hematology Flashcards

1
Q

clinical manifestations of severe anemia (<60g/L)

A

integument =pallor, jaundice, pruritus
eyes = icteria conjunctiva and sclera, retinal hemorrhage, blurred vision
mouth = glossitis, smooth tongue
cardiovascular = tachycardia, increase pulse pressure, systolic murmurs intermittent claudication, angina, HF, AMI
pulmonary = tachypnea, orthopnea, dyspnea at rest
neurological = headache, vertigo, irritability, depression, impaired thought process
GI = anorexia, hepatomegaly, splenomegaly, difficulty swallowing, sore mouth
msk = bone pain
general = sensitivity to cold, weight loss, lethargy

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2
Q

anemia acute and long term interventions

A
Ultimate goal of therapy is to address the cause of the anemia
Acute interventions: 
Replace blood loss with RBC 
Volume replacement 
Drug therapy  
Oxygen therapy
Long term interventions: 
Diet 
Lifestyle changes
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3
Q

anemia nursing interventions

A
Age related interventions:  a decline in RBC is expected (10g/L males; 2g/L females) after age 70
Symptoms may include: 
Fatigue
Ataxia
Confusion
 Pallor 
Worsening cardiac or pulmonary issues
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4
Q

iron deficiency anemia etiology

A

Inadequate supplies of iron lacking from diet
Malabsorption (GI surgery),
Blood loss (peptic ulcer, gastritis, esophagitis, diverticuli, hemorrhoids, and neoplasia, menstrual bleeding, postmenopausal bleeding, pregnancy, chronic kidney disease)
Hemolysis (dialysis treatment

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5
Q

ida diagnostic studies

A

Lab Values: Hct, Hgb, Rbc count, reticulocyte count, serum iron, serum ferritin, serum transferrin, TIBC, stool for OB
Endoscopy and Colonoscopy are used to detect GI bleeding
Bone marrow biopsy if all other tests are inconclusive

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6
Q

ida collaborative care

A

Collaborative Care:
Identification and treatment of underlying cause
Drug Therapy
Oral: ferrous sulphate of ferrous gluconate
IM or IV: iron dextran, iron sucrose, sodium ferric gluconate (Ferriecit)
Nutritional Therapy
Transfusion of packed RBC’s

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7
Q

iron supplements

A

Daily dose of 150-200 mg of elemental iron given in divided doses (3-4)
Ferrous sulphate preferred over ferrous gluconate
May stain teeth; suggest use of straw
Should be taken an hour before food (if possible)
Vitamin C enhances absorption
Enteric coated pills are counterproductive
GI adverse effects: constipation, diarrhea, heartburn
Causes black stools
May need stool softener
If needing IM dose, use separate needle for drawing up medication and injecting (z-track method)

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8
Q

ida nutritional therapy

A

Organ meats
Other meats (tuna, halibut, turkey, oysters, lean ground beef, lamb chop)
Beans (black, pinto, and garbanzo)
Whole-grain breads, brown rice, bran flakes, oatmeal
Dried fruits
Leafy green vegetables

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9
Q

ida blood transfusion and hemorrhage

A

Acute loss of total blood volume (leading to hypovolemia shock)
Gradual blood loss: plasma increases thus diluting the RBC and ability to carry oxygen throughout the body
Clinical signs more important than lab values
Acute blood loss will result in hypotension before Hgb and Hct drop.
Once the body compensates with volume, the Hgb, Hct and RBC will drop (ratio changes not #)
Pain may be an important sign of internal bleeding; also numbness

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10
Q

ida fluid replacement

A
Fluid replacement may include:
Dextran
Hetastarch
Albumin
Crystalloid electrolyte solutions (lactated ringers, 0.9% NaCL)
Blood products may include: 
Platelets
Plasma
Cryoprecipitate
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11
Q

sickle cell disease nursing interventions

A
Characterized by abnormal form of Hgb in the blood
Collaborative Care aimed at:
Preventing sequelae from the disease
Alleviating symptoms of the disease
Minimizing end target organ damage
Promptly treating sequelae
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12
Q

patient teaching for sickle cell disease

A

Patient teaching:
Avoid triggers: high altitude, extreme temperatures
Minimize stress
Adequate fluid hydration
Treat infections promptly
Screen for retinopathy starting by preteen years (10 years old)
Immunizations should be up to date

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13
Q

sickle cell crisis interventions

A

Resp failure most common cause of death: careful monitoring
Encourage rest to reduce metabolic requirements
Deep vein thrombosis prophylaxis with anticoagulants
Fluids and electrolytes
Priapism: managed with pain meds, fluids and nifedipine
During aplastic crisis RBC exchange transfusion program may be implemented

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14
Q

sickle cell disease interventions for pain

A

Ongoing treatment for pain may result in tolerance by the pt; higher doses of opioids may be required
Folic acid supplements
NSAIDS, antineuropathic pain (TCA’s, antiseizure medications), local anesthetics, nerve blocks, transelectrodermal nerve stimulator (TENS), acupuncture, or a combination of these strategies
Bone marrow transplantation only cure; rarely done in Canada
Healthcare team: occupational therapist and physiotherapists may assist the pt with ongoing pain and resulting depression; psychologists may help with CBT

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15
Q

hemophilia collaborative care

A
  1. Prevent hemorrhage
    No contact sports
    Pt wears gloves when performing household chores to prevent cuts and abrasions
    Pt learns to promptly treat bleeding
    Pt learns to distinguish which bleeding can be treated at home and which requires medical treatment
  2. Treat hemorrhage
    Replace clotting factors: Factor VIII & IX
    Fresh Frozen plasma rarely used anymore
    Desmopressin acetate (DDAVP) for mild cases
    Antifibrinolytic therapy (tranexamic acid)
    Minor hemorrhage should be treated for 72 hrs
  3. Treat symptoms from hemorrhage
    Bedrest until pain, swelling resolves and movement returns to affected joints
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16
Q

hemophilia acute intervention

A

Stop the bleeding by applying pressure, ice or packing with fibrin foam or Gelfoam
Administer specific coagulation factor; watch for sensitivity (antibody reaction)
Manage life-threatening complications as a result of hemorrhage or adverse effects

17
Q

hemophilia joint bleeding

A

In addition to other interventions…total rest to prevent crippling effects of hemarthrosis
No ASA, but other pain meds should be given
When bleeding stops, mobilize the joint with passive range of motion
Weight bearing resumes when swelling resolves

18
Q

hemophilia antifibrinolytics desmopressin acetate (DDAVP)

A

MOA: causes an increase in plasma factor VIII (von Willebrand factor), and an increase in t-PA
Contraindicated: in known sensitivity and those with nephrogenic diabetes insipidus
Adverse events: thrombotic events like acute cerebrovascular thrombosis and AMI
CV: dysrhythmias, orthostatic hypotension, brady
CNS: headache, dizziness, fatigue, hallucinations, convulsions
GI: nausea, vomiting, abdominal cramps, diarrhea
Administered: PO, IV, Intranasal
Interactions:
Estrogen/ oral contraceptives + tranexamic acid = additive effects resulting in increased coagulation
Caution with DDAVP + lithium, or heparin, or ETOG, or epinephrine
Pharmacokinetics:
Onset of Action (IV): 15-30 min
Peak Plasma Concentration: 1-2 h ours
Half Life: 2 hours