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DCMV SP22 RNSG 1441 > Nursing Care of H&L Disorders > Flashcards

Nursing Care of H&L Disorders Flashcards

1
Q

S&S of anemia

A 
Extreme weakness
Dyspnea
Fever 
Hypoxia
Weight loss
Slight jaundice with pallor
Lower extremity edema
Intermittent constipation & diarrhea
Flatulence, N, and indigestion
Palpitations
Dysphagia
Hand/feet tingling
Partial or total paralysis
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2
Q

What is the pathophysiology of:
Aplastic anemia
Iron-deficiency anemia
Pernicious anemia

A

Impaired production of RBCs

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3
Q

What is the pathophysiology of:
Sickle cell anemia
Thalassemia

A

Increased destruction of RBCs

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4
Q

What is the pathophysiology of anemia r/t:
Trauma- hypovolemia
Chronic infection
Renal failure

A

Massive or chronic blood loss

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5
Q

Aplastic anemia

A

Decrease of bone marrow function
Depression of erythrocyte production, which results in lowerd hgb and RBCs
All formed elements of blood are defective

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6
Q

What may develop due to Aplastic anemia?

A

Leukopenia and thrombocytopenia

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7
Q

Primary causes of aplastic anemia

A

Congenital

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8
Q

Secondary causes of aplastic anemia

A

Viral invasion
Meds
Chemicals
Radiation/Chemo

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9
Q

Diagnostic tests r/t aplastic anemia

A

CBC- all values low (except RBCs- they have longer life span)
Bone marrow aspiration- pale,yellow, fatty marrow
Total Iron-binding capacity
Serum iron level
Peripheral blood smears

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10
Q

Medical management of aplastic anemia

A

Bone Marrow and Stem Cell transplant
Blood transfusions
Antibiotics
Immunosuppressant agents (if autoimmune) -
-Antithymocyte globulin, Cyclosporine,
Methyprednisolone
Medications that stimulate bone marrow
-Colony-stimulating factors, Epogen-RBCs,
Neupogen- WBCs

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11
Q

Nursing interventions for aplastic anemia

A

Prevent infection
Neutropenic precautions
Hand hygiene
Avoid contact with those who have an infection
Bleeding precautions
Eliminate intake of raw meats, fruits, or veggies
Report S&S of infection or bleeding
Observe for blood in urine/stool, or petechiae
Use soft toothbrush or swab mouth
Avoid enemas or other rectal insertions
No nose picking or blowing nose forcefully
Avoid IMs
Avoid trauma, falls, bumps, and cuts
Avoid contact sports
Avoid aspirin
Use electric razor
Use lubrication and gentleness during intercourse

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12
Q

Nutrients needed for RBC formation

A

Iron- meats, green leafy vegetables, seafood
Folic acid- dark green, leafy veggies, citrus foods, avocados, seeds, nuts
Vitamin B12- shellfish, cheese, eggs, veggie burgers

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13
Q

Dietary deficiencies that lead to impaired RBC production

A

Iron
Folic acid
B12

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14
Q

Pernicious anemia is a lack of what vitamin?

A

Vitamin B12

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15
Q

Another term for pernicious anemia

A

Macrocytic anemia (large cells)

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16
Q

Pernicious Anemia

A

Autoimmune dx
Abscence of the intrinsic factor due to destruction of parietal cells
-essential for absorptoin of vitamin B12, transport of vitamin B12 is prevented, and affects the frowth and maturation of RBCs

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17
Q

Pernicious anemia has a insidious onset after what age?

A

40; higher in women

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18
Q

Perniciuos anemia has highest incidence in what descent?

A

African

Scandinavian

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19
Q

What can you get pernicious anemia from?

A

Gastrectomy
Bowel resection
Crohn’s
Other autoimmune diseases

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20
Q

What kind of diet is required with pernicious anemia?

A

Diet that includes :
Citrus fruits
Leafy green vegetables
Fortified cereals

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21
Q

S&S of pernicious anemia

A

Soreness/burning of the tongue

Chronic B12 deficiency can cause irreparable nerve damage (B12 is needed for production of myelin)

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22
Q

Diagnositc tests for pernicious anemia

A

Schilling test
Serum megaloblastic anemia profile
Bone marrow aspiration (revelas abnormal RBC development)
Gastric analysis (decreased hydrochloric acid secretion)

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23
Q

Medical management of pernicious anemia

A

Lifelong B12 injections, folic acid supplements, and iron supplements
-1000 mg vitamin B12 IM for life
*Daily for 2 weeks, weekly for 1 month, monthly
for life
-Intra-nasal form of B12 once a week
PRBCs if anemia is severe
CBC- every 3-6 months for life
Death can occur in 1-3 years if no treatment

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24
Q

Who is at risk for Vitamin B12 deficiency?

A

Strict vegetarians

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25
Q

NIs for pernicious anemia

A

Mouth care- several times a day
High protein, vitamins, and minerals diet
Light weight blanket- cold sensitivity
Interventions should conserve energy and prevent injury
Teach about lifelong vitamin B12 treatment

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26
Q

Folic acid deficiency

A

Can occur in pregnancy
Can occur with sickle cell disease
ETOH can aggravate deficiency
Certain medications can cause it (ones used to treat cancer, RA, and seizures)

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27
Q

Amino acid sources

A 
Eggs
Meat
Milk and milk products
Poultry
Fish
Nuts
Legumes
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28
Q

Folic acid sources

A 
Green leafy veggies
Asparugus, broccoli
Organ meats
Whole grain breads
Enriched cereal
Fish
Legumes
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29
Q

Spina bifida

A

Linked to folic acid deficiency in the mother

Babies have early exposure to latex products during surgery and develop allegy

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30
Q

Another term for iron deficiency anemia

A

Microcytic anemia

smaller than normal cells

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31
Q

Iron deficiency anemia

A

Insufficent intake of iron, excess blood loss, or lack of stomach acid

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32
Q

What is the most common type of anemia in all ages?

A

Iron deficiency anemia

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33
Q

Infants and children who have a high milk intake are at a higher risk for what?

A

Iron deficiency anemia

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34
Q

What is the most common cause of iron deficiency anemia?

A

Excess iroin loss in adults

Inadequate intake of iron in children

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35
Q

What is a common source of iron deficiency anemia

A

Chronic intestinal or uterine bleeding

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36
Q

Iron deficiency anemia may be caused by

A 
bleeding from gastric or duodenal ulcer
Esophageal varices
Hiatal hernias
Colonic diverticulitis
Tumors
Celiac disease
Sprue
Malabsorption- less common
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37
Q

When can iron deficiency anemia occur?

A

When the body’s demand for iron exceeds it’s absorption

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38
Q

How much blood loss from upper GI is required for melena?

A

50-75 mLs

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39
Q

What is a common cause of iron deficiency anemia in young adult women?

A

Menstrual blood loss

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40
Q

Diagnositc tests for iron deficiency anemia

A 
History- especially children
Reiculocyte count
CBC
Serum iron levels- (Ferritin- major iron storage protein)
\+ Direct Coombs antigobulin test
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41
Q

What does a direct coombs antiglobulin test look for?

A

Antibodies that may bind to RBCs and cause premature RBC destruction

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42
Q

Hemolysis

A

premature RBC destruction

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43
Q

Food sources of Iron

A 
Organ meats
Muscle meats
Eggs
Shellfish
Whole-grain bread and cereal
Iron-enriched breads and cereal
Legumes
Nuts
Dried fruits
Dark green vegetables
Orange juice
Grape juice
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44
Q

Medical management for iron deficiency anemia

A 
Ferrous sulfate- 900 mg/day given with citrus fruits and juices;Oral or injection (z-track-staining)
Iron administered orally or injection
IM dextran or IV venofer
Ascorbic acid
Nutritional counseling
Treatment of underlying conditions
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45
Q

NIs for iron deficiency anemia

A

Plan rest periods
Diet adequate in iron
Teach SE of iron therapy (dark, tarry stool)
Balance between rest/activites
Report N/D
Do not take with tetracycline antibiotics
Toxic to children

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46
Q

Teaching for iron deficiency anemia

A

Stew acidic foods in iron cookware
Can give iron-fortified formula
Pregnancy can deplete mother’s iron stores
For children, give liquid iron through a straw (avoids teeth staining)
Best solid food iron source for children is infant cereal
Infants need more than just milk

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47
Q

Erythropoietin

A

Protein made in the kidneys

Stimulates bone marrow to produce RBCs

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48
Q

Erythropoietin can:

A

Cause: hives, dyspnea, swelling of face, lips, tongue or throat
Increase: risk of blood clots

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49
Q

Hemolyteic anemias cause what?

A

Increased destruction of RBCs

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50
Q

Main types of hemolytic anemias

A

Sickle cell anemia

Thalassemia

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51
Q

More types of hemolytic anemias

A 
G6PD deficiency
Aquired hemolytic anemia
Immune hemolytic anemia
Malaria
Tick-borne diseases
Snake venom
Toxic chemicals
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52
Q

Hemolytic anemia

A

Marrow produces enough RBCs, but they are destroyed

R/T defects of the cell membrane of RBC, inherited enzyme defects, or trauma

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53
Q

Causes of hemolytic anemia include

A

Infections
Drug reactions
Certain cancers
Delivery of a newborn with Rh+ blood while mom is Rh-

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54
Q

What is the most common genetic disorder?

A

Sickle cell anemia

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55
Q

What is sickle cell?

A

Abnormal crescent/sickle shape RBC containing hemoglobin S

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56
Q

Sickle cell anemia is a _____, _______, ______ condition

A

Severe;chronic;incurable

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57
Q

The sickle cell cases the RBC to be …..

A

Unable to carry as much O2, which causes pt. to become more sickled due to lack of O2

Crises cna be life threatening- Hypoxia and ischemia

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58
Q

Sickle cell anemia is seen in descendants from?

A 
People of:
Africa
Saudi arabia
India
Meditarranean area
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59
Q

1 in _____ african americans have sickle cell anemia

A

400

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60
Q

Sickle cell trait occcurs in the person wtih…

A

One defective gene and one normal one

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61
Q

Often the carrier of ____________ shows no S&S

A

sickle cell anemia

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62
Q

Infants with sickle cell anemia do not show S&S until what age?

A

> 6 months

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63
Q

Sickles RBCs live how many days?

A

10-20 days

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64
Q

Sickle cell anemia crisis lasts how many days?

A

4-6 days; may come in clusters or far apart

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65
Q

What happens in sickle cell disease?

A

When O2 is released to the tissues, the abnormal hemoglobin becomes more viscous and crystallizes, causing the erythrocyte to change from a round shape to an elongated crescent shape.

As the sickles cells clump together, circulations slows, resulting in obstruction with severe hypoxia and necrosis

Precipitated by infection, fever, hypoxemia, dehydration, high altitudes, cold, or emotional stress

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66
Q

G6PD deficiency

A

Glucose-6-phosphate dehydrogenase
Genetic disorder
In affected individuals, a defect in the enzyme G6PD causes RBCs to break down prematurely.

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67
Q

G6PD deficiency occurs most often in?

A

Males

68
Q

S&S of sickle cell anemia

A 
Asymptomatic until a crisis
Pain in joints and back
Loss of appetite
Dehydration
Irritability with weakness
Fatigue
Fever
Dyspnea
Cough
Strokes- in children
Joint deformity
Abdominal elargement (pooling in liver and spleen)
Jaundice
Extremity edema
Skin irritation and ulceration
Priapism
69
Q

Complications of sickle cell anemia

A

Multisystem failure
Infarctions
Hemorrhage
Retinal damage

70
Q

Diagnostic tests for sickle cell anemia

A

Hemoglobin electrophoresis (7-10g/dL)
Peripheral blood smear (shows sickled cells)
CBC
MRI
X-rays
Sickledex test (along with hgb electrophoresis, can determine whether trait or disease)

71
Q

Medical management of sickle cell anemia

A

Supportive care
Alleviate S&S
Antibiotics
Pneumovax, haemophilus influenza and hepatits immunizations

72
Q

Medical management of sickle cell anemia during a crisis

A 
O2
Rest
IVFs
Pain management
RBC exchanges (NOT TRANSFUSIONS)
Folic acid
Hydroxyurea therpay (reduces hemolysis)
Bone marrow transplant
73
Q

NIs for sickle cell anemia

A 
Supportive care
Hydration
Frequent VS and O2 sats
Analgesia
Watch for fever and infection
Blow nose gently
Genetic counseling
Good diet (increased need for folic acid)
I&O
74
Q

Evaluation of NIs for sickle cell anemia

A

Activity levels increase
Client reports no SOB on exertoin
Client explains treatment plan, meds, and diet
Client remains free of injury

75
Q

Client teaching to avoid sickle cell crisis

A 
Avoid high altitudes and air travel
Increase fluid intake, avoid dehydration
Notify MD of D/V
High risk for pregnant women to develop pulmonary and/or renal conditions
ROM, encourage physical activity as tolerated (but not during a crisis)
Avoid trauma
Avoid extreme temperatures
Avoid ETOH and smoking
Wear loose clothing
Genetic counseling
76
Q

Effects of sickle cell disease on the brain

A

Thrombosis
Hemorrhage
Stroke

77
Q

Effects of sickle cell disease on the heart

A

Failure

78
Q

Effects of sickle cell disease on the abdominal organs

A

Hepatomegaly
Gallstones (cholethiasis)
Splenic enlargement
Splenic infarction

79
Q

Effects of sickle cell disease on the bones and joints

A

Hand and foot syndrome

80
Q

Effects of sickle cell disease on the eye

A

Retinal or conjunctival hemorrhage

Blindness

81
Q

Effects of sickle cell disease on the lungs

A

Atelectasis
Infarctoin
Pneumonia

82
Q

Effects of sickle cell disease on the kidney

A

Dilute urine
Diuresis
Hematuria

83
Q

Effects of sickle cell disease on the penis

A

Priapism

84
Q

Effects of sickle cell disease on the skin

A

Stasis ulcers

85
Q

Sickle cell crisis: Acute attack

What does it cause?

A

Causes occlusion and ichemia of distal blood vessels

86
Q

Sickle cell crisis: Acute attack

Where is the pain felt?

A

Pain in hands and feet

87
Q

Sickle cell crisis: Acute attack

What physical and emotional factors trigger an attack?

A 
Dehydration
Change in O2 tension (changes in altitude)
Infection
Fever
V/D
Overexertion
Changes in climate (especially the cold)
ETOH
Smoking
Stress
88
Q

Sickle cell crisis: Aplastic crisis

What is it caused by?

A

Premature destruction of RBCs, = profound anemia

89
Q

Sickle cell crisis: Aplastic crisis

Medical management

A

Transfusions of PRBCs

NOTE: watch for iron build up

90
Q

Sickle cell crisis:Vaso-occlusive

A

Obstruction of the small blood vessels in the hands and feet, resulting in edema, impaired ROM, and pain

91
Q

Sickle cell crisis:Sequestration

A

Blood pools in the spleen and liver resulting in hepatosplenomegaly; can progress to CV collapse and death

92
Q

Sickle cell crisis:Vaso-occlusive

Palliative Tx:

A

Pain meds

O2

93
Q

Sickle cell crisis:Sequestration

Treatment

A

Pain meds
Volume expanders
Transfusions
Splenectomy

94
Q

Sickle cell crisis nursing Dx of pain

A

Pain r/t thrombotic crisis

95
Q

Sickle cell crisis nursing Dx of pain interventions

A 
Position in alignment
Protect joints
Position with slow, gentle movements
Apply warm, moist compresses to relieve discomfort
Administer and monitor pain meds
96
Q

Sickle cell crisis nursing Dx of impaired skin integrity

A

Impaired skin integrity r/t alteration in circulation to tissues, resulting in hypoxia and inadequate nurtition

97
Q

Sickle cell crisis nursing Dx of impaired skin integrity interventions

A

Remove constrictive clothing
Maintain room and body warmth
ROM
Inspect extremities for adequate circulation
Monitor gases for indictors of adeqaute tissue perfusion

98
Q

Thalassemia

A

Insufficient production of normal Hgb - abnormal synthesis

Recessive genetic disorder

99
Q

Thalassemia affects what ethnic groups?

A

Ethnic groups with origins near the mediterranean area

100
Q

Thalassemia has what kind of forms

A

Major and minor

101
Q

Thalassemia is AKA..

A

Cooley’s anemia

102
Q

Treatment for major thalassemia

A

Blood transfusions
Folate therapy
Chelation therapy
Bone marrow transplant- may help

103
Q

Treatment for minor thalassemia

A

None-

Body adapts to reduction of normal Hgb

104
Q

Anemia of Chronic Infection/Disease

ACI or ACD

A

Human body limits the amount of iron available when potentially harmful things get into our body
Bacteria and cancer cells depend upon iron to sustain life
Iron gets shuttle to ferritin so the harmful invader cannot get the iron

105
Q

ACI or ACD low normal range

A

9.5-10.5 g/dL

106
Q

Anemia of Chronic Renal Failure

A

Kidneys are unable to secrete the hormone erythropoietin
Toxins may also depress bone marrow
Aluminum may accumulate in the bone marrow of dialysis patient and can contribute to anemia

107
Q

Disseminated Intravascular Coagulation (DIC)

A

Overstimulation of clotting and anti-clotting processes in response to disease and injury
Clotting and hemorrhage issues

108
Q

DIC is caused by

A 
Infection (sepsis)
Obstetric complications
Neoplastic disorders
Hematological disorders
Trauma
109
Q

Clots normally lyse in ______ while in DIC clots lyse_____

A

7-10 days; immediately

110
Q

S&S of DIC

A 
Bleeding              GI bleeding
Hemoptysis         Hematuria
Dyspnea              Pulmonary edema
Diaphoresis         PE
Cold, mottled digits
Purpura on the chest and abdomen- 1st sign
Petechiae           Hypotension
Abdominal tenderness
Tachycardia       Absent peripheral pulses
Restlessnes      Confusion
Seizures            Coma
111
Q

Diagnostic tests for DIC

A

Decreased fibrinogen levels
Increased PT and PTT
Increased fibrin split products
Increased D-Dlmers

112
Q

Treatment of DIC- Supportive

A 
Administer blood
FFP
Platelets
Vitamin K
Cryoprecipitate
113
Q

Treatment of DIC- controversial

A

IV heparin

114
Q

Nurse teaching for DIC

A

Involve the family
Critical situation= IVs, N/G, Foley
Emotional support

115
Q

Thrombocytopenia

Idiopatic Thrombocytopenia Purpura (ITP)

A

Platelets reduced below 150,000/mm3; may be due to decreased production or decreased survival
Autoimmune disease, platelets are coated with antibodies. Although they function normally, are destroyed by macrophages in the spleen

116
Q

ITP is assosciated with…

A 
Aplastic anemia
Leukemia
Tumors
Chemo
Infection
Antibody destruction
Viral overload
Drug induced
117
Q

ITP chronic form in common in who?

A

Women aged 20-40

118
Q

Acute form common in children (ITP)

A

Bleeding beneath the skin

Follows viral infection

119
Q

S&S of ITP

A 
Petechiae
Ecchymosis
Bleeding from mucous membranes
Splenomegaly from entrapment of blood in the spleen
Bleeding in brain
Nosebleeds
120
Q

Diagnostic tests for ITP

A

CBC
Peripheral blood smear
Coags
Bone marrow aspiration (may show that precursor cells for platelets, the magarkaryocytes, are adequate)(Platelets live for a few hours rather than 7-10 days)

121
Q

Medical management of ITP

A 
Corticosteroid therapy (prolongs platelet life)
Splenectomy
IV immunoglobulin
Immunosuppressive drugs
PRBCs to treat hemorrhage
Platelet transfusions (counts <20K)
Vitamin K
Anti-D antibody therapy (new)
122
Q

Meds assosciated with thrombocytopenia

A 
ASA
Digitalis
Lasix
NSAIDs
ORal hypoglycemics
PCN
Quinidine
Rifampicin
Sulfonamides
Thiazides
123
Q

NIs for thrombocytopenia

A 
Meticulous aseptic technique
Careful positioning and moving of client
Watch for S&S of increased ICP
Bleeding precautions
      *Avoid trauma, soft toothbrush, high fiber diet
      blow nose gently
Transfusions- monitor for reaction
124
Q

Heparin Induced Thrombocytopenia (HIT)

A

Development of thrombocytopenia due to heparin administration
HIT can predispose to thrombosis

125
Q

What is HIT caused by?

A

Abnormal antibodies that activate platelets

126
Q

Hemophilia

A

Hereditary coagulation disorder
Distrubance of clotting factor
2 types- A and B
X-linked hereditary trait (only affects males, women are carriers though)

127
Q

Hemophilia A

A

most common

Absence of factor VIII

128
Q

Hemophilia B

A

Christmas disease

Deficiency in factor IX

129
Q

Von Wilebrand’s disases

A

Mild factor VIII

130
Q

Hemophilia- what happends after repeated bleeds?

A

Muscles become weak, scarred, and shorter than normal (sometimes permanently)
They can no longer protect the joints

131
Q

Hemophilia- joints above and below the muscle cannot move prperly. They may ______

A

bleed more often

132
Q

Hemophilia- what happends if nerves are damaged during muscle bleeds?

A

Muscle may become weake or paralyzed

133
Q

Diagnositc tests for hemophilia

A

Normal INR and PT
Prolonged aPTT
Factors VIII and IX are absent

134
Q

S&S of hemophilia

A

Internal & External bleeding
Ecchymoses from slight trauma
Hemarhrosis (indicates severe disease; seen in knees ankles and elbow; exibits pain, edema, erythema and fever)
Excessive blood loss from small cuts and dental procedures

135
Q

Medical management of hemophilia

A 
Minimize bleeding- avoid trauma
Relieve pain- no aspirin
Minor bleeds- ice packs
Transfusions (child needs Hep B vaccine)
Factor VIII or IX concentrate
Cryoprecipitate (rich in factor VIII)
Manufactured VIII or IX (less risk of viral transmission)
136
Q

Treatment for Hemophilia A

A

Inhalation of desmopressin (DDAVP) which can stimulate body to release more clotting factors

137
Q

Treatment for hemophilia B

A

Transfuse factor IX

138
Q

NIs for hempophilia

A 
Apply pressure & cold (ice)
Control hemorrhages
Educate family
Monitor transfusions
Pain management
Genetic counseling
No ASA products
Avoid injury
Medic alert bracelet
Diet
Dental care & preventive dental care
Non-contact sports
Soft, age appropriate toys
Immobilize affect part
Notify MD
Teach good diet to avoid obesity
Avoid over protection
139
Q

Von Willebrand’s disease

A

Inherited bleeding disorder
Characterized by abnormally slow coagulation of blod
Mild deficiency of factor VIII
Common in post-partum period

140
Q

How is Von Willebrand’s disease different from hemophilia?

A

VW’s disease is not limited to males like hemophilia

141
Q

S&S of von willebrand’s disease

A

Spontaneous episodes of:
GI bleeding
Epistaxis
Gingival bleeding

142
Q

Primary polycythemia

A

Polycythemia Vera (PV)

143
Q

How are primary and secondary polycythemia different and similiar?

A

Etiologies and pathophysiology differe although S&S and compliactions are similiar

144
Q

Polycythemia Vera

A

Myeloproliferative- characterized by excessive bone marrow production

145
Q

S&S of PV

A

Increase in erythrocytes, granulocytes, and platelets
Stem cell abnormality
Pathologic response is a malignancy of blodd cells

146
Q

Secondary polycythemia

A

Caused by hypoxia
Hypoxia stimulates erythropoietin in the kidneys, which in turn stimulates erythrocyte production (people who live in mountains, COPD)

147
Q

S&S of secondary polycythemia

A 
Gradual onset
Mainly affects men in middle age
Venous distention and platelet dysfunction can cause organ infarction
Florid or dark, flushed face
Esophageal varices
Epistaxis
GI bleeding
Petechiae
148
Q

Medical management of polycythemia

A

Repeated phlebotomy
Myelosuppressive agents, such as Myleran, Hydrea, and radioactive phosphorus are often given to inhibit bone marrow activity
Main cause of morbidity and mortality is thrombosis

149
Q

Nursing actions for polycythemia

A

Controlling chronic pulmonary disease and avoiding high altitudes (secondary)
Proper hydration to avoid fluid overload

150
Q

NIs for the nursing DX Ineffective tissue perfusion r/t polycythemia

A

Comfy position
Provide passive ROM q2-4 hours
Report S&S of thrombosis
Avoid trauma

151
Q

NIs for the nursing DX activity inolerance r/t polycythemia

A

Avoid high NA+ food
Encourage adequate exercises
Explain disease course

152
Q

Lymphadenopathy

A

Swelling of lymph glands

153
Q

Lymphagenopathy causes

A

Infection
Cancer
Autoimmune disease

154
Q

Lymphangitis

A

Inflammation of one or more lymphatic vessels

155
Q

S&Sof lymphangitis

A 
Clinical symptom of infection important*
Fine red streaks from affected area
Groin or axilla
Not localized- edema is diffuse
Chills
Fever
Local pain
H/A
Myalgia
156
Q

Medical management/NIs of lymphadenopathy/lymphangitis?

A

PCN or other antibiotics
Moist heat to area
Elevate extremity
Use aseptic technique

157
Q

Lymphedema

A

Primary or secondary disorder
Accumulation of lymph in soft tissue due to obstruction, increased amount of lymph in area of removal of nodes(usually occurs for strep or staph infection in an extremity)
Extreme edema &tightness resulting in pain and pressure
Often a result of mastectomies

158
Q

Lypmphedema- extreme edema & tightness in affected extremity resulting in pain and pressure is aggravated by?

A

Standing pressure
Pregnancy
Obesity
Warm environments

159
Q

Medical management/NIs for lymphedema

A 
Diuretics
Antibiotics
SCDs
Elastic stocking or sleep
Elevate extremity
Restricted Na+ diet
Avoid constrictive clothing/trauma
Meticulous skin care
Be supportive- body image disturbance may occur
160
Q

Nursing problems for blood and lymphatic disorders

A 
Risk for infection
Risk for injury (trauma, bleeding, falls)
Knowledge deficit
Pain (acute,chronic)
Impaired gas exchange
Activity intolerance
Ineffective coping
Impaied skin integrity
Disturbed body image
161
Q

Splenomegaly

A

Enlarged spleen

May not enlarge, but still destroys RBC and platelets?

162
Q

Splenectomy problems

A 
Bleeding
Pneumonia
Atelectasis
Pancreatitis
Fistulas
OPSI- overwhelming post-op infection (1 week - 20 years)
163
Q

Cullen’s sign

A

Sign of retroperitoneal bleeding/hemorrhage

Superficial edema and bruising in the subQ fatty tissue around the umbilicus

164
Q

Grey-Turner’s sign

A

Sign of retroperitoneal bleeding/hemorrhage
Takes 24-48 hours to appear
Bruising/blue discolaration of the flanks
***A flank = the side of a person’s body between ribs and hip! Who knew?! Not me!

165
Q

Kehr’s sign

A

Acute pain in the tip of the shoulder due to the presence of blood or other irritants in the peritoneal cavity when a person is lying down with the legs elevated
**Pain in left shoulder is sign of a ruptured spleen

166
Q

Neutropenic precautions

A 
Reverse isolation
No raw meats, veggies, or fruit
No fresh flowers
Visitors= cannot show any S&S of infection; not a lot of visitors
Good handwashing
167
Q

What is anemia?

A

Deficiency of RBCs, hemoglobin, or both

DCMV SP22 RNSG 1441 (7 decks)

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