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NURS 405 > NURS 405 Week 5 Wednesday > Flashcards

NURS 405 Week 5 Wednesday Flashcards

1
Q

Iron-Deficiency Anemia

A
  • Decreased RBC production
  • Most common nutritional disorder in the world
  • Most susceptible- very young, poor diets, women in reproductive years
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2
Q

Causes of Iron-Deficiency Anemia

A
  • Inadequate dietary intake (5-10% ingested iron is absorbed)
  • Malabsorption
  • Blood loss: 2mL whole blood contain 1 mg iron
  • Hemolysis
  • Pregnancy
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3
Q

Clinical Manifestation of Iron Deficiency Anemia

A

Early: asymptomatic
General: pallor, glossitis (inflammation of the tongue), cheilitis (inflammation of the lips)
- headache, paresthesia, burning sensation of the tongue (from lack of Fe in the tissues)

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4
Q

Iron Deficiency Anemia Diagnostic

A

Low iron level, normal or low transferrin level
CBC
Microcytic, hypochromic RBCs
Stool – occult blood
May need endoscopy or colonoscopy for diagnosis

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5
Q

Iron Deficiency Treatment

A
  • Treat underlying cause
  • Replace iron, nutrition, oral or parenteral iron supplementation, transfusions of RBCs
  • Enhance absorption of iron
  • Patient teaching
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6
Q

Oral Fe

A

Inexpensive / convenient

  • 1 hour prior to food, best absorbed in acidic
    1. Absorbed best by duodenum and proximal jejunum (enteric coated are not necessary)
    2. Daily dose = 150-200 mg daily of elemental Fe (can take this 3-4 x per day)
    3. Fe best absorbed in acidic environment (take 1 hour prior to food)
    4. Undiluted liquid Fe can stain teeth (drink through a straw!)
    5. GI side effects: heartburn, constipation, diarrhea, black stools.
  • SE: heartburn, constipation, diarrhea, black stools
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7
Q

IM / IV Fe

A

Parenteral Fe: IM or IV, switch needles between draw and administartion due to Fe staining skin

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8
Q

Thalassemia

A

Decreased RBC production
- Caused by group of inherited microcytic disease
- Common in ethnic groups - Mediterranean / Asia / middle east / Africa
- Problem with globulin protein –> abnormal Hgb synthesis and hemolysis
Autosomal recessive – 2 types:
minor (heterozygous) 🡪 mild form
major (homozygous) 🡪 severe

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9
Q

Megaloblastic Anemia

A

Decreased RBC Production
- Abnormally large (macrocytic) red blood cells
Group of disorders caused by impaired DNA synthesis and presence of megaloblasts
Easily destroyed because of fragile cell membranes
4 classifications

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10
Q

Pancytopenia

A

Decreased RBCs, WBCs, Platelets

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11
Q

Acute Blood Loss

A

Loss of volume (trauma, surgery, GIB, …) 🡪 hypovolemic shock
Body responds by increasing plasma volume
With fluid resuscitation a dilutional anemia also occurs
Labs will not reflect an acute bleed for 2-3 days (until the fluids can shift)

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12
Q

Chronic Blood Loss

A

Abnormal menstrual bleeding or slow GI bleeding
If rate of RBC loss > rate of generation 🡪 dilutional anemia
Intestinal absorption of iron is not fast enough to replace what is lost

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13
Q

Hemolytic Anemia

A

Increased RBC destruction
- Genetic or acquired :physical, infectious agents or toxins
- General manifestations of anemia
SPECIFIC
- JAUNDICE
- Enlargement of spleen (primary site of RBC destruction) and liver
** Maintenance of renal function is a major focus of treatment **

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14
Q

Categorical Causes of Anemia

A
  1. Decreased / Abnormal RBC production
  2. Blood Loss
  3. RBC Destruction
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15
Q

Decreased RBC Production Examples

A
  1. Deficient nutrients
    - Iron / Cobalamin / Folic Acid
  2. Decreased erythropoietin (KIDNEY)
  3. Decreased iron availability in (LIVER)
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16
Q

Blood Loss Examples

A
  1. Chronic Hemorrhage
    - Bleeding duodenal ulcer
    - Colorectal cancer
    - Liver disease
  2. Acute Trauma
  3. Ruptured aortic aneurysm
  4. GI Bleeding
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17
Q

Increased RBC destruction Examples

A
  1. Hemolysis
    - Sickle cell disease
    - Medication
    - Incompatible blood
    - Trauma (cardiopulmonary bypass)
18
Q

Hypochormic

A

Pale Color

19
Q

Normochromic

A

Normal Color

20
Q

Microcytic

A

Small cell

21
Q

Macrocytic

A

Big Cells

22
Q

MCV

A

Red blood cell size (Mean Cell Volume)

23
Q

MCH

A

Mean cell hemoglobin - amount of Hgb in the cell (color)

24
Q

MCHC

A

Mean cell hemoglobin concentration - Hbg concentration in relationship to cell volume

25
Q

Normocytic, normochromic - etiology?

A

Acute blood loss, CKD, CA, starvation, sickle cell anemia, pregnancy
(you don’t have enough RBC due to condition)

26
Q

Microcytic, Hypochromic - etiology

A

Fe-deficiency anemia
vitamin B6 or copper deficiency
lead poisoning

27
Q

Macrocytic, normochromic - etiology

A

Cobalamin (vitamin B12) deficiency, folic acid deficiency, liver disease

28
Q

Erythropoietin

A

Glycoprotein primarily produced in the kidneys (10% liver) –> stimulate erythropoiesis (production of RBC)

29
Q

MOA Erythropoietin

A

Kidney sense low O2 due to low RBC –> increase erythropoietin production –> stimulates erythropoietin in bone marrow –> erythropoiesis –> increase blood O2 levels , so decrease EPO production

30
Q

Thalassemia Minor

A

Body adapts to reduction of Hgb

Often does not require treatment, asymptomatic

31
Q

Thalassemia Major

A

can be life threatening, may cause physical and mental growth and development delays, splenomegaly, hepatomegaly, and cardiomyopathy, prominent jaundice
Treatment: blood transfusions, chelating agents that bind iron, zinc, vit C, splenectomy
Goal = keep Hgb around 10 g/dL
Fe supplements should NOT BE GIVEN!
Stem cell transplants = only cure for thalassemia

32
Q

Cobalamin (Vitamin B12) Deficiency - Meg

A

Type of megaloblastic anemia
Dietary deficiency
Deficiency of gastric intrinsic factor (H. Pylori, pernicious anemia - absence of IF)
Malabsorption (Celiac, Crohn’s, small bowel resection)
Chronic alcoholism
Increases requirement (pregnancy)
long-term H2 blockers, PPIs, strict vegetarians

33
Q

Folic Acid Deficiency -Meg

A 
Type of megaloblastic anemia
Dietary 
Malabsorption (Celiac, Crohn’s, small bowel resection)
Chronic alcoholism
Increases requirement (pregnancy)
Chronic hemodialysis
34
Q

Drug induced Suppression of DNA synthesis - Meg

A

A type of megaloblastic anemia

Long list of drugs (see UpToDate) that interfere with purine or pyrimidine metabolism

35
Q

Inborn Errors - Meg

A

A type of megaloblastic anemia

Defective folate metabolism

36
Q

Nursing Management for Megaloblastic Anemias

A

Determine cause
Genetic counseling – early detection and treatment, patients with positive family history should be evaluated for symptoms
Safety – diminished sensitivity to heat and pain from neurologic impairment (protect from burns, falls, trauma)
Monitor for patient’s adherence to treatment
Assess neurologic difficulties
Patient may need more frequent assessments for gastric CA (risk may be increased in patients with pernicious anemia)

37
Q

Vitamin B 12 Deficiency - Treatment

A

Gastrointestinal Manifestations:
Sore, red, beefy tongue, anorexia, nausea, vomiting, and abdominal pain

Neuromuscular manifestations:
Weakness, ataxia, impaired cognition, paresthesia of feet and hands

Dx: Macrocytic RBCs, Serum B12 levels are reduced, folate normal suggests B12 (cobalamin) deficiency

Tx: Without cobalamin administration, individuals will die in 1 to 3 years
As long as supplemental cobalamin is used, the anemia can be reversed
Can replace with intramuscular, oral or nasal B12 (Latest studies support oral in high doses)

38
Q

Folic Acid Deficiency- Treatment

A

Folic acid required for DNA synthesis

Signs/sx similar to B12 deficiency anemia except:
NO NEUROLOGIC SYMPTOMS!

Folate levels are low, B12 levels are normal
Treatment:
Folic acid: 1 mg/day orally

Malabsorption or chronic alcoholism: up to 5 mg/day

39
Q

Anemia of Chronic Disease

A 
Caused by: 
Chronic inflammation
Autoimmune and infectious disorders
Heart Failure
Malignant diseases
Bleeding

Diagnostics:
elevated serum ferritin, normal folate and B12 levels

Treatment:
correct underlying problem, erythropoietin if from renal disease and anemia from CA

40
Q

Aplastic Anemia (rare)

A

Pancytopenia! ☹ (decreased RBCs, WBCs, Platelets)

Can be chronic or acute related to sepsis or hemorrhage.

Usually acquired
Idiopathic or Autoimmune 
Chemical agents, toxins
Drugs
Radiation viral or bacterial infections

Clinical manifestations: abrupt or insidious: fatigue, dyspnea, CV and cerebral responses, increased risk for bleeding, susceptible to infection, sepsis, death. Watch for fever!

Diagnostics: CBC. Normocytic/normochromic anemia. Reticulocytes are low, bleeding times are increased. Bone marrow biopsy.

Treatment: stem cell transplants, high-dose immunosuppression or corticosteroids.

41
Q

Nursing Implications Blood Loss

A

Replace volume to prevent shock
Identify the source of hemorrhage and stop
Watch for s/s shock – don’t rely on labs alone
Pain, shock
LR, Albumin, and Plasma Expanders
Once volume is corrected, focus on RBCs (takes 2-5 days to make more RBCs in response to erythropoietin)
May need PRBC transfusions

NURS 405 (3 decks)

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