PATHO-- RBC's, anemias, alterations in homeostasis Flashcards

1
Q

aplastic anemia

A

stem cell disorder characterized by reduction of hematopoietic tissue in bone marrow and pancytopenia (reduction in WBC, RBC, platelets)

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2
Q

aplastic anemia etiologies

A

toxic, radiant, or immunologic injury to bone marrow stem cells

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3
Q

aplastic anemia clinical manifestations

A

late symptoms–fatigue, tachycardia, weakness, lethargy. Pancytopenia

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4
Q

labs of aplastic anemia findings

A

RBC’s are normocytic and normochromic

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5
Q

aplastic anemia treatment

A

bone marrow transplant

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6
Q

anemia of chronic renal failure

A

failure of renal function impairs erythropoietin production and bone marrow compensation

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7
Q

anemia of chronic renal failure labs

A

decreased RBC count with low HCT and HGB level

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8
Q

anemia of chronic renal failure treatment

A

dialysis and administration of erythropoietin

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9
Q

RBC appearance in labs anemia of chronic renal failure

A

normocytic, normochromic

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10
Q

pernicious anemia etiology

A

lack of intrinsic factor causes vitamin B-12 deficiency due to malabsorption of vitamin b-12

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11
Q

pernicious anemia lab findings

A

low RBC, WBC, and platelets, increased MCV

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12
Q

RBC appearance in labs pernicious anemia

A

microcytic

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13
Q

pernicious anemia clinical manifestations

A

pallor, fatigue, sore tongue, anaorexia, nausea and vomiting, abdominal pain

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14
Q

pernicious anemia neurological manifestations

A

Paresthesias of hands and feet, reduced vibratory position and sense, muscle weakness, impaired thought process

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15
Q

folate deficiency anemia etiologies

A

poor dietary intake,

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16
Q

folate deficiency anemia cells

A

macrocytic, normochromic

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17
Q

iron deficiency anemia etiologies

A

inadequate diet, malabsorption of iron, blood loss

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18
Q

iron deficiency anemia pathogenesis

A

body’s Fe+ stores depleted, lack of Fe+ for bone marrow which leads to iron deficient RBC production

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19
Q

iron deficiency anemia clinical manifestations

A

pallor, fatigue, hypoactivity, pica, glossitis

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20
Q

iron deficiency anemia lab findings

A

hypochromic and microcytic RBC’s, low MCV, MCH, and MCHC, TIBC increased

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21
Q

iron deficiency anemia treatment

A

PO ferrous sulfate or IV ferrous gluconate

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22
Q

thalassemia etiology

A

is a GENETIC DISORDER group associated with presence of mutant genes

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23
Q

thalassemia pathogenesis

A

increased RBC destruction (hemolysis) results in decreased RBC survival rate

24
Q

thalassemia lab findings

A

hypochromic and microcytic RBC’s, MCV, MCH, and MCHC are low, erythroblastic hypoplasia

25
Q

thalassemia treatment

A

blood transfusions, splenectomy, bone marrow transplantation, genetic counseling

26
Q

sickle cell anemia etiology

A

genetic defect of hemoglobin synthesis, results in hemoglobin instability, autosomal recessive disorder

27
Q

sickle cell anemia pathogenesis

A

predisposes RBC’s to early destruction due to abnormalities in structure, sickled cells cause vascular occlusion

28
Q

lab findings sickle cell anemia

A

severe anemia, RBC’s of different shapes and sizes

29
Q

sickle cell anemia treatment

A

O2, pain management, fluids, stem cell transplant

30
Q

hemolytic disease of the newborn

A

fetal RBC’s cross the placenta, stimulate production of maternal antibodies against antigen on fetal RBC’s not inherited by mother, maternal antibodies cross into fetal circulation and destroy fetal cells

31
Q

complications of hemolytic disease of the newborn for the newborn

A

anemia, reticulocytosis, nucleated RBC’s in blood of infant

32
Q

how to prevent hemolytic disease of the newborn

A

Standard dose of anti-Rh immune globulin (RhoGAM) is given to mother
before or after delivery, in some cases in eutero transfusion or early delivery

33
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 (tachycardia & postural drop in BP), and increase in severity with
continued blood loss

34
Q

acute blood loss treatment

A

blood volume replacement therapy

35
Q

thrombocytopenia

A

common cause of general bleeding: has 2 types– ITP and acquired thrombocytopenia

36
Q

ITP–idiopathic thrombocytopenia purpura

A

autoimmune, platelets function normally but live only 1-3 days. acute= after viral illness. chronic= women aged 20-40

37
Q

acquired thrombocytopenia

A

diminished or defective platelet production, splenic sequestration, medications, platelet dilution

38
Q

thrombocytopenia pathogenesis

A

general mechanisms: decreased platelet production, decreased platelet survival, intravascular dilution of circulating platelets

39
Q

thrombocytopenia lab findings

A

low platelet count, prolonged bleeding time, abnormal peripheral smear

40
Q

thrombocytopenia clinical manifestations

A

platelet count is less than 150,000 (50,000 for spontaneous bleeding from slight trauma, below 20,000 life threatening), bruising (purpura, petechae), internal bleeding.

41
Q

treatment for thrombocytopenia

A

based on identified cause

42
Q

hemophilia

A

most common inherited genetic disorder; excessive bleeding

43
Q

hemophilia etiology

A

x linked recessive disorder (mother to son), 25% due to genetic mutation (not family history)

44
Q

types of hemophilia

A

hemophilia A–classic hemophilia, factor VIII deficiency
hemophilia B– Christmas disease, factor 9 deficiency

45
Q

treatment for hemophilia

A

patient/family education,
hemophilia A= cryoprecipitate or factor VIII concentrate
hemophilia B= fresh frozen plasma or cryoprecipitate

46
Q

hemophilia clinical manifestations

A

hemarthrosis (oozing of blood into soft tissue, muscle, joint capsule). Knee is most common site. Begins with a slight tear and joint expands with blood, leads to degenerative arthritis.

47
Q

Von willebrand disease

A

disorder of factor VIII and platelet function, excessive bleeding

48
Q

etiology of vwd

A

autosomal dominant inheritance

49
Q

pathogenesis of vwd

A

VW factor is needed to stabilize factor VIII and for platelet adherence. Bleeding occurs when VWF is decreased or absent

50
Q

vwd clinical manifestations

A

nose bleed, mucosal bleed, bruising, GI hemorrhage, menorrhagia, hemarthrosis (rare)

51
Q

vwd lab tests

A

prolonged bleeding time, normal platelet count

52
Q

vwd treatment

A

replace VWF

53
Q

disseminated intravascular coagulation

A

acquired bleeding syndrome, clotting and bleeding occur simultaneously. NOT a disease itself, develops second to other conditions

54
Q

etiology of DIC

A

trauma, burns, shock

55
Q

pathogenesis of DIC

A

continued release of thromboplastic material causes abnormal levels of thrombin in plasma–> essential to clot breakdown—> leads to emboli

56
Q

clinical manifestations of DIC

A

Bleeding; often from 3 or more sites, Weakness, malaise, fever, CNS bleeding, altered LOC