochromic, and hypoproliferative RBCs)

A

underproduction

*usually a mild anemia (10-14) but can become severe if underlying disorder is untreated.

46
Q

Anemia of chronic disease findings include ______ in serum ferritin, increase in ____ stores, and normal folate and _______ levels.

A

increase, iron, cobalamin

*treating underlying cause is best- rarely use blood transfusions, and a conservative use of erythropoietin therapy.

47
Q

What is pancytopenia?

A

A decrease in all blood cell types (RBC, WBC-neutropenic-risk for infection, and platelets-risk for bleeding)

48
Q

Aplastic anemia is characterized by ________ and _______ bone marrow.

A

pancytopenia, hypocellular (less cells than usual)

  • 70% of aplastic anemia is idiopathic
  • Ranges from chronic to critical
49
Q

Aplastic anemia has a low incidence (affecting 2 of 1 million persons) and its etiology includes two major types: 1.) ______ and 2.)______

A
  1. ) Congenital- chromosomal alterations

2. ) Acquired- results from exposure to ionizing radiation, chemical agents, viral and bacterial infections

50
Q

Clinical manifestations of Aplastic anemia include what?

A
  • Abrupt or gradual development
  • Symptoms caused by suppression of any or all bone marrow elements
  • General manifestations of anemia
  • fatigue, dyspnea
  • cardiovascular and cerebral responses
  • neutropenia
51
Q

What are some diagnostic studies for Aplastic anemia?

A

Diagnosis confirmed by LAB studies

  • Low Hgb, WBC, and platelet values
  • Low reticulocyte count
  • Prolonged bleeding time (b/c decrease in platelets)
  • Elevated serum iron and TIBC
  • Hypocellular bone marrow with increased fat content (yellow marrow)
52
Q

What is the nursing and collaborative management for Aplastic anemia?

A
  • Identify and remove causative agent (when possible)
  • Provide supportive care until pancytopenia reverses
  • Prevent complications from infection
  • Prevent hemorrhage
53
Q

Name some nursing interventions for those at risk for infection

A
  • Isolation
  • Asepsis
  • Limit visitors
  • Private room
  • Monitor for S & S of infection
  • Antibiotics in timely manner
  • Monitor labs- WBC
  • **Think PRIORITIES
54
Q

Name some nursing interventions for those with increased bleeding

A
  • Check body secretions of occult blood
  • Assess for petechiae, bruising
  • Use soft toothbrush
  • Avoid injections-if possible
  • Use electric razor
  • Administer blood products (with order)
  • Monitor labs
  • Safety precautions
  • warn about aspirin, advil etc (NSAIDs….can cause GI bleeding)
55
Q

Acute blood loss is caused by sudden hemorrhage such as:

A
  • Trauma
  • Complications of surgery
  • Conditions or diseases that disrupt vascular integrity
    • hypovolemic shock-HR increases, BP decreases, watch urine output-need 30 mL per hour at least!
    • compensatory increased plasma vol. with diminished o2-carrying RBCs
56
Q

Clinical manifestations of acute blood loss include 1.) _____ and 2.) _____.

A
  1. ) Pain
    - internal hemorrhage (tissue distention, organ displacement, nerve compression)
    - retroperitoneal bleeding (numbness, pain in the lower extremities)
  2. ) Shock
    - a major complication
57
Q

Diagnostic studies for acute blood loss include values that may seem ______ or ____ for 2-3 days.

A

normal, high

58
Q

What is collaborative care for acute blood loss?

A
  • Replacing blood volume to prevent shock
  • Identifying the source of the hemorrhage and stopping blood loss
  • Correcting RBC loss
  • Providing supplemental iron
59
Q

Sources of chronic blood loss include: bleeding _____, hemorrhoids, ______ and postmenopausal blood loss.

A

ulcers, menstrual

60
Q

Management of chronic blood loss includes:

A
  • Identifying the sources
  • Stopping the bleeding
  • Providing supplemental iron as needed
61
Q

What is hemolytic anemia?

A

Destruction of hemolysis of RBCs at a rate that exceeds production

  • caused by problems intrinsic or extrinsic to the RBCs
    • Intrinsic forms are usually hereditary and result from defects in RBCs themselves.
    • RBCs are normal in acquired forms which are more common; damage is caused by external factors.
62
Q

Hemolytic anemia has general symptoms of anemia, specific symptoms include ______, and enlargement of the _____ and ______.

A

Jaundice- b/c of bilirubin
spleen, liver (destroyed RBC move to these locations to get absorbed)

**maintenance of renal function is a major focus of treatment.

63
Q

Sickle cell disease is a group of ______, autosomal _______ disorders.

A

inherited, recessive

  • Characterized by the presence of abnormal form of Hgb in the RBC
  • Genetic disorder usually identified in infancy or early childhood
  • incurable and often fatal
  • Predominant in african american
64
Q

The etiology and pathophysiology of Sickle cell disease is abnormal hemoglobin, HgbS, causes the RBC to ______ and ______.

A

stiffen, elongate

  • Erythrocytes take on a sickle shape in response to decrease in O2 levels- cannot pass through vascular system, which causes a lot of pain.
  • Substitution of valine for glutamic acid on the B-globin chain of hemoglobin
65
Q

Sickling episodes have a major pathophysiologic event that are triggered by ___ O2 tension in the blood; ______ is the most common precipitating factor; initially, sickling is _______with re-oxygenation.

A

low, infection, reversible

*for infection interventions- wash hands, flu shot, avoid crowded areas, avoid high altitude

66
Q

What is sickle cell crisis?

A
  • Severe, painful, acute exacerbation of sickling causes a vaso-occluive crisis
  • Severe capillary hypoxia eventually leads to tissue necrosis
  • Life-threatening shock is a result of severe O2 depletion of the tissues and a reduction of the circulating fluid volume.
67
Q

What are the clinical manifestations of sickle cell disease?

A
  • Typical pt is asymptomatic except during sickling episodes.
  • Symptoms may include: (read chart from notes)
    • pain from tissue hypoxia and damage
    • pallor of mucous membranes
    • jaundice from hemolysis (prone to gallstones (cholelithiasis)
68
Q

What are the complications from sickle cell disease?

A
  • Infection is a major cause of morbidity and mortality
  • the function of the spleen becomes compromised from sickled RBCs (autosplenectomy is a result of scarring)
  • Pneumococal pneumonia most common
  • Severe infections can cause aplastic crisis (can lead to shutdown of RBC production)
69
Q

What are diagnostic studies of sickle cell disease?

A
  • Peripheral blood smear
  • Sickling test
  • Electrophoresis of hemoglobin (extracts diff. cells from plasma)
  • Skeletal x-rays
  • Magnetic resonance imaging (MRI)
  • Doppler studies (how well extremities are perfused by blood flow)
  • X-rays
70
Q

What is collaborative care is directed toward sickle cell disease?

A
  • Alleviating symptoms and complications
  • *administer O2
  • Minimizing end-organ damage
  • Promptly treating serious sequelae
  • Teach pt to avoid high altitude
  • Maintain adequate fluid intake
  • Treat infections promptly
  • Avoid crowds to avoid infection
  • *under treatment is a major problem
  • *pain management
  • often pain med tolerant
  • require continuous & breakthrough analgesia with morphine and hydromorphone (IV through PCA pump)
  • multimodal &interdisciplinary approach involving emotional & adjunctive measures
71
Q

What is polycythemia?

A

production and presence of increased numbers of RBC

*include primary & secondary

72
Q

Primary is characterized by polycythemia ____ - a chromosomal mutation that affects RBCs & WBC, which results in increased volume and ______; this predisposes patient to clotting, splenomegaly and ________ (males >60)

A

vera, viscosity, hepatomegaly

73
Q

Secondary polycythemia occurs as a result of ______ state that stimulated increased production of RBC’s or malignant or benign tumor tissue.

A

hypoxic

74
Q

What are clinical manifestations of Polycythemia?

A
  • Hypertension
  • Headache, vertigo, dizziness, tinnitus and visual disturbances
  • Generalized pruritis related to histamine release from increased numbers of basophils
  • paresthesias (tingling)
  • possible angina, heart failure, intermittent claudication and thrombophlebitis
  • hemorrhagic phenomena caused by vessel rupture can result in petechiae, ecchymosis, epistaxis and GI bleeds

***ALL of the above symptoms are caused by blood vessel distention, impaired blood flow, circulatory stasis, thrombosis and tissue hypoxia caused by hypervolemia and hyperviscosity

75
Q

What is the management of Polycythemia?

A
  • Treatment is aimed at reducing blood vol. and viscosity and bone marrow activity
  • Phlebotomy to keep hematocrit 45-48
  • Myelosupression agent to suppress bone marrow activity
  • Paxil or low dose aspirin to manage erythromelalgia
76
Q

What is the nursing management of polycythemia?

A
  • *Maintaining adequate oxygenation
    • smoking cessation
    • avoid high altitudes
    • Maintain adequate hydration (monitor I &O to avoid either over or under hydration;
    • Maintain mobilization (encourage active or passive activities as indicated to prevent venous stasis and thrombus formation)
77
Q

Acquired hemolytic anemia is caused by three categories of extrinsic factors. What are the three?

A
  1. ) Physical factors- ex: dialysis
  2. ) Immune reactions
  3. ) Infectious agents and toxins- ex: malaria
78
Q

What is the treatment and management of acquired hemolytic anemia?

A
  • Supportive care until the causative agent can be eliminated or made less injurious
  • Emergency preparedness is essential for potential hemolytic crises (hydration, electrolyte replacement, corticosteriods, blood products, splenectomy)
  • Folic acid replacement and immuno-suppresive agents for chronic conditions.
79
Q

________ is low platelet count and characterized by less than _______ platelets.

A

Thrombocytopenia, 150,000

80
Q

Hemophilia and Von Willegrand disease are inherited disorder of specific ______ factors

A

clotting

81
Q

Majority of ______ disorders are acquired and caused by certain food, drugs (chemotherapy), and herbs. Other causes include ______ disease, increased platelet _________, splenomegaly, bone marrow failure, hemolytic ______ syndrome.

A
  • platelet,
  • autoimmune: (immune thrombocytopenic purpura- platelets only survive 1-3 days)
  • consumption
  • uremic
82
Q

______ induced thrombocytopenia results from an immune ______ response to heparin therapy and causes venous and _____ clot formation, infarctions and ____.

A

Heparin, mediated, arterial, stroke

*Ex: from DVT

83
Q

What are the clinical manifestation of thrombocytopenia?

A

-Bleeding: epistaxis, gingival, petechiae, ecchymosis and possible severe hemorrhage

84
Q

What is the management of immune thrombocytopenia?

A
  • If asymptomatic-no therapy unless platelet count <30,000
  • Corticosteroids used to treat immune thrombocytopenia
  • Splenectomy if non responsive to steroids (platelets do not get trapped and then circulate in body instead)
  • immunoglobulin
  • platelet transfusion
85
Q

What is the management of thrombotic thrombocytopenia purpura?

A
  • Treat underlying cause (infection) or remove the causative agent
  • Corticosteroids
  • Plasmapheresis (plasma exchange) to reverse the process
86
Q

What is the management of heparin induced thrombocytopenia?

A
  • discontinue heparin/administer protamine sulfate (antidote)
  • Administer thrombin inhibitors
  • May begin coumadin therapy when platelets at 100,000
  • Plasmapheresis
87
Q

______: Sex linked recessive genetic disorder caused by defective or deficient coagulation factor. Has A and B.

A

Hemophilia

88
Q

What kind of hemophilia is the most common and has factor VIII deficiency?

A

A

89
Q

What kind of hemophilia is called the Christmas disease and has factor IX (9) deficiency?

A

B

90
Q

What is Von Willebrand disease?

A

Deficiency of von willebrand coagulation protein

  • *most common coagulation disease in humans
  • not a type of hemophilia, diff type of clotting disease
91
Q

What are clinical manifestations of Hemophilia and Von Willebrand disease?

A
  • Slow persistant, prolonged bleeding
  • Delayed bleeding
  • Uncontrollable hemorrhage
  • Epistaxis
  • Hematuria and GI bleeds
  • Neurologic signs such as pain, anesthesia and paralysis from nerve compression by blood
  • Diagnostics- no change in PT or platelets
  • prolonged bleeding time and PTT because of reduction in factor assays VIII, IX
92
Q

What is the management of Hemophilia and Von Willebrand disease?

A
  • *prevent and treat bleeding
  • replacement of deficient clotting factor
  • preventative care
  • use of blood replacement with acute bleeds
  • most common complication is providing factor replacement too late and stopping too soon (minor bleeds support for 72 hrs, Surgery and trauma may require support for 10-14 days)
93
Q

What are nursing implications for hemophilia and Von Willebrand disease?

A
  • advise genetic counseling
  • acute interventions
    • Stop bleeding (apply pressure/ice, packing area with gel-foam or fibrin foam, apply topical hemostatic agents such as thrombin)
    • Administer specified coagulation factor and monitor for signs of hypersensitivity
    • Assess and manage life threatening complications from major bleeds
    • With joint involvement- total rest of joint; packing joint with ice and provide analgesics to control pain- avoid Aspirin, when bleeding ceases, encourage mobilization of affected joint.
94
Q

Disseminated Intravascular Coagulation (DIC) results from serious ______ and thrombotic disorder that results from abnormally initiated and ________ clotting followed by subsequent decrease in clotting factors and platelets- may lead to ________ hemorrhage.

A

bleeding, accelerated, uncontrollable

95
Q

DIC always results from an underlying problem that must be treated to resolve the condition ( ____, septicemia, malignancies, obstetric complications, hemolytic processes caused by _______ transfusions, infections or immunologic disorders). It is not a disease, but rather an abnormal response of the ______ process

A

shock, incompatible, clotting

96
Q

The manifestations of DIC include bleeding in a person with no _____ history or obvious cause should be suspect, _______ signs can include weakness, malaise and fever

A

previous, nonspecific

97
Q

The bleeding manifestations of DIC include:

A
  • pallor
  • petechiae (red/purple spots on skin from minor hemorrhage)
  • purpura (confluent and extensive patch of petechiae and ecchymoses (purple patch >3mm)
  • oozing around IV sites
  • hematoma (bruise you can feel)
  • occult hemorrhage hemoptysis (blood sputum)
  • orthopnea (difficultly breathing while supine)
  • tachycardia
  • hypotension
  • GI bleeds
  • hematuria (blood in urine)
  • neurologic changes
  • bone and joint pain
98
Q

The thrombotic manifestations of DIC include:

A
  • cyanosis
  • ischemic tissue necrosis
  • dyspnea
  • tachypnea
  • pulmonary emboli
  • acute res. distress syndrome (ARDS)
  • abdominal pain and paralytic ilius
  • kidney damage
  • oliguria leading to renal failure
99
Q

What are the diagnostics of DIC?

A
  • prolonged prothrombin time (PT) , partial thromboplastin time (PTT), activated partial thromboplastin time (aPTT), and thrombin time
  • reduced fibrinogen
  • reduced platelets
  • reduced factor assays
  • D-dimer elevated (This substance is used to rule out blood clot or stroke in the blood)
100
Q

What is the management of DIC?

A
  • stabilize pt with O2, volume replacement
  • recognize pt who are at risk
  • assess for occult/overt bleeding tendencies
  • therapy to resolve underlying disease or problem
  • administer blood products as needed
  • use of anticoagulant therapy for thrombotic tendencies controversial but sometimes heparin or low molecular weight heparin used
101
Q

What is neutropenia?

A

Reduction in total WBC (neutrophil) count less than 4000 and only confirmed by differential counts (determines the % of each type of WBC)

102
Q

Normal neutrophil count is _____ -_____. Moderate neutropenia is ____ - _____ and
severe neutropenia is a neutrophil count of less than ____

A
  • 4,000-10,000
  • 500-1000
  • 500

**the faster the drop and the longer the duration, the greater risk of life threatening infection, sepsis and death.

103
Q

What are some common problems of neutropenia?

A
  • drug induced- chemotherapy, antimicrobial agents, gold, penicillamine, mepacrine
  • hematologic disorders
  • autoimmune disorders (lupus, rheumatoid arthritis)
  • infections
  • severe sepsis, bone marrow cancers, nutritional deficiencies, transfusion reaction, hemodialysis
104
Q

What are nursing interventions of neutropenia?

A
  • institute appropriate isolation and neutropenic precautions
  • hand washing
  • limit visitors
  • monitor signs of systemic and localized infection
  • monitor WBC count and differential
  • eliminate fresh fruits, uncooked veggies, pepper
  • administer prescribed antibiotics in a timely manner
  • eliminated fresh flowers/plants from room
  • teach pt and family how to avoid infection and signs and symptoms of infection.

Adult I (3 decks)

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