Hematology Flashcards

(150 cards)

1
Q

What is Anemia?

A

Lower than normal hemoglobin and fewer than normal circulating erythrocytes; a sign of an underlying disorder

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2
Q

What are the two types of Anemia?

A

Hypoproliferative
Hemolytic

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3
Q

Explain Hypoproliferative anemia.

A
  • Defect in production of erythrocytes (RBCs)

Caused by iron, vitamin B12, or folate deficiency (vegans and vegetarians at risk) , decreased erythropoietin production by kidneys, cancer, bone marrow damage

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4
Q

Explain Hemolytic anemia.

A
  • Excess destruction of erythrocytes (RBCs)

Caused by altered erythropoiesis, or direct injury to the erythrocyte.

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5
Q

What laboratory findings are associated with iron deficiency anemia (hypoproliferative) ?

(TABLE 29-1: Classification of Anemias)

A

CBC findings: ↓ MCV (microcytic)

Other labs: :↓ Iron, ↓ Ferritin

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6
Q

What laboratory findings are associated with vitamin B12 deficiency anemia (hypoproliferative)?

(TABLE 29-1: Classification of Anemias)

A

CBC findings: ↑ MCV (macrocytic / megaloblastic)

Other labs: ↓ Vitamin B12

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7
Q

What laboratory findings are associated with folate deficiency anemia (hypoproliferative) ?

(TABLE 29-1: Classification of Anemias)

A

CBC findings: ↑ MCV (macrocytic)

Other labs: ↓ Folate

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8
Q

What laboratory findings are associated with anemia caused by decreased erythropoietin production (such as in chronic kidney disease)(hypoproliferative) ?

(TABLE 29-1: Classification of Anemias)

A

CBC findings: Normal MCV

Other labs: ↓ Erythropoietin level, ↑ Creatinine, ↑ Ferritin , ↓ Iron

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9
Q

What laboratory finding is typically seen with anemia related to cancer or inflammation (hypoproliferative) ?

(TABLE 29-1: Classification of Anemias)

A

CBC findings: Normal MCV

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10
Q

What causes bleeding anemia?

(TABLE 29-1: Classification of Anemias)

A

Gastrointestinal bleeding

Epistaxis (nosebleeds)

Trauma

Genitourinary bleeding

Menorrhagia

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11
Q

What laboratory findings occur with anemia due to acute or chronic bleeding?

(TABLE 29-1: Classification of Anemias)

A

CBC findings: ↓ H&H

Other labs: ↓ Iron, ↓ Ferritin

Note:
Hgb and Hct may initially be normal immediately after bleeding begins.

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12
Q

What laboratory findings occur with hemolytic anemia caused by altered erythropoiesis such as sickle cell disease or thalassemia (Hemolytic anemia)?

(TABLE 29-1: Classification of Anemias)

A

CBC findings: ↓ MCV

Other findings: Fragmented RBCs, Abnormal RBC shapes

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13
Q

What laboratory finding may occur with hemolysis caused by hypersplenism (Hemolytic anemia ?

(TABLE 29-1: Classification of Anemias)

A

CBC findings: ↑ MCV

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14
Q

What blood cell finding may indicate autoimmune hemolytic anemia?

(TABLE 29-1: Classification of Anemias)

A

Presence of spherocytes

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15
Q

What blood smear finding is associated with mechanical heart valve–related anemia (Hemolytic anemia ?

(TABLE 29-1: Classification of Anemias)

A

Fragmented red blood cells

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16
Q

What are the two main categories of hemolytic anemia?

A

Inherited hemolytic anemia

Acquired hemolytic anemia

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17
Q

What inherited diseases can cause hemolytic anemia?

A

Sickle cell disease

Thalassemia

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18
Q

What enzyme deficiency can cause inherited hemolytic anemia?

A

Glucose-6-phosphate dehydrogenase (G6PD) deficiency

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19
Q

What antibody-related conditions can cause acquired hemolytic anemia?

A

Autoimmune hemolytic anemia

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20
Q

What non–antibody-related conditions can cause acquired hemolytic anemia?

A

Disseminated intravascular coagulation (DIC) - most common!!

Hypersplenism

Infection

Liver disease

Mechanical heart valve

Microangiopathic hemolytic anemia

Paroxysmal nocturnal hemoglobinuria

Toxins

Trauma (highlighted)

Uremia

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21
Q

What types of infections can cause hemolytic anemia?

A

Bacterial infections

Parasitic infections

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22
Q

How does anemia manifest itself?

A
  • Fatigue, weakness, malaise (due to lack of blood oxygen)
  • Pallor or jaundice
  • Cardiac, GI, neurologic and respiratory symptoms (lack of oxygen)
  • Tongue changes: smooth, red tongue
  • Nail changes: brittle and ridged
  • Angular cheilitis:
  • Pica: eating dirt
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23
Q

What type of anemia results from red blood cell destruction?

a) Iron deficiency
b) Hemolytic
c) Hypoproliferative
d) None of the above

A

b) Hemolytic

Rationale: Hemolytic anemia results from red blood cell destruction. In hemolytic anemias, premature destruction of erythrocytes results in the liberation of hemoglobin from the erythrocytes into the plasma. The bilirubin concentration rises, and increased erythrocyte destruction leads to tissue hypoxia, which in turn stimulates erythropoietin production, reflected in an increased reticulocyte count.

remember, reticulocytes are immature erythrocytes

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24
Q

What diagnostic testing do we do for Anemia?

A
  • Hemoglobin and hematocrit
  • Reticulocyte count
  • RBC indices
  • Iron studies
  • Vitamin B12
  • Folate
  • Haptoglobin level: if low=hemolytic anemia (this protein made in liver, it rids hemoglobin that is outside if RBC)
  • Erythropoietin levels (will be high)
  • Bone marrow aspiration
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25
What is the medical management of Anemia?
* Correct or control the cause * Transfusion of packed RBCs * Immunosuppressive therapy (if cause of anemia is caused by antibodies/autoimmune disorder)
26
What are the treatment of chronic types of Anemia?
* Dietary therapy * Iron or vitamin supplementation: iron, folate, B12: make sure to teach patient proper iron supplementation (e.g. take on empty stomach and with vit C. Iron absorption reduced by food and milk )
27
What is Sickle Cell disease?
A type of hereditary hemolytic anemia. RBCs are sickle shaped, may adhere to walls and decrease blood flow which causes ischemia/infection, pain and swelling. Fever is sign of sickle cell crisis.
28
What is Thalassemia?
Type of hereditary hemolytic anemia. where the patient have impaired hemoglobin production and small RBC's - O2 carrying capability reduced.
29
What allows oxygen to attach to RBCs?
Hemoglobin
30
What is Hypochromia?
↓Hemoglobin in RBC seen in Thalassemia
31
What is Microcytosis?
Small RBC seen in Thalassemia
32
What is Glucose-6-phosphate dehydrogenase deficiency?
Type of Hemolytic Anemia. Patients are deficient in enzyme required to stabilize cell wall (scaffolding) of RBCs, this makes them easy to hemolyze
33
What is Immune hemolytic anemia?
Form of anemia where antibodies attack RBC's
34
What is Hereditary hemochromatosis?
Too much iron in blood stream due to excess Fe absorption in GI tract=excess Fe deposits on organs.
35
What is Iron deficiency anemia?
Low iron in diet makes it hard for RBC's to form Type of Hypoproliferative anemia.
36
How can renal disease cause anemia?
Kidneys produce erythropoietin. Kidney disease can impact this production. Keep in mind dialysis patients (receive EPO) Type of Hypoproliferative anemia.
37
What is anemia caused by inflammation?
Type of Hypoproliferative anemia. R/T chronic diseases such as rheumatoid arthritis, chronic infections, many cancers
38
What is aplastic anemia?
Type of Hypoproliferative anemia. T cells attack and damage bone marrow stem cells, marrow replaced by fat. Can result in neutropenia, thrombocytopenia as well
39
What is Megaloblastic anemia?
Large RBC's: * Folic acid deficiency * Vitamin B12 deficiency Both needed for normal DNA synthesis. Lack of this will make the RBC's produce abnormally.
40
What is Neutropenia?
Decreased production or increased destruction of neutrophils (<2000/mm3) Neutropenia increases the risk of infection.
41
What lab indicate neutrophil count?
Absolute neutrophil count (ANC) low indicates high risk for infection.
42
How do we treat neutropenia medically ?
Depend on cause. If cancer is the reason we would be treating cancer etc. Neupogen/filgrastim is a drug that we can use to treat neutropenia. Stimulates bone marrow to produce neutrophils.
43
What are the nursing managements in our patients w/ Neutropenia?
patient education, preventing and managing complications
44
What are the three major mechanisms that cause neutropenia? (Chart 29-5: Causes of Neutropenia)
Decreased production of neutrophils Ineffective granulocytopoiesis Increased destruction of neutrophils
45
What conditions can cause neutropenia due to decreased production of neutrophils? (Chart 29-5: Causes of Neutropenia)
Aplastic anemia (due to medications or toxins) Chemotherapy Metastatic cancer, lymphoma, leukemia Radiation therapy
46
What conditions can cause neutropenia due to increased destruction of neutrophils? (Chart 29-5: Causes of Neutropenia)
Bacterial infections Hypersplenism Immunologic disorders (e.g., systemic lupus erythematosus) Medication-induced neutropenia Viral infections (e.g., infectious hepatitis, mononucleosis)
47
What lifestyle or home environment changes can help decrease infection risk? (Chart 29-7: Home Care Checklist – The Patient at Risk for Infection)
Patients may need to modify: Diet, Activity level, Home environment to reduce infection exposure.
48
What hygiene practices help reduce infection risk? (Chart 29-7: Home Care Checklist – The Patient at Risk for Infection)
Good hand hygiene, Oral hygiene, Total body hygiene, Maintaining skin integrity.
49
What environmental exposures should patients avoid to reduce infection risk? (Chart 29-7: Home Care Checklist – The Patient at Risk for Infection)
Avoid: Cleaning birdcages, Cleaning litter boxes, Gardening/soil exposure, Fresh flowers in stagnant water.
50
What nutritional recommendations help reduce infection risk? (Chart 29-7: Home Care Checklist – The Patient at Risk for Infection)
High-calorie diet, High-protein diet, Fluid intake of about 3000 mL/day - unless restricted
51
What social precautions should patients take to prevent infection? (Chart 29-7: Home Care Checklist – The Patient at Risk for Infection)
* Avoid people with infections, * Avoid crowded environments.
52
What respiratory interventions help prevent infection when mobility is limited? (Chart 29-7: Home Care Checklist – The Patient at Risk for Infection)
Perform deep breathing exercises, Use an incentive spirometer every 4 hours while awake.
53
What sexual health precautions are recommended to reduce infection risk? (Chart 29-7: Home Care Checklist – The Patient at Risk for Infection)
Use adequate lubrication with gentle vaginal manipulation during intercourse, Avoid anal intercourse.
54
What signs and symptoms of infection should patients report to their healthcare provider? (Chart 29-7: Home Care Checklist – The Patient at Risk for Infection)
Fever, Chills, Cough (wet or dry), Breathing problems, White patches in the mouth, Swollen glands, Nausea or vomiting, Persistent abdominal pain, Persistent diarrhea, Urinary changes, Red, swollen, or draining wounds, Skin sores or lesions, Persistent vaginal discharge, Severe fatigue.
55
What self-monitoring skills should patients demonstrate? (Chart 29-7: Home Care Checklist – The Patient at Risk for Infection)
Patients should be able to: Monitor for signs of infection, Recognize abnormal symptoms.
56
What communication instructions should patients understand regarding infection symptoms? (Chart 29-7: Home Care Checklist – The Patient at Risk for Infection)
Patients should know: Who to contact, How to report symptoms, When to report signs of infection.
57
What is Lymphopenia?
Lymphocyte count less than 1500/mm3
58
What are causes of Lymphopenia?
* Exposure to radiation * Long-term use of corticosteroids - immunosuppresses patients because lymphocyte count drops. * Infections * Neoplasms * Alcohol abuse - malnourished
59
What is Polycythemia?
Increased volume of RBCs - ↑ hematocrit May be caused by dehydration.
60
What is secondary polycythemia?
Excessive production of erythropoietin from : Reduced amounts of oxygen, Cyanotic heart disease, Nonpathologic conditions or neoplasms [think high altitude living (Leadville, CO)], COPD, Obs sleep apnea, heavy smoker)
61
What does moving from lower elevation to higher elevation do to our bodies?
Lower altitude we will have normal RBC count.. Moving to higher elevation our WOB will increase due to thinner air and our kidneys will start to release more erythropoietin to produce more RBCs for increased O2 delivery. This is why people living at high altitude often develop secondary polycythemia due to increased erythropoietin production.
62
How do we treat Polycythemia?
Treatment not needed if condition is mild Treat underlying cause Therapeutic phlebotomy - bleeding the patient.
63
Is the following statement true or false? Polycythemia is a form of anemia.
False Rationale: Polycythemia is caused by excessive production of erythropoietin. Examples of conditions causing polycythemia include smoking, obstructive sleep apnea, chronic obstructive pulmonary disease, severe heart disease, living at high altitudes or exposure to low levels of carbon monoxide. Secondary polycythemia can result from neoplasms that stimulate erythropoietic production.
64
Bleeding disorders are :
Failure of hemostatic mechanisms.
65
What are causes of Bleeding disorders?
* Trauma * Platelet abnormality - too little or not working properly * Coagulation factor abnormality - occur deeper within the body such as subQ hematomas, joint space bleeding
66
What are our medical managements in patients w/ bleeding disorders?
* Specific blood products (i.e. platelet transfusion) * if fibrinolysis is excessive we can use a hemostatic agent such aminocaproic acid is given to control bleeding.
67
What are our nursing managements in patients w/ bleeding disorders?
* limit injury, * assess for bleeding, * bleeding precautions
68
What is Thrombocytopenia?
Low platelets. Have many different causes such as bone-marrow related, platelet destruction or increased use of platelets for clotting.
69
What is Immune thrombocytopenic purpura (ITP) ?
Primary ITP is acquired immune disorder that causes platelet antibodies. Secondary ITP is related to underlying disorders such as lupus or RA.
70
What is Hemophilia?
A-deficient/defective Factor VIII; B-deficient/defective Factor IV; bleeding in joints
71
What is Von Willebrand disease?
Deficiency in v WFactor-mucosa-associated bleeding (nose-bleeds, heavy menses, easy bruising, long bleeds from cuts/surgical incisions)
72
True / False Platelet defects can lead to bleeding disorders.
True
73
How does poor nutritional status increase infection risk? (Chart 29-6: Risk Factors – Development of Infection and Bleeding in Patients with Hematologic Disorders)
Low protein stores lead to: Decreased immune response, Impaired immune function (anergy)
74
How does deconditioning or decreased mobility increase infection risk? (Chart 29-6: Risk Factors – Development of Infection and Bleeding in Patients with Hematologic Disorders)
Decreased mobility leads to: Reduced respiratory effort, Pooling of respiratory secretions, Increased risk of infection
75
How can antibiotic therapy increase infection risk? (Chart 29-6: Risk Factors – Development of Infection and Bleeding in Patients with Hematologic Disorders)
Antibiotics may cause superinfection, often fungal infections.
76
How can sepsis increase bleeding risk? (Chart 29-6: Risk Factors – Development of Infection and Bleeding in Patients with Hematologic Disorders)
Sepsis leads to increased platelet consumption, raising bleeding risk.
77
How does increased intracranial pressure (ICP) increase bleeding risk? (Chart 29-6: Risk Factors – Development of Infection and Bleeding in Patients with Hematologic Disorders)
Elevated blood pressure may cause rupture of blood vessels.
78
How does liver dysfunction increase bleeding risk? (Chart 29-6: Risk Factors – Development of Infection and Bleeding in Patients with Hematologic Disorders)
The liver produces clotting factors. Liver dysfunction causes decreased clotting factor synthesis.
79
How does renal dysfunction increase bleeding risk? (Chart 29-6: Risk Factors – Development of Infection and Bleeding in Patients with Hematologic Disorders)
Renal dysfunction causes decreased platelet function.
80
How does alcohol abuse increase bleeding risk? (Chart 29-6: Risk Factors – Development of Infection and Bleeding in Patients with Hematologic Disorders)
Alcohol causes: Bone marrow suppression → decreased platelet production, Impaired platelet function Liver dysfunction → decreased clotting factor production.
81
What is Dysproteinemia?
Increases bleeding risk in patients w/ bleeding disorders. Protein coats surface of platelet, leading to decreased platelet function; protein causes increased blood viscosity, which leads to stretching of capillaries an increased risk for rupture and bleeding.
82
What rectal or vaginal products should patients at risk for bleeding avoid? (Chart 29-8: Home Care Checklist – The Patient at Risk for Bleeding)
Suppositories Enemas Tampons
83
Why should patients at risk for bleeding avoid constipation? (Chart 29-8: Home Care Checklist – The Patient at Risk for Bleeding)
Straining during bowel movements can increase risk of bleeding.
84
What physical activities should patients avoid to reduce bleeding risk? (Chart 29-8: Home Care Checklist – The Patient at Risk for Bleeding)
Contact sports Aggressive manual labor
85
What personal hygiene practices reduce bleeding risk? (Chart 29-8: Home Care Checklist – The Patient at Risk for Bleeding)
Use an electric razor for shaving Use a soft-bristled toothbrush
86
What should patients do before dental work or invasive procedures? (Chart 29-8: Home Care Checklist – The Patient at Risk for Bleeding)
Patients should notify their healthcare provider before undergoing: * Dental work * Any invasive procedures
87
What medications and substances should patients at risk for bleeding avoid? (Chart 29-8: Home Care Checklist – The Patient at Risk for Bleeding)
* Aspirin-containing medications * Alcohol
88
What symptoms should patients be able to recognize related to bleeding? (Chart 29-8: Home Care Checklist – The Patient at Risk for Bleeding)
* Easy bruising * Bleeding gums * Nosebleeds * Blood in urine or stool * Prolonged bleeding from cuts
89
What are the three main mechanisms that cause thrombocytopenia? (TABLE 29-3: Causes and Management of Thrombocytopenia)
Decreased platelet production Increased platelet destruction Increased platelet consumption
90
What is the management for thrombocytopenia caused by medications such as sulfa drugs or methotrexate? (TABLE 29-3: Causes and Management of Thrombocytopenia)
Discontinue the medication
91
What is the management for thrombocytopenia caused by chronic alcohol abuse? (TABLE 29-3: Causes and Management of Thrombocytopenia)
Refrain from alcohol Referral for substance use disorder treatment
92
How is thrombocytopenia caused by chemotherapy managed? (TABLE 29-3: Causes and Management of Thrombocytopenia)
Delay chemotherapy Reduce dose Platelet transfusion
93
What conditions can cause antibody-related platelet destruction? (TABLE 29-3: Causes and Management of Thrombocytopenia)
Immune thrombocytopenic purpura (ITP) Systemic lupus erythematosus (SLE) Malignant lymphoma Chronic lymphocytic leukemia (CLL)
94
How is thrombocytopenia caused by medications that trigger immune destruction of platelets managed? (TABLE 29-3: Causes and Management of Thrombocytopenia)
Discontinue the medication
95
How is thrombocytopenia caused by infection (sepsis or post-viral infection) managed? (TABLE 29-3: Causes and Management of Thrombocytopenia)
Treat the infection
96
How is thrombocytopenia caused by splenic sequestration managed? (TABLE 29-3: Causes and Management of Thrombocytopenia)
Splenectomy may be required if severe
97
How is thrombocytopenia caused by disseminated intravascular coagulation (DIC) managed? (TABLE 29-3: Causes and Management of Thrombocytopenia)
Treat the underlying cause triggering DIC
98
How is thrombocytopenia caused by major bleeding managed? (TABLE 29-3: Causes and Management of Thrombocytopenia)
Transfusion support Surgical intervention if needed
99
How is thrombocytopenia caused by severe pulmonary embolism or severe thrombosis managed? (TABLE 29-3: Causes and Management of Thrombocytopenia)
Treat the clot
100
What is our assessment for patients with Anemia?
* Health history and physical exam * Laboratory data - CBC's * Presence of symptoms and impact of those symptoms on patient’s life; fatigue, weakness, malaise, pain (sickle cell) * Nutritional assessment (vegan, vegetarian) * Medications * Cardiac and GI assessment (GI bleed may cause anemia) * Blood loss: menses, potential GI loss * Neurologic assessment (not enough oxygen to brain will affect mentation)
101
What are Collaborative Problems and Potential Complications of the Patient with Anemia ?
* Heart failure * Angina r/t low oxygenation * Paresthesia: damage to peripheral nerves= pins/needles sensation e.g. from sickle cell * Confusion: less oxygen to brain * Injury related to falls - orthostatic hypotension * Depressed mood - less oxygen to brain.
102
What are our Planning and Goals for the Patient with Anemia?
Understand and treating : * decreased fatigue * attainment or maintenance of adequate nutrition * maintenance of adequate tissue perfusion * compliance with prescribed therapy e.g iron supplements. B12, folate * absence of complications
103
What are our interventions for the patient w/ anemia?
* Balance physical activity, exercise, and rest * Maintain adequate nutrition * Maintain adequate perfusion * Patient education to promote compliance with medications and nutrition * Monitor VS and pulse oximetry; provide supplemental oxygen as needed * Monitor for potential complications
104
What are our assessments of patients w/ Sickle Cell disease?
* Health history and physical exam * Pain assessment * Laboratory data: CBC's, C- shaped hemoglobin * Presence of symptoms and impact of those symptoms on patient’s life: swelling, fever, pain * Sickle cell crisis assessment * Blood loss: menses, potential GI loss * Cardiovascular and neurologic assessment
105
What are collaborative problem and potential complications that we may see in patients with Sickle Cell Disease?
* Hypoxia, ischemia, infection * Avoid dehydration to prevent the blood from getting too viscous. * CVA: stroke * Anemia * Acute and chronic kidney disease - filtration difficulty * Heart failure - lack of O2 * Impotence - less perfusion * Poor compliance * Substance abuse: chronic pain=chronic pain med use
106
What are our interventions for patients w/ sickle cell disease?
* Pain management due to chronic pain * Manage fatigue due to anemia * Infection prevention * Promote coping * Education of disease process * Monitor for complications
107
Name 4 Acquired Coagulation Disorders that are not hereditary.
* Liver disease: Because most coagulation factors synthesized here (NASH, Cirrhosis) * Vitamin K deficiency: nutrition may impact (eat leafy greens!) * Complications of anticoagulant therapy (e.g., Heparin-induced thrombocytopenia - HIIT - to much patient may bleed out) ) * Disseminated intravascular coagulation (DIC)
108
What is Disseminated Intravascular Coagulation (DIC)?
Not as disease but sign of underlying disorder. Possibly life threatening if severe enough. Altered hemostasis mechanism causes massive clotting in microcirculation. As clotting factors are consumed in one area, bleeding occur in other areas. Symptoms are related to tissue ischemia and bleeding
109
What may trigger DIC?
Sepsis - always keep DIC in mind with septic patients. Trauma, Shock, Cancer, Abruptio placentae, Toxins, and Allergic reactions
110
S/S r/t DIC :
Tissue ischemia Bleeding
111
How do we diagnose/detect DIC?
Lab tests
112
How do we treat DIC?
* treat underlying cause, * correct tissue ischemia caused by clotting. * replace fluids and electrolytes - maintain blood pressure, * replace coagulation factors, * use heparin or LMWH (low molecular weight heparin)
113
Explain the Patho behind DIC Mainly for review.
1) Significant illness occur (sepsis, trauma, malignancy,complication from pregnancy) 2) Pathologic activation of coagulation and impaired fibrinolysis (initially) 3) Causes both further bleeding and thrombus formation in microcirculation 4) Occur at the same time : * Consumption of platelets and clotting factors → bleeding. * Thrombus formation → Tissue ischemia → End-organ damage → end organ failure,
114
What S/S should we be assessing for to detect DIC?
Be aware of patients who are at risk for DIC (trauma, sepsis) and assess for signs and symptoms of the condition Assess for signs and symptoms and progression of thrombi and bleeding
115
What two major clinical problems must be assessed in disseminated intravascular coagulation (DIC)? (Chart 29-10: Assessment – Assessing for Thrombosis and Bleeding in Disseminated Intravascular Coagulation)
Microvascular thrombosis (clotting) Microvascular and frank bleeding - DIC causes both excessive clotting and bleeding simultaneously.
116
What integumentary signs indicate microvascular thrombosis in DIC? (Chart 29-10: Assessment – Assessing for Thrombosis and Bleeding in Disseminated Intravascular Coagulation)
* Decreased temperature and sensation * Increased pain * Cyanosis of extremities, nose, or earlobes * Focal ischemia * Superficial gangrene
117
What integumentary signs indicate bleeding in DIC? (Chart 29-10: Assessment – Assessing for Thrombosis and Bleeding in Disseminated Intravascular Coagulation)
* Petechiae (including periorbital and oral mucosa) * Bleeding gums * Oozing from wounds * Bleeding at injection or catheter sites * Epistaxis - nosebleed * Diffuse ecchymoses * Subcutaneous hemorrhage * Joint pain
118
What circulatory findings may indicate microvascular thrombosis in DIC? (Chart 29-10: Assessment – Assessing for Thrombosis and Bleeding in Disseminated Intravascular Coagulation)
Decreased pulses Capillary refill > 3 seconds
119
What circulatory sign may indicate bleeding or hemodynamic instability in DIC? (Chart 29-10: Assessment – Assessing for Thrombosis and Bleeding in Disseminated Intravascular Coagulation)
Tachycardia
120
What respiratory findings may indicate microvascular thrombosis in DIC? (Chart 29-10: Assessment – Assessing for Thrombosis and Bleeding in Disseminated Intravascular Coagulation)
Hypoxia Dyspnea Chest pain with deep inspiration Decreased breath sounds over areas of embolism *** Think PE
121
What respiratory findings may indicate bleeding complications or lung injury in DIC? (Chart 29-10: Assessment – Assessing for Thrombosis and Bleeding in Disseminated Intravascular Coagulation)
High-pitched bronchial breath sounds Tachypnea Signs of acute respiratory distress syndrome (ARDS)
122
What gastrointestinal findings may indicate bleeding in DIC? (Chart 29-10: Assessment – Assessing for Thrombosis and Bleeding in Disseminated Intravascular Coagulation)
Hematemesis Melena (tarry stools) Bright red rectal bleeding Retroperitoneal bleeding s/s: * Firm, distended abdomen * Abdominal tenderness * Increased abdominal girth
123
What renal findings may indicate microvascular thrombosis in DIC? (Chart 29-10: Assessment – Assessing for Thrombosis and Bleeding in Disseminated Intravascular Coagulation)
Decreased urine output Increased creatinine Increased BUN
124
What renal finding may indicate bleeding in DIC? (Chart 29-10: Assessment – Assessing for Thrombosis and Bleeding in Disseminated Intravascular Coagulation)
Hematuria
125
What neurologic findings may indicate microvascular thrombosis affecting the brain in DIC? (Chart 29-10: Assessment – Assessing for Thrombosis and Bleeding in Disseminated Intravascular Coagulation)
Decreased alertness Decreased orientation Decreased pupillary reaction Reduced response to commands Decreased strength and mobility
126
What neurologic findings may indicate bleeding or neurologic complications in DIC? (Chart 29-10: Assessment – Assessing for Thrombosis and Bleeding in Disseminated Intravascular Coagulation)
Anxiety Restlessness Altered level of consciousness Headache Visual disturbances Conjunctival hemorrhage
127
What are Collaborative Problems and Potential Complications of the Patient with DIC ?
* Kidney injury * Gangrene * Pulmonary embolism or hemorrhage * Acute respiratory distress syndrome - PE may cause ARDS * Stroke - clot travel to brain.
128
What are planning and treatment goals w/ DIC?
* Maintenance of hemodynamic status * Maintenance of intact skin and oral mucosa * Maintenance of fluid balance - ensure blood doesn't get too viscous. * Maintenance of tissue perfusion - ischemia * Enhanced coping * Absence of complications
129
What are our interventions for patients w/ DIC?
* Assessment and interventions should target potential sites of organ damage * Monitor and assess carefully * Avoid trauma and procedures that increase the risk of bleeding, including activities that would increase ICP
130
Is the following statement true or false? Disseminated intravascular coagulation is caused by alteration of normal hemostatic mechanisms.
True Rationale: Normal hemostatic mechanisms are altered in DIC. The inflammatory response generated by the underlying disease initiates the process of inflammation and coagulation within the vasculature. Normal anticoagulation pathways are impaired and fibrinolysis is suppressed allowing small clots to form. As platelets and clotting factors are consumed by the microthrombi, coagulation fails, leading to excessive clotting and bleeding.
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What is Polycythemia Vera?
Too many blood cells. Bone marrow is hypercellular and increased production of erythrocytes, leukocytes and platelets. Blood become viscous. It is a proliferative disorder of the myeloid stem cells. Median age is 60 yrs and survival after onset 14-20 yrs.
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What are the clinical manifestations of Polycythemia Vera?
Manifestations are r/t blood viscosity. Neuro: headache, dizziness, vision changes, TIA GI: early satiety, abdominal pain/discomfort (splenomegaly?) Cardio-vasc: ruddy complexion, angina (hard to pump blood that is thicker) , claudication (pain in legs/arms while exercising - DVT), dyspnea, HTN, thrombophlebitis Generalized pruritus, and erythromelalgia (burning pain and erythema in fingers or toes, uric stones (gout)
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What diagnostic studies would we do to identify Polycythemia Vera?
* elevated H&H * presence of an acquired mutation in the JAK2 gene (positive for this gene = positive diagnosis)
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What are risks associated w/ Polycythemia Vera?
* thrombosis complications (CVA, MI) * bleeding from dysfunctional platelets
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What are the treatments for Polycythemia Vera?
* Phlebotomy (initially 500 mL or once or twice a week)= bleed the patient * Chemotherapeutic agents to suppress marrow function * Aggressive management of atherosclerosis * Allopurinol to prevent gout * Aspirin for pain * Platelet aggregation inhibitors * Interferon-alfa
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What is Systemic Lupus Erythematosus ?
Inflammatory, autoimmune disorder affecting almost all organs body, antibodies attack. More likely in women, African americans, Indigenous population, Hispanics and Asians. Cause not known
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What are the clinical manifestations of Systemic Lupus Erythematosus ?
*Fever * Fatigue * Skin rashes * Joint pain
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What are the most common involved systems with Systemic Lupus Erythematosus?
* Mucocutaneous * Musculoskeletal * Renal * Nervous * CV * Respiratory
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How do we diagnose Lupus?
+antinuclear antibody (ANA), antiDNA test, CBC
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How do we manage Lupus medically?
Preventing progressive loss of organ function Immunosuppression : * Monoclonal antibodies * Corticosteroids * Antimalarial agents * NSAIDS
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What are our nursing managements focusing on for patients w/ lupus?
* Fatigue * Impaired skin integrity * Body imaging disturbance * Avoid sun - may cause rashes. * Periodic screenings * Health promotion techniques * Dietary consults * Risk for infections - due to immunosuppression drugs, * Osteoporosis - corticosteroid use may lead to osteoporosis.
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What skin conditions are associated w/ lupus?
Rash, and lesions
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Which medication may cause hypoproliferative anemia?
Chloramphenicol
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What is the definitive method of establishing the diagnosis of iron deficiency anemia?
Bone marrow aspiration.
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What are foods rich in iron?
Food sources rich in iron include organ meats (e.g., beef or calf’s liver, chicken liver), other meats, beans (e.g., pinto, black, and garbanzo beans), leafy green vegetables, raisins, and molasses. Eating iron-rich foods with a source of vitamin C (e.g., orange juice) improves iron absorption. Oral iron is best absorbed on an empty stomach, making it important for patients to be instructed to take the supplement approximately 1 hour before or 2 hours after meals.
146
True / False Aplastic anemia is a life - threatening condition.
True : Aplastic anemia is a life-threatening condition associated with bone marrow failure evidenced by pancytopenia (i.e., anemia, neutropenia, and thrombocytopenia; lower-than-normal counts of erythrocytes, neutrophils, and platelets)
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Which agents are associated with aplastic anemia?
benzene and benzene derivatives (i.e., airplane glues, paint remover, dry cleaning solutions). Certain toxic materials, including inorganic arsenic, glycol ethers, plutonium, and radon,
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With Hemochromatosis patients are at increased risk of developing :
Clots
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What medication do we give for HIT , when discontinuing Heparin?
Argatroban
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Cryoprecipitate is given to treat :
DIC It is given to replace fibrogen, factor VIII and XIII