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Pathophysiology > Chapter 13 > Flashcards

Chapter 13 Flashcards

1
Q

Anemia

A
  • a deficit of red cells

- can be relative or absolute

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2
Q

Relative Anemia

A
  • normal total red cell mass with disturbances in regulation of plasma volume
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3
Q

Absolute Anemia

A
  • actual decrease in numbers of red cells
  • decreased production
  • increased destruction
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4
Q

Aplastic Anemia

A
  • Body stops making enough new blood cells
  • insidious onset of symptoms
  • late symptoms include weakness, fatigue, lethargy, pallor (paleness), dyspnea, palpitations, transient murmurs and tachycardia related to low RBCs
  • thrombocytopenia
  • neutropenia
  • fatal unless successful bone marrow transplant
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5
Q

Treatment of Aplastic Anemia

A
  • Identify and avoid further toxic exposure
  • type HLA and ABO to identify serologically defined loci and potential donors
  • maintain minimally essential levels of hemoglobin and platelets
  • prevent and manage infection
  • determine efficacy of bone marrow transplantation
  • administer immunosuppressive therapy
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6
Q

Anemia of Chronic Renal Failure

A
  • failure of the renal endocrine function impairs erythropoietin production and bone marrow compensation
  • decreased RBC count with low hematocrit and hemoglobin level
  • 95% respond to erythropoietin therapy
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7
Q

Treatment of Anemia of Chronic Renal Failure

A
  • dialysis
  • administration of erythropoietin
  • Replacement of iron, folate, and B12
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8
Q

Anemia Related to Vitamin B12 or Folate Deficiency (pernicious anemia)

A
  • pernicious anemia due to lack of intrinsic factor leading to vitamin B12 deficiency
  • Folate deficiencies from dietary deficiencies, alcoholism, cirrhosis, pregnancy, or infancy
  • disruption in DNA synthesis of blast cells produces megaloblasts due to deficiencies
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9
Q

Clinical Manifestations of Pernicious Anemia

A
  • low RBC (properly functioning), WBC, and platelet counts with increased MCV (Mean Corpuscular Volume); megaloblastic dysplasia
  • peripheral nerve degeneration
  • shillings test indicates low B12
  • gastric analysis reveals achlordydria
  • megoblastic madness
    (MVC = Blood cell volume; Megaloblast = abnormally big RBC, doesnt function properly)
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10
Q

Treatment of Pernicious Anemia

A
  • recognize that megaloblastic anemia is present
  • ascertain if vitamin B12 folate or a combined deficiency is the cause
  • diagnose underlying disease and mechanism responsible
  • for B12 administer B12 parenterally or orally and K supplements
  • For folate administer folic acid
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11
Q

Iron Deficiency Anemai

A
  • most common nutritional deficiency in the world
  • insufficient iron for hemoglobin synthesis
  • hypochromic, microcytic RBCs; Low MCV, MCH, and MCHC
  • Serum ferritin level decreased; serum iron level decreased; total iron binding capacity (TIBC) increased
  • excellent prognosis
    (MCH = Mean corpuscular Hemoglobin; MCHC = mean corpuscular hematocrit)
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12
Q

Symptoms of Iron Deficiency Anemia

A
  • pica (craving for non food substances)
  • Koilonychias (spoon shaped nails)
  • Blue sclerae
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13
Q

Treatmen of Iron Deficiency Anemia

A
  • oral administration of ferrous sulfate or intravenous ferric gluconate (only in severe cases)
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14
Q

Thalassemia

A
  • increased RBC destruction (hemolysis) resulting in decreased RBC survival rates
  • associated with mutant genes that auppress the rate of globin chain synthesis
  • classified by the polypeptide chains with deficient synthesis (alpha and beta thalassemia)
  • most clinically severe form: thalassemia major
  • prognosis depends on type
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15
Q

Symptoms of Thalassemia

A
  • Hypochromic, microcytic RBCs
  • MCV, MCH, and MCHC are low
  • Erythroblastic hyperplasia (bone marrow)
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16
Q

Treatment of Thalassemia

A
  • blood transfusions
  • splenectomy
  • chelation therapy
  • bone marrow transplantation
  • genetic counseling
17
Q

Sickle Cell Anemia

A
  • genetically determined defect of hemoglobin synthesis resulting in hemoglobin instability and insolubility
  • sickled cells cause vascular occulsion
  • severe anemia, RBCs of different shapes and sizes, recurrent painful episodes
18
Q

Treatment and Prognosis of SIckle cell Anemia

A
  • treatment: stem cell transplant

- Prognosis: death if no/unsuccessful transplant

19
Q

Glucose 6 Phosphate Dehydrogenase Deficiency

A
  • genetic disorder resulting in RBC membrane destruction; most common
  • Do not have hemolytic anemia unless challenged by drugs, infection
20
Q

Treatment and Prognosis of Glucose 6 Phosphate Dehydrogenase Deficiency

A

Treatment is preventive: avoidance of drugs that trigger hemolytic episodes
Prognosis: good unless has fava bean susceptibility

21
Q

Hemolytic Disease of the Newborn

A
  • Fetal RBCs cross the placenta, stimulate production of maternal antibodies against antigen on fetal RBC not inherited from mother
  • Maternal antibodies cross into the fetal circulation causing destruction of fetal cells
22
Q

Treatment and Prognosis of Hemolytic Disease of the Newborn

A

Treatment: standard dose of anti-Rh immune globulin (RhoGAM) is given to the mother before or after delivery . In sever cases, in utero blood transfusion and early delivery
Prognosis: Death, possible retardation, or barely perceptible hemolytic process

23
Q

Antibody Mediated Drug Reactions

A
  • exposure to a drug causes destruction and lysis of the sensitized person’s own RBCs
  • Mechanisms include: hapten mechanisms, neoantigen formation, membrane modification, and autoantibody induction
  • May have schisocytes
24
Q

Treatment and Prognosis of Antibody Mediated Drug Reactions

A

Treatment: Recognize and discontinue offending medications, sometimes steroids given
Prognosis: good unless severe hemolysis

25
Q

Acute Blood Loss

A
  • may be from trauma or secondary to a disease process
  • Symptoms develop with activity at 20% loss of blood volume and increase in severity with continued blood loss
  • shock and death can occur with 50% loss of circulating volume
26
Q

Treatment and Prognosis of Acute Blood Loss

A

Treatment: blood volume replacement therapy with crystalloids, colloids, and fresh whole blood
Prognosis: Excellent with treatment unless blood loss is severe

27
Q

Polycythemia

A
  • Excess RBCs resulting in increased blood viscosity, leading to clinical symptoms such as hypertension
  • Types of polycythemia are categorized by cause
  • 3 types: Polycythemia Vera, Secondary Polycythemia, Relative Polycythemia
28
Q

Polycythemia Vera

A
  • Neoplastic transformation of bone marrow stem cells
  • Absolute increase in RBC mass, leukocytosis, and thrombocytosis
  • Increased uric acid due to excess proliferation
  • oxygen saturation normal
29
Q

Treatment and Prognosis of Polycythemia Vera

A

Treatment: reducing increased blood volume, viscosity, RBC mass and platelet count with phlebotomy (drawing blood), radioactive phosphorous, and chemotherapeutic agents
Prognosis: poor unless properly managed, no cure

30
Q

Secondary Polycythemia

A
  • due to chronic hypoxemia with resultant increase in erythropoientin production
  • increased RBC production without increase in WBCs or platelets
31
Q

Treatment and Prognosis of Secondary Polycythemia

A

Treatment: Identify and manage underlying cause of hypoxemia; phlebotomy may be used to decrease cardiovascular workload
Prognosis: depends on underlying condition

32
Q

Relative Polycythemia

A
  • due to dehydration with spurious increase in RBC produtction
  • 2 grps (disturbed fluid balance, stress polycythemia)
  • elevated hematocrit, hemoglobin, and RBC count
33
Q

Treatment and Prognosis of Relative Polycythemia

A

Treatment: Recognize and manage underlying cause; fluid administration with management of long term conditions
Prognosis: excellent if managed properly

34
Q

Blood transfusion tests

A

Before transfusion therapy can occur, various donor
tests are performed on the blood unit sample. These include ABO and Rh(D); syphilis; HIV antigen and antibodies; hepatitis B and C antigens; and human T-cell lymphotropic virus. Blood centers, which are producing plasma for fractionation, also test for alanine aminotransferase. 68 Speciic pretransfusion testing using blood samples from the recipient and the donor unit must be done to ensure that the blood component will not harm the recipient and that the blood component
will have an acceptable survival time when transfused. ABO and Rh typing and RBC antibody detection tests are performed, and then a cross-match between the donor unit and the recipient is performed.

35
Q

Blood transfusion

A

Medical indications for transfusion therapy are restoration or maintenance of oxygen-carrying capacity, blood volume, hemostasis, and leukocyte function. Red cell transfusions are administered to improve tissue oxygenation in the context of anemia or acute blood loss

Pathophysiology (34 decks)

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