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Pathophysiology Final > Hematological Conditions - Anemia > Flashcards

Hematological Conditions - Anemia Flashcards

1
Q

Blood

A
  • plasma

- blood cells

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2
Q

Blood cells

A

Erythrocytes
Leukocytes
(Granulocytes/Agranulocytes (monocytes and lymphocytes)
Thrombocytes - clotting cells (platelets)

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3
Q

Differentials

A

the numbers and differences between the numbers of the 5 different types of white blood cells

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4
Q

Primary Function of Red Blood Cells

A

Transport gasses and assist in acid base balance

  • transport oxygen (O2) from lungs to systemic tissues
  • Carry carbon dioxide from the tissues to the the lungs
  • because RBCs transport oxygen, erythrocyte disorders can lead to tissue hypoxia. This hypoxia accounts for many signs and symptoms of anemia
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5
Q

Primary Function of White Blood Cells

A

Protect the body from infection

phagocytosis - most common

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6
Q

Primary function of Platelets

A

promote blood coagulation

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7
Q

Blood functions to transport (4)

A
  • nutrients
  • hormones
  • metabolic waste products
  • CO2
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8
Q

Blood functions to regulate…

A
  • acid base balance
  • fluid electrolyte balance
  • temperature control
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9
Q

How much fluid volume does blood compose?

A

8% of total body weight

  • 55% plasma
  • 45% formed elements
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10
Q

Albumin - 58% of proteins circulating in blood and maintaining oncotic pressure

A
  • low albumin (seen in cancer states, liver disease, HF) you will see peripheral edema
  • important value to look at to see if the liver is being affected
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11
Q

Clotting mechanisms

A
  • vascular injury and subendothelial exposure
  • platelet plug formation
  • fibrin clot development
  • clot retraction and dissolution
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12
Q

How much ingested iron is absorbed in the body?

A
  • 5-10%
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13
Q

Clotting Mechanisms

A
  • vascular injury and subendothelial exposure
  • platelet plug formation
  • fibrin clot development
  • clot retraction and dissolution
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14
Q

Clotting Mechanisms

A
  • platelets become stickier
  • aspirin inhibits platelet stickiness, so this phase of the clotting process, when the platelets become sticky - we give the enteric coated ASA to keep them from being sticky. Anticoagulant effects.
  • known platelet disorders
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15
Q

Spleen

A

produces RBC during fetal development, filters the blood, and removes defective RBC from circulation, recycles iron from hemoglobin catabolism, filters out bacteria, especially gram+ cocci. Involved in storage, stores platelets and RBC. Any trauma to the spleen or RUQ can cause massive hemodynamic response and internal bleed

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16
Q

Lymph System

A

lymph fluid, lymphatic ducts, lymphatic capillaries and lymphatic nodes

  • Carries fluid from the interstitial fluid to the blood
  • How proteins and nutrients get from the GI tract into the blood
  • Intermediary, between interstitial and vascular spaces
  • Important in preventing edema
  • > 200 lymph nodes - filter pathogens and foreign pathogens
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17
Q

Liver

A
  • produces procoagulants
  • regulates excess iron (stores it)
  • when iron is deficient, the liver produces less hepcidin which means more iron is released from the GI tract and more iron is absorbed
  • hepcidin - regulates the release of stored iron from enterocytes in the GI tract, and from macrophages
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18
Q

Age-related Considerations

A
  • More vulnerable to clotting issues, less ability to fight infection
  • Anytime older adults go out of range with normal values, they have less reserve capacity. They fall ill more quickly because they cannot produce the needed new blood cells as quickly and are more likely to experience clinical manifestations
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19
Q

Assessment of Hematological System - Subjective Data

A 
- important health information 
past health history 
hematological history
social and occupational history
self-care history
activities of daily living
nutrition-metabolic history
elimination pattern 
neurological history
sleep history
sexual-reproductive history 
values and beliefs - jehovahs witnesses
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20
Q

Past Health History

A
  • what have they had before?
  • blood loss? Blood cancers? Any medication that restricts their blood from functioning properly? Any blood thinners or anticoagulants? Immunosuppressants - interfere with the body’s ability to produce WBC and fight infection? Any surgery’s or traumas that have resulted in significant blood loss?
  • medications? Rx and OTC
  • Surgery or other treatments (chemotherapy)
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21
Q

Objective Assessment - Physical examination

A
  • lymph node assessment (should include: symmetry, size, degree of fixation, tenderness, and texture) normal lymph nodes are small, mobile, firm, and nontender
  • palpation of the liver or spleen: usually you cannot feel them. not palpable/when palpating the abdomen. if enlarged, measured as # of cm below the rib border
  • skin assessment (cyanosis or pallor may occur in a patient with a hematological condition: or digital clubbing): assess H2T for rashes. If rash is present. Add pressure to determine if blanchable or non-blanchable (petichial rash, clotting disorders, purple flecks or large patches of purple)
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22
Q

Diagnostic Studies of the Hematological System - Laboratory Studies

A
  • Complete blood count (CBC)
    (RBC, WBC, platelets)
  • Iron metabolism (Iron, TIBC (total iron binding capacity), Ferritin (blood protein that contains iron), transferrin saturation)
  • PT, INR (go together, warfarin), aPTT (heparin) (anticoagulants that end in -eban cannot be trend using PT, IRN, PTT which means they can run into clotting problems unbeknownst
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23
Q

Other Diagnostics

A 
Radiological Studies
Biopsy 
- bone marrow examination 
- lymph node biopsy 
molecular cytogenetics and gene analysis
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24
Q

Three broad causes of anemia

A
  1. Decreased RBC production
  2. Blood loss
  3. Increased RBC destruction
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25
Q

Decreased RBC production

A

Iron deficiency - most common cause of decreased RBC production

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26
Q

Blood Loss

A

Acute

Chronic

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27
Q

Increased RBC destruction

A

sickle cell disease

Instrinsic (abnormal Hgb)

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28
Q

Anemia is classified as:

a) morphological
b) etiological

A

morphological
- cellular characteristics
- descriptive, objective laboratory infections
- based on erythrocyte size and color.
Etiological
- underlying cause
- related to the clinical conditions causing anemia
- although the morphological system is the most accurate means of classifying anemias, it is easier to discuss client care by focusing on the cause of the anemia

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29
Q

Anemia is not a disease, it is a manifestation of. a pathological process

A

Asking why?

  • why are the RBC low
  • subjective/objective assessment matters - have things from the physical exam that should be backed up with diagnostic tests
  • then look into meds
  • the entire time asking “why” is this happening and what pathological process is happening here that I need to understand
  • identified through history and physical exam and classified by laboratory review
  • it is classified by laboratory review of the CBC, reticulocyte count, and peripheral blood smear. once anemia is identified, further investigation is done to determine its cause
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30
Q

Clinical Manifestations

A
  • caused by the body’s response to tissue hypoxia - compensatory chest pain, rise in troponin because the heart is having to work harder. fatigue because the muscles are not getting the oxygen they need, increased resp rate, lower BP - peripheral system wants to make it as easy as possible so vasodilation
  • three states of anemia (> 100 is the normal range for hemoglobin)
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31
Q

Mild Anemia

A

hemoglobin between 100 - 120 up to the lower end of normal. will not create symptoms, if symptoms develop, it is because the client has an underlying disease or is experiencing a compensatory response to heavy exercise. maybe palpitations and mild dyspnea and mild fatigue.

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32
Q

Moderate Anemia

A

60-100. patients continue to live. cardiopulmonary symptoms are increased and may be experienced even on rest.

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33
Q

Severe Anemia

A

hemoglobin < 60. many clinical symptoms, throughout many systems, need immediate intervention to preserve life

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34
Q

jaundice

A

increased concentration in serum bilirubin because when the RBC breaks down it releases bilirubin. usually our body can handle it, but when they are being destroyed to quickly the body cant keep up and we will get jaundice

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35
Q

Treatment of Anemia

A
  • blood or blood transfusions

- correcting the cause is the goal of anemia

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36
Q

Anemia - a deficiency in the

A
  • number of erythrocytes (red blood cells)
  • Quantity or quality of hemoglobin
  • volume of packed RBCs (hematocrit)
37
Q

Normal Hemoglobin levels

A

120-150

38
Q

Clinical Manifestations - Integumentary Manifestations

A
  • Pallor (decreased hemoglobin, decreased blood flow to skin)
  • Jaundice (increased concentration of serum bilirubin)
  • Prutitus (increased serum and skin bile salt concentrations)
  • in addition to skin, the sclera of the eyes and mucous membranes should be evaluated for jaundice because they reflect the integumentary changes more accurately, especially in a dark-skinned individual
39
Q

Clinical Manifestations Anemia - cardiopulmonary manifestations

A
  • additional attemtps by the heart and lungs to provide adequate O2 to the tissues
  • cardiac output maintained by increasing the heart rate and stroke volume
  • in extreme cases, or when concomitant heart disease is present, angina pectoris and myocardial infarction may occur if myocardial O2 needs cannot be met
  • heart failure, cardiomegaly, pulmonary and systemic congestion, ascites, and peripheral edema may develop if the heart is overworked for an extended period of time
40
Q

Nursing Assessment Anemia - subjective data

A 
- important health informtation 
past health history
medications
surgery or other treatments
dietary history
symptoms
41
Q

Objective data Anemia

A
  • general
  • integumentary
  • respiratory
  • cardiovascular
  • gastro-intestinal
  • neurological
  • possible diagnostic findings
42
Q

Nursing Management of Anemia - Goals

A
  • assume normal activities of daily living
  • maintain adequate nutrition
  • develop no complications related to anemia
43
Q

Anemia - Nursing Implementation

A
  • bood or blood product transfusions
  • drug therapy (ex.erythropoietin and vitamin supplements)
  • volume replacement
  • dietary and lifestyle changes
  • oxygen therapy
  • client teaching (nutrition intake, compliance with safety precautions to prevent falls and injury)
44
Q

Anemia - ultimate goal of therapy

A

correcting the cause of the anemia

45
Q

Anemia - Age-Related Consideration

A
  • common in older adults
    chronic disease
    nutritional deficiencies
  • signs and symptoms may go unrecognized or may be mistaken for normal aging changes
    (in healthy older men, a modest decline in hemoglobin occurs with age at about 10g/L between ages 70 and 88 years. d/t decreased production of androgens. minimal decrease in hemoglobin in healthy women.
  • S&S in older adults - pallor, confusion, ataxia, fatigue, worsening cardiovascular and respiratory problems
  • many older adults with anemia have a nutritional type of anemia.
46
Q

Decreased Erythrocyte Production

A
  • Erythropoietin (EPO) is a glycoprotein primarily produced in the kidney’s
  • increased number of stem cells committed to RBC production
  • Shortens the time to mature RBCs
47
Q

Lifespan of an RBC

A

120 days

48
Q

Three alterations in erythropoiesis may decrease RBC production:

A
  1. decreased hemoglobin sythesis (may lead to iron-deficiency anemia, thalassemia, and sidroblastic anemia)
  2. Defective DNA synthesis in RBCs (e.g., cobalamin (vit b12) deficiency, folic acid deficiency, may lead to megaloblastic anemias
  3. Diminished availability of erythrocyte precursors may result in aplastic anemia and anemia of chronic disease
49
Q

Decreased Hgb Synthesis: Iron-Deficiency Anemia

A
  • one of the most common chronic hematological disorders and the most common nutritional disorder in the world
  • iron is present in all RBCs as heme in hemoglobin and in a stored form
  • Heme accounts for two-thirds of the body’s iron
50
Q

Those most susceptible to iron-deficiency are:

A
  1. the very young
  2. those on poor diets
  3. Women in their reproductive years
51
Q

Iron-Deficiency Anemia - Etiology

A
  • Inadequate dietary intake
  • malabosrption (as iron absorption occurs in the duodenum, malabsorption syndromes may involve disease of the duodenum in which the absorption surface is altered or destroyed)
  • Blood loss (major sources of chronic blood loss involve the GI and GU systems - peptic ulcer, gastritis, esophagitis, diverticula, hemorrhoids and neoplasia, menstrual bleeding) (dialysis treatment may induce iron-deficiency anemia as a result of blood lost in the dialysis equipment and frequent blood sampling)
  • Hemolysis
52
Q

Iron Deficiency Anemia - Clinical Manifestations

A
  • pallor is the most common finding
  • glossitits is the second most common (inflammation of the tongue)
  • cheilitis (inflammation of the lips)
  • headache, paresthesias, and a burning sensation of the tongue. caused by lackof iron in the tissues
53
Q

Iron-Deficiency Anemia - Diagnostic Studies

A
  • Laboratory findings (hb, hct, MCV (size of RBCs), reticulocytes, serum iron, TIBC (total iron binding capacity), transferrin, ferritin, bilirubin, serum B12, folate - both B vitamins necessary for RBC proliferation)
  • stool guaiac test/fecal occult blood test
  • endoscopy
  • colonoscopy
  • bone marrow biopsy
54
Q

IDA - collaborative care

- Goal is to treat the underlying Cause

A
  • increased intake of iron
  • nutritional therapy
  • oral or occasional parenteral iron supplements
  • tranfusion of packed RBCs
55
Q

IDA - Drug Therapy

A
  • Oral Iron (inexpensive, convenient, factors to consider - enteric-coated or sustained-release capsules are counterproductive, and daily dose is 150-200mg (can be ingested three or four daily doses)
  • iron is absorbed best from the duodenum and proximal jejunum, therefore enteric-coated or sustained-release capsules, which release iron farther down the GI tract, are counterproductive and expensive.
  • best absorbed as ferrous sulphate in an acidic environment (to avoid binding the iron with food, should be taken about an hour before meals, when the duodenal mucosa is most acidic. Taking iron with vitamin C or orange juice also enhances absorption.
  • liquid should be diluted and ingested through a straw
56
Q

Adverse Effects of Oral Iron

A
  • heartburn
  • constipation
  • diarrhea
  • may individuals who need supplemental iron cannot tolerate ferrous sulphate because of the effects of the sulphate base. however, ferrous gluconate may be an acceptable substitute
57
Q

Parenteral Iron

A
  • Indicated for malabsorption, oral iron intolerance, need for iron beyond normal limits, poor client compliance
  • can be given IM or IV
  • IM may stain skin
  • An iron-dextran complex (INFeD) contains 50 mg/mL of elemental iron in 2 mL. Sodium ferrous gluconate and iron sucrose are alternatives and may provide less risk of life-threatening anaphylaxis.
  • because IM solutions may stain the skin, separate needles should be used for withdrawaing the solution and for injecting the medication. A z-track injection technique should be used.
58
Q

IDA - Nursing Management

At-risk Groups

A
  • premenopausal women
  • pregnant women
  • persons from low socioeconomic backgrounds
  • older adults
  • individuals experiencing blood loss
59
Q

IDA - Nursing Management

A
  • diet teaching
  • supplementation
  • Discuss diagnostic studies
  • Emphasize compliance
  • Iron therapy for 2-3 months after hemoglobin levels return to normal
  • Clients who require lifeling iron supplementation should be monitored for potential liver problems related to iron storage
60
Q

Anemia of Chronic Disease Decreased # of RBC Precursors

A
  • Underproduction of RBCs
  • Mild shortening of RBC survival
  • Chronic inflammatory, autoimmune, infectious, or malignant diseases can lead to anemia of chronic disease.
  • RBCs are usually normocytic, normochronic, and hypoproliferative. The anemia is usually mild, but it can be more severe. This type of anemia is primarily immune-driven.
61
Q

Anemia of Chronic Disease - Causes

A
  • renal disease (primary factor: decreased erythropoietin)
  • chronic liver disease
  • inflammatory, autoimmune, infectious, or malignant disease
  • any condition that causes increased RBC destruction (autoimmune hemolysis) accompanied by failure to increased erythropoiesis will contribute to anemia
  • Myelosuppression and decreased erythropoiesis caused by disease, medications (chemotherapy) or radiation will contribute to normochromic (enough hemoglobin in the red blood cells, but not enough red blood cells), normocytic (regular sized RBC just not enough of them) anemia
  • Examoles of chronic endocrine diseases include hypopituitary, hypothyroid, and adrenal deficiency
62
Q

Anemia of Chronic Disease Findings

A

increased serum ferritin (because of the infection or inflammation causing the anemia)
increase iron stores
normal folate and cobalamin levels (vitamin Bs)

63
Q

Treating Underlying cause is best

A
  • rarely blood transfusion
  • erythropoietin therapy (used for anemia related to renal disease and may be used for anemia related to cancer and its therapy. however, it is used conservatively because of the risk of thromboembolism and mortality is increased in some clients)
64
Q

Acute Blood Loss

A
  • result of sudden hemorrhage from: trauma, complications of surgery, disrupted vascular integrity
65
Q

Concerns with Acute Blood Loss

A
  • hypovolemic shock

- Reduced plasma volume (diminished O2 because fewer RBCs are available)

66
Q

Acute Blood loss - Clinical Manifestations

A
  • Cause (Body’s attempt to maintain adequate blood volume and O2)
  • Pain (Internal Hemorrhage - tissue distension, organ displacement, nerve compression)
  • it is essential to understand that the clinical S&S the client is experiencing are more important than the lab values.
  • Ex. an adult with bleeding ulcer who had 750-mL hematemesis within the past 30 minutes may have postural hypotension, but may have normal values for hb and hct. over the ensuing 36-48 hr most of the blood volume deficit will be replaced by the movement of fluid from the extravascular into the intravascular space. only at these latter times will the hemoglobin and hematocrit reflect blood loss.
67
Q

Acute Blood Loss - Pain

A 
Retroperitoneal bleeding
- abd pain and distention 
- severe back and lower quadrant pain
- femoral neuropathy 
Shock is the major complication
68
Q

Acute Blood Loss - Diagnostic Studies

A
  • laboratory data do not adequately assess RBC problems for 2-3 days
  • however, once the plasma volume has been replaced, the RBC mass will be less concentrated. At this time, RBC, hemoglobin, and hematocrit levels are low and reflect the actual blood loss.
69
Q

Acute Blood Loss - Collaborative Care

A
  • replacing blood volume to prevent shock
  • identifying the source of the hemorrage
  • Stopping blood loss
  • Correcting RBC loss
  • Providing supplemental iron
  • IV fluids used in emergencies include dextran, hetastarch, albumin, and/or crystalloid electrolyte solutions such as lactated Ringers
  • The body needs 2-5 days to manufacture more RBCs in response to increased erythropoietin. Consequently blood transfusions (packed RBCs) may be needed if the blood loss is significant
70
Q

Acute Blood Loss - Nursing Management

A
  • may be impossible to prevent if caused by trauma
  • postoperative clients (monitor clients)
  • no need for long-term treatment
71
Q

Chronic Blood Loss - Sources similar to iron-deficiency anemia

A
  • Bleeding ulcer
  • Hemorrhoids
  • Menstrual and postmenopausal blood loss
  • the effects of chronic blood loss usually are related to the depletion of iron stores and are considered as iron-deficiency anemia
72
Q

Management of Chronic Blood Loss

A
  • identify source
  • stop bleeding
  • use supplemental iron if needed
73
Q

Increased RBC Destruction: Hemolytic Anemia

A
  • Destruction or hemolysis of RBCs at a rate that exceeds production
  • Intrinsic hemolytic anemia (abnormal hemoglobin, enzyme deficiencies, RBC membrane abnormalities - usually hereditary)
74
Q

Extrinsic Hemolytic Anemia

A
  • more common than intrinsic
  • Acquired
  • Damage caused by external factors
  • The spleen is the primary site of destruction of RBCs that are old, defective, or moderately damaged.
75
Q

Hemolytic Anemia - Jaundice and Enlarged Spleen and Liver

A

Jaundice - destroyed RBCs cause increased bilirubin

Enlarged spleen and liver - hyperactive with macrophage phagocytosis of defective RBCs

76
Q

Accumulation of hemoglobin molecules can obstruct renal tubules

A

Tubular necrosis

77
Q

Acquired Hemolytic Anemia - Three extrinsic categories

A
  1. physical factors
  2. Immune reactions
  3. Infectious agents and toxins
78
Q

Physical Factors - Acquired Hemolytic Anemia

A
  • physical destruction of RBCs results from extreme force on the cells
  • hemodialysis, extracorporeal circulation ( Circulation of the blood outside the body, as through a heart-lung machine or artificial kidney), prosthetic heart valves.
  • the force needed to push blood through abnormal vessels, such as those that have been burned or affected by vascular disease (diabetes mellitus), may physically damage RBCs/
79
Q

Immune Reactions

A
  • antigen-antibody reactions destroy RBCs
  • Isoimmune reactions (antibodies develop against antigens, blood transfusions)
  • Autoimmune reactions (develop antibodies against their own RBCs) - autoimmune hemolytic reactions may be idiopathic, developing with no prior hemolytic history as a result of immunoglobulin G covering the RBCs, or secondary to other autoimmune diseases, leukemia, or lymphoma, or reactions to drugs (penicillin, ibuprofen, metformin)
80
Q

Infectious Agents and toxins

A
  • foster hemolysis in three ways
    1. invading RBCs and destroying contents
    2. Releasing hemolysis substances
    3. Generating an antigen-antibody reaction
81
Q

what is the only way the body loses iron?

A

blood loss

82
Q

where does absorption of iron take place?

A

duodenum and jejunum
- if someone has a portion of bowel removed this has important implications for iron absorption and many drug absorptions

83
Q

where is 2/3 of the body’s iron stored?

A

as the heme part of the hemoglobin molecule

84
Q

where is 1/3 of the body’s iron stored?

A

as ferritin in the bone marrow, liver, spleen, and macrophages

85
Q

What is transferrin

A
  • made in the liver and used for the production of the iron - the degree to which transferrin is saturated is an accurate picture of how much iron is available to the RBCs
86
Q

what happens when iron stores are depleted after it is used and not replaced?

A

hemoglobin production decreases

87
Q

when is iron recycled in the body?

A

after RBCs are phagocytized by macrophages in the liver and spleen

88
Q

is iron deficiency more common in men or women, and why?

A

in women. very uncommon in men. because of menstruation

Pathophysiology Final (7 decks)

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