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Adult Health > Chapter 31 exam 1 (b) > Flashcards

Chapter 31 exam 1 (b) Flashcards

1
Q

What are 3 ways to have anemia?

A
  • Deficient nutrients; Iron, Cobalamin (B12), Folic Acid
  • Decreased erythropoietin (kidneys)
  • Decreased iron deficiency (liver)
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2
Q

If you have decreased iron deficiency (liver), you have ____?

A

Anemia

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3
Q

If you have decreased erythropoietin (kidneys) you have ____?

A

Anemia

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4
Q

if you have deficient nutrients; Iron, Cobalamin (B12), Folic acid you have ____?

A

Anemia

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5
Q

What is the meaning of CYTIC? Example, Microcytic and Macrocytic.

A

SIZE

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6
Q

What is the meaning of CHROMIC?

A

COLOR

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7
Q

What morphologic change has an etiology caused by Acute Blood Loss, Hemolysis, Chronic Kidney Disease, Aplastic Anemia, Sickle Cell Anemia?

A

Normocytic & normochromic

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8
Q

What morphologic change has an etiology caused by IRON DEFICIENCY?

A

Microcytic (small) & hypochromic (pale color)

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9
Q

What morphologic change has an etiology caused by COBALAMIN (B12) DEFECIENCY, FOLIC ACID DEFICIENCY

A

Macrocytic/ Megaloblastic (big) & normochromic

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10
Q

What is an example of a condition that causes NORMOCYTIC & NORMCHROMIC morphologic change?

A

Sickle Cell Anemia, Acute blood loss, hemolysis, Aplastic Anemia

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11
Q

What is an example of a condition that causes MICROCYTIC (small) & HYPOCHROMIC morphologic change?

A

Iron Deficiency

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12
Q

What is an example of a condition/conditions that cause Macrocytic (megaloblastic) & Normochromic. *Pregnant can have this.

A

B12 & Folic Acid Deficiency

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13
Q

What is another name for MICROCYTIC?

A

MEGALOBLASTIC meaning large in size.

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14
Q

A DECREASE in Hemoglobin synthesis is caused by?

A

IRON DEFICIENCY

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15
Q

This causes ________?

  • Decreased Hemoglobin Synthesis
  • Defective DNA Synthesis
  • Decreased # of RBC precursors (think pieces to help build RBC)
A

Decreased RBC production

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16
Q

Defective DNA Synthesis is affected by what TWO deficiency’s. *Think pregnant woman

A

Cobalamin (Vitamin B12) deficiency & Folic acid deficiency

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17
Q

Blood Loss Anemia can be split into what TWO categories?

A

Acute and Chronic

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18
Q

ACUTE blood loss anemia is caused by what?

A

TRAUMA & Blood vessel RUPTURE

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19
Q

Chronic blood loss anemia is caused by what?

A
  • Gastritis (inflammation)
  • Menstrual flow
  • Hemorrhoids
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20
Q

Trauma & Blood vessel rupture are considered ACUTE or CHRONIC blood loss anemia?

A

ACUTE

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21
Q

-Gastritis (inflammation)
-Menstrual flow
-Hemorrhoids
are considered ACUTE or CHRONIC blood loss anemia?

A

CHRONIC

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22
Q

Increased RBC destruction hemolytic anemias can be broken down into what TWO type of Hemolytic anemias?

A

INTRINSIC & EXTRINSIC (Aquired Hemolytic anemia)

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23
Q
  • Abnormal hemoglobin (Hb S–sickle cell anemia)
  • Enzyme deficiency (G6PD: glucose-6-phosphate dehydrogenase)
  • Membrane abnormalities (paroxysmal nocturnal hemoglobinuria, hereditary spherocytosis

this is INTRINSIC or EXTRINSIC (Acquired Hemolytic Anemia)

A

INTRINSIC

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24
Q
  • Physical trauma (prosthetic heart valves, extracorporeal circulation)
  • Antibodies (isoimmune and autoimmune)
  • Infectious agents and toxins

this is INTRINSIC or EXTRINSIC (Acquired Hemolytic Anemia)

A

EXTRINSIC

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25
Q

Clinical Anemia Manifestations of the INTEGUMENT

A

Pallor and Jaundice

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26
Q

Clinical Anemia Manifestations of the EYES

A

Blurred Vision, Rectinal hemorrhage

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27
Q

Clinical Anemia Manifestations of the MOUTH

A

Glossitis (inflammation), smooth tongue

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28
Q

Clinical Anemia Manifestations of the CV

A
  1. Palpatations
  2. BOUNDING pulse
  3. Increased HR, Increased pulse pressure, MURMURS & BRUITS, Angina (chest pain), MI
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29
Q

Clinical Anemia Manifestations of the PULMONARY

A

Increased HR, orthopnea (problems laying supine breathing), dyspnea @ rest

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30
Q

Clinical Anemia Manifestations of the Neurologic

A

Vertigo, irritability, depression. Imparied thought process

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31
Q

Clinical Anemia Manifestations of the GI

A

Anorexia, difficulty swallowing, sore mouth, hepatomegaly, splenomagaly

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32
Q

Clinicall Anemia Manifestations of the Musculoskeletal

A

Bone Pain

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33
Q

What is a GENERAL clinical manifestation of overall ANEMIA?

A

FATIGUE

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34
Q

How do you calculate MEAN CORPUSCULAR VOLUME (MCV)?

A

(Total Hematocrit + Total # RBCs) X 10

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35
Q

I am a immature erythrocyte (makes RBCs) and I have nucleus.

A

Reticulocytes

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36
Q

I am a MATURE erythrocyte and I have (no nucleus or i have a nucleus)

A

no nucleus

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37
Q

Definition of _______
iron-bindingblood plasmaglycoproteinsthat control the level of freeironin biologic fluids; needed to transport iron in the formation of hemoglobin

A

Transferrin

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38
Q

Measures the body’s capacity to bind iron with transferrin

A

TIBC

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39
Q

This deficiency develops from; Inadequate dietary intake, Malabsorption (GI issues), Blood loss, Hemolysis

A

Iron-deficiency

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40
Q

This is One of the most common chronic hematologic disorders. What is Fe?

A

Iron-deficiency

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41
Q

What deficiency am I?
- Pallow, Glossitis (inflamed tongue), Chelitis (inflamed lips), HA (headache), paresthesias (tingling sensation), burning sensation on Tongue

A

Iron-deficiency

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42
Q

I am best absorbed in the duodenum and proximal jejunum.

A

Iron

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43
Q

What is the daily dosage of Iron for treatment?

A

150-200 mg of elemental iron

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44
Q

When is the best time to take Iron before meals?

A

1 hour before meals.

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45
Q

Taking Iron with (what vitamin) and (what juice) ENHANCES iron absorption.

A

Vitamin C & Orange Juice

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46
Q

Why would you have to INGEST iron with meals?

A

Gastric side effects caused from orange juice and vitamin C. (The absorption through fluid is faster than digesting)

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47
Q

The patient’s teeth is STAINED from drinking (Undiluted liquid iron, or diluted iron through a straw)?

A

Diluted Iron through a straw

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48
Q

GI side effects of Iron (3)

A

heartburn, constipation, and diarrhea

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49
Q

heartburn, constipation, and diarrhea are GI side effects of ________

A

Iron

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50
Q

Iron Deficiency Anemia: INTERVENTION
After teaching the patient about Iron supplements how long should they patient continue it after hemoglobin has returned to normal?

A

2-3 months

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51
Q

INTERVENTIONS for what ______ DEFECIENCY?
-Teaching: compliance with supplements and diet
-Supplements need to be continued for 2-3 months after hgb has returned to normal
�

A

Iron Deficiency Anemia

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52
Q

What NURSING DIAGNOSES can be made for IRON DEIFICIENCY ANEMIA?

A
  • Fatigue
  • Altered Nutrition: Less than body requirements
  • Ineffective self-health management
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53
Q

What TWO types of Megaloblastic/ Macrocytic (Big RBC) Anemias are there?

A

Cobalamin (B12) Deficiency & Folic Acid (Folate) Deficiency

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54
Q

What is Cobalamin?

A

Vitamin B12 Deficiency

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55
Q

What is another name for Cobalamin (B12) Deficiency

A

Pernicious anemia

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56
Q

What is another name for Pernicious Anemia and what is it?

A

It is Cobalamin (Vitamin B12) Deficiency in which there is LOW VITAMIN B12

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57
Q

What is the cause/etiology of Cobalamin (B12) Deficiency?

A

Lack of adequate intrinsic factor (this helps with absorption)

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58
Q

WHAT MEGALOBLASTIC ANEMIA IS THIS?
Clinical Manifestations: tissue hypoxia, shiny/beefy tongue, N/V, anorexia, ABD pain; NEUROLOGIC PROBLEMS <– (extremely important to remember)

A

Cobalamin (B12) Deficiency aka Pernicious Anemia

- This deficiency has neurologic problems Folic Acid Deficiency does not!!!

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59
Q

WHAT MEGALOBLASTIC ANEMIA IS THIS?

Diagnostic Studies: Serum folate levels, SCHILLING TEST (ingestion of radioactive cobalamin), endoscopy

A

Cobalamin (B12) Deficiency aka Pernicious Anemia

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60
Q

WHAT MEGALOBLASTIC ANEMIA IS THIS?
Collaborative Care: IM (injection) or IHN (inhalation) cobalamin (daily for 2wks, wkly until hct is normal, monthly for life)

A

Cobalamin (B12) Deficiency aka Pernicious Anemia

61
Q

Without Cobalamin how long will the patient live?

A

1-3 years

62
Q

Why is Folate important?

A

Required for DNA synthesis

63
Q

WHAT MEGALOBLASTIC ANEMIA IS THIS? Clinical Manifestations: similar to cobalamin deficiency; NO NEUROLOGIC SYMPTOMS

A

Folic Acid (Folate) Deficiency

64
Q

What is the etiology for Folic Acid (Folate) Deficiency

A

Lack of adequate intrinsic factor

65
Q

Whats is the ETIOLOGY of B12 Deficiency and Folate Deficiency?

A

Lack of adequate intrinsic factor

66
Q

What is the DIAGNOSTIC TEST for Folic Acid (Folate) Deficiency?

A

Low serum folate levels

67
Q

WHAT ANEMIA IS THIS?
By performing Collaborative Care: Replacement therapy
- Encourage patient to eat foods high in folate: Green leafy vegetables, liver, meat, fish, legumes, whole grains

A

Folic Acid (Folate) Deficiency

68
Q

The most COMMON type of Megaloblastic anemia is?

A

PERNICIOUS ANEMIA aka Cobalamin deficiency

69
Q

What disease development cannot be prevented? Cobalamin and Folic Acid Deficiency’s are what?

A

Megaloblastic Anemias

70
Q

What TWO things can you do to have symptom reversal in Megaloblastic anemias?

A

Early detection and treatment

71
Q

What do you want to ENSURE/PROTECT for a patient who has Meagloblastic anemia?

A

-Ensure that injuries are not sustained because of the diminished sensations to heat and pain resulting from the neurologic impairment
-Protect patient from falling, burns, and trauma.

72
Q

What kind of appropriate SCREENINGS do you perform in a patient with Megaloblastic anemia?

A

Screen for Gastric Cancer (remember B12 and Folic Acid Deficiency are related to absorption problems)

73
Q

What do you CAREFULLY ASSESS for in patients with Megaloblastic Anemia?

A

Neurological difficulties

74
Q

What is “not enough blood being produced” Anemia.

A

Aplastic

75
Q

Decrease of all blood cell types RBCs, WBCs, and Platelets and hypocellular bone marrow?

A

Pancytopenia

76
Q

If a patient is Aplastic what signs and symptoms do they have?

A

S/S: Range from chronic condition managed with erythropoietin or blood transfusions to a critical condition with hemorrhage and sepsis

77
Q

Range from chronic condition managed with erythropoietin is signs and symptoms of what?

A

Aplastic Anemia

78
Q

blood transfusions to a critical condition with hemorrhage and sepsis signs and symptoms of what?

A

Aplastic Anemia

79
Q

What are the TWO type of Aplastic Anemia (how can you get it?

A

Congenital (born with it) and acquired

80
Q

MANIFESTATIONS of what type of Anemia?
-can manifest abruptly (over days) or insidiously over weeks to months
-can vary from mild to severe
-Symptoms caused by suppression of any or
all bone marrow element fatigue and dyspnea (SOB)

A

Aplastic Anemia

81
Q

MANIFESTATIONS of what type of Anemia?

  • cardiovascular and cerebral responses
  • neutropenia (low neutrophil count) - risk for infection & septic shock and death
  • Even a low-grade fever (above 100.4° F [38° C]) should be considered a medical emergency
  • Thrombocytopenia is manifested by a predisposition to bleeding (e.g., petechiae, ecchymosis, epistaxis)
A

Aplastic Anemia

82
Q

What type of DIAGNOSTIC test/ LABS can you do to check for APLASTIC ANEMIA?

A

CBC, diff/plt, retic count, PT/PTT/INR, Fe, TIBC

83
Q

Idiopathic/ autoimmune, chemical agents and toxins, durgs, radiation, viral & bacterial infection are CAUSES of what type of APLASTIC ANEMIA?

A

Acquired

84
Q

Fanconi syndrome, thrombocytopenia, Schwachman-Diamond Syndrome are CAUSES of what type of APLASTIC ANEMIA?

A

Congenital

85
Q

In NSG & collaborative management what type of IMMUNOSUPRRESSIVE THERAPY can you give the Patient?

A

Cytoxan

86
Q

What are Aplastic Anemia: NSG & Collaborative Management?

A
  • Immunosuppressive therapy: cytoxan
  • Antithymocyte globulin
  • Hematopoietic stem cell transplant: Need
  • HLA-matched donor
  • Supportive blood transfusions
87
Q

What are CAUSES of Anemia of Chronic DIsease?

A

Causes: inflammatory, autoimmune, infectious, malignant disease processes

88
Q

What is the meaning of “Anemia of inflammation”?

A

underproduction of RBCs & shorter RBC lifespan

89
Q

What is “underproduction of RBCs & shorter RBC lifespan

A

Anemia of inflammation

90
Q

What are the SIZE & COLOR of Chronic Disease?

A

Normocytic, normochromic, hypoproiferative (don’t make enough)

91
Q

What are manifestations of Anemia of Chronic Disease?

A

Manifestation: fatigue, pallor; ferritin & Fe stores, NL folate & cobalamin

92
Q

What are interventions that treat Anemia of Chronic Disease?

A

(treat cause (pRBCs, epogen subcut)

93
Q

This is an Anemia cause by erythrocyte destruction: Autosomal, recessive, SINGLE POINT MUTATION on beta-hgb chain

A

Sickle Cell Anemia

94
Q

What are the 4 types of Sickle Cell Anemia?

A
  • Sickle Cell Anemia (most SEVERE)
  • Sickle Cell-THALLASSEMIA (inherits two anemias one from each parent - less common and less severe)
  • Sickle cell Hgb C disease - inherits two anemias – one from each parent (less common and less severe)
  • Sickle cell trait – very mild to asymptomatic (carrier)
95
Q

I am very mild to asymptomatic (carrier). What Sickle Cell am I?

A

Sickle cell trait

96
Q

What type of Sickle cell is…. it inherits two anemias – one from each parent (less common and less severe)

A

Sickle cell Hgb C disease

97
Q

What type of Sickle cell is… – inherits two anemias – one from each parent (less common and less severe)

A

Sickle cell THALLASSEMIA

98
Q

What is the MOST SEVERE type of Sickle Cell?

A

SICKLE CELL ANEMIA

99
Q

Sickle Cell Anemia causes pain where?

A

ALL OVER YOUR BODY

100
Q

What happens to the Brain, Eye, Lung, Heart, and Kidney in Sickle Cell Anemia?

A

Brain-Thrombosis or Hemorrhage
Eye-Hemorrhage, Retinopathy, BLINDNESS
Lung- Acute chest syndrome, pulmonary embolism, pneumonia
Heart - Heart failure
Kidney - Hematuria (blood in urine) & Renal Failure

101
Q

What happens to the Spleen, Bones & Joints, Liver-gallbladder, Penis, and Skin in Sickle Cell Anemia?

A

Spleen-Splenic Atrophy
Bones & Joints- Hand and food Syndrome OSTEONECROSIS
Liver & Gallbladder - Hepatomegaly, Gallstones
Penis- priapism (cant get erect)
Skin - Stasis ulcers of hands, ankles, and feet

102
Q

THIS IS WHAT?
Increased # of RBCs
Increased Blood Viscosity (hyperviscosity)
Increased Volume (hypervolemia)

A

Polycythemia

103
Q

What is Polycythemia (3)

A

Increased # of RBCs
Increased Blood Viscosity (hyperviscosity)
Increased Volume (hypervolemia)

104
Q

Primary polycythemia is __ ________

A

not preventable

105
Q

In Polycythemia what is SECONDARY (treat what?)

A

hypoxemia

106
Q

What are manifestations of Polycythemia?

A

INCREASED blood viscosity, organ congestion, enlarged spleen & liver, hypercoagulopathies, clotting

107
Q

INCREASED blood viscosity, organ congestion, enlarged spleen & liver, hypercoagulopathies, clotting. This is what anemia?

A

Polycythemia

108
Q

What NURSING INTERVENTIONS for Polycythemia?

A
  • Adequate oxygenation
  • Control COPD symptoms
  • Teach patient to stop smoking
  • Avoid high altitudes
  • Perform phlebotomy
  • Myelosuppressive drugs used: monitor S/Es, ensure compliance. Suppress production of RBC’s
109
Q

What are the NURSING MANAGEMENT for Thrombocytopenia?

A
  • Diagnoses: Risk for bleeding, deficient knowledge
  • Administer appropriate ordered medications
  • Observe and document patient response
  • Teaching: avoid heparin, medication management, when to call MD
110
Q

What are the 3 types of Thrombocytopenia?

A
  • Immune Thrombocytopenic purpura (ITP): ABNL PLT destruction
  • Thrombotic Thrombocytopenic Purpura (TTP): ABNL agglutination of PLTs
  • Heparin-Induced Thrombocytopenia (HIT): Immune response to heparin
111
Q

Immune response to Heparin is what ANEMIA?

A

Heparin-Induced Thrombocytopenia (HIT)

112
Q

ABNL agglutination of PLTs is what ANEMIA?

A

Thrombotic Thrombocytopenic Purpura (TTP)

113
Q

ABNL PLT destruction is what ANEMIA?

A

Immune Thrombocytopenic purpura (ITP)

114
Q

CAUSES/ MANIFESTATIONS of Thrombocytopenia

A

decreased Platelets (<150000/mcL)

115
Q

Treatment: ITP

A

steriods, immunosuppressives, PLT transfusion, splenectomy

116
Q

Treatment:TTP

A

Plasmaphoresis, steriods, dextran, chemotherapy, splenectomy

117
Q

Treatment: HIT

A

Lepirudin, protamine sulfate (antidote for heparin), warfarin, thrombolytics

118
Q

Etiology (the cause) & Pathophysiology of Leukemia is?

A

no single causative agent, combo environmental & genetic influences

119
Q

What are the 4 types of Leukemia?

A
  • AML: Acute myelogenous leukemia – 85% of acute leukemias
  • ALL: Acute lymphocytic leukemia – 15%
  • CML: Chronic myelogenous leukemia – Philadelphia chromosome, eventually ends in a “blastic phase”
  • CLL: Chronic lymphocytic leukemia – most common in adults
120
Q

Collaborative Care for Leukemia is?

A
  • Drug therapy

- Hematopoietic stem cell transplantation

121
Q

What is makes up 85% of acute leukemia?

A

AML - Acute myelogenous leukemia

122
Q

What makes up of 15%, type of leukemia?

A

ALL - Acute lymphocytic leukemia

123
Q

What is Philedelphia chromosome

A

CML - Chronic myelogenous leukemia

124
Q

What is the most COMMON type of Leukemia in ADULTS?

A

CLL - Chronic lymphocytic leukemia

125
Q

AML - Acute myelogenous leukemia other types of treatment are?

A

Autologus or altogenic HEMATOPOIETIC STEM CELL TRANSPLANT

126
Q

ALL - Acute lymphocytic leukemia other types of treatment are?

A

Cranial radiation therapy, Hematopoietic stem cell transplant,

127
Q

CML - Chronic myelogenous leukemia other types of treatment are?

A

Radiation, Hematopoietic stem cell tranplant, e-interferon, leukapharesis

128
Q

CLL - Chronic lymphocytic leukemia other types of treatment are?

A

Radiation, SPENECTOMY, colony-stimulating factors, Hematopoietic stem cell tranplant,

129
Q

What are the 2 type of Acute Leukemias?

A

AML - Acute myelogenous leukemia,ALL - Acute lymphocytic leukemia

130
Q

What are the 2 type of Chronic Leukemias?

A

CML - Chronic myelogenous leukemia,CLL - Chronic lymphocytic leukemia

131
Q

What is the Onset of AML?

A

Increase in incidence with advancing age, peak incidence betwee 60-70 yr of age

132
Q

What is the Onset of ALL?

A

Before 14 yr of age, peak incidence b/w 2-9 yr of age and older adults

133
Q

What is the Onset of CML?

A

25-60 yr of age peak incidence around 45 yr of age

134
Q

What is the Onset of CLL (most common in adults)

A

50-70 yr of age rare below 30 yr of age, PREDOMINANCE IN MEN

135
Q

What is the Manifestations of AML?

A

FATIGUE, WEAKNESS, HEADING, MOUTH SORES, BLEEDING, FEVER

136
Q

What is the Manifestations of ALL?

A

FEVER, PALLOR, WEAKNESS, BONE JOINT, GENERALIZED LYMPHADENOPATHY, INTRACRANIAL PRESSURE, SECONDARY TO MENINGEAL INFILTRATION, NERVE DYSFUNCTION

137
Q

What is the Manifestations of CML?

A

NO SYMPTOMS IN EARLY DISEASE, weakness fever, sternal tenderness, increase in sweating

138
Q

What is the Manifestations of CLL (most common in adults)

A

NO SYMPTOMS FREQUENTLY, detection often during examination, fatigue, SPLENOMEGALY AND LYMPHADENOPATHY, HEPATOMEGALY

139
Q

What is the Diagnostic Findings of AML?

A

Low RBC, Hb, Hct, low platelet, low to high WBC count

140
Q

What is the Diagnostic Findings of ALL?

A

presence of Philedelphia chromosome 20-25%

141
Q

What is the Diagnostic Findings of CML?

A

presence of Philedelphia chromosome is 90% in patient

142
Q

What is the Diagnostic Findings of CLL (most common in adults)?

A

Mild anemia and Thrombocytopenia with disease progression

143
Q

Nursing Management: Leukemia - Nursing Assessment?

A

Subjective: Health Hx, Medications, Surgical Hx
Objective: General, ROS, possible diagnostic findings REVIEW OF SYMPTOMS

144
Q

Nursing Management: Leukemia - Nursing Diagnoses?

A
  • Fatigue
  • Altered nutrition: Less than body requirements
  • Ineffective self-health management
  • Risk for infection
  • Pain
145
Q

Nursing Management: Leukemia - Planning?

A

what kind of nursing interventions will you anticipate performing due to the problems you identified the patient as having?

146
Q

Nursing Management: Leukemia - Nursing implementation

A

What specific actions did you take to assist the patient with coping with the problems you identified from your assessment data?

Acute intervention – things you can do now (or soon)
Ambulatory and home care (discharge planning)

147
Q

Nursing Management: Leukemia - Evaluation

A

how well did your interventions work for this patient? Is the patient satisfied with the response? Are you satisfied with the response? Why or why not?

148
Q

What are Blood Transfusion Reactions?

A
  • Acute transfusion reactions
  • Acute hemolytic reactions (body is reactions to antibody)
  • Febrile reactions
  • Allergic reactions (itching/ rash)
  • Circulatory overload (too much blood too fast)
  • Sepsis
  • Transfusion-related lung injury (TRALI)
  • Massive blood transfusion reaction

Adult Health (9 decks)

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