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

(56 cards)

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
thalassemia treatment
blood transfusions, splenectomy, bone marrow transplantation, genetic counseling
26
sickle cell anemia etiology
genetic defect of hemoglobin synthesis, results in hemoglobin instability, autosomal recessive disorder
27
sickle cell anemia pathogenesis
predisposes RBC's to early destruction due to abnormalities in structure, sickled cells cause vascular occlusion
28
lab findings sickle cell anemia
severe anemia, RBC’s of different shapes and sizes
29
sickle cell anemia treatment
O2, pain management, fluids, stem cell transplant
30
hemolytic disease of the newborn
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
complications of hemolytic disease of the newborn for the newborn
anemia, reticulocytosis, nucleated RBC's in blood of infant
32
how to prevent hemolytic disease of the newborn
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
acute blood loss
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
acute blood loss treatment
blood volume replacement therapy
35
thrombocytopenia
common cause of general bleeding: has 2 types-- ITP and acquired thrombocytopenia
36
ITP--idiopathic thrombocytopenia purpura
autoimmune, platelets function normally but live only 1-3 days. acute= after viral illness. chronic= women aged 20-40
37
acquired thrombocytopenia
diminished or defective platelet production, splenic sequestration, medications, platelet dilution
38
thrombocytopenia pathogenesis
general mechanisms: decreased platelet production, decreased platelet survival, intravascular dilution of circulating platelets
39
thrombocytopenia lab findings
low platelet count, prolonged bleeding time, abnormal peripheral smear
40
thrombocytopenia clinical manifestations
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
treatment for thrombocytopenia
based on identified cause
42
hemophilia
most common inherited genetic disorder; excessive bleeding
43
hemophilia etiology
x linked recessive disorder (mother to son), 25% due to genetic mutation (not family history)
44
types of hemophilia
hemophilia A--classic hemophilia, factor VIII deficiency hemophilia B-- Christmas disease, factor 9 deficiency
45
treatment for hemophilia
patient/family education, hemophilia A= cryoprecipitate or factor VIII concentrate hemophilia B= fresh frozen plasma or cryoprecipitate
46
hemophilia clinical manifestations
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
Von willebrand disease
disorder of factor VIII and platelet function, excessive bleeding
48
etiology of vwd
autosomal dominant inheritance
49
pathogenesis of vwd
VW factor is needed to stabilize factor VIII and for platelet adherence. Bleeding occurs when VWF is decreased or absent
50
vwd clinical manifestations
nose bleed, mucosal bleed, bruising, GI hemorrhage, menorrhagia, hemarthrosis (rare)
51
vwd lab tests
prolonged bleeding time, normal platelet count
52
vwd treatment
replace VWF
53
disseminated intravascular coagulation
acquired bleeding syndrome, clotting and bleeding occur simultaneously. NOT a disease itself, develops second to other conditions
54
etiology of DIC
trauma, burns, shock
55
pathogenesis of DIC
continued release of thromboplastic material causes abnormal levels of thrombin in plasma--> essential to clot breakdown---> leads to emboli
56
clinical manifestations of DIC
Bleeding; often from 3 or more sites, Weakness, malaise, fever, CNS bleeding, altered LOC