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NURS 8022 EXAM 2
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Exam study book Recent Trends in International Migration of Doctors, Nurses and Medical Students of OECD - ISBN: 9789264318656 (NURS 8022 EXAM 2)
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NURS 8022 EXAM 2 LATEST ACTUAL EXAM QUESTIONS AND CORRECTDETAILED ANSWERS WITH RATIONALES (VERIFIED ANSWERS) |
ALREADY GRADED A+
Hematopoiesis - ANSWER: Process of blood cell production in adult bone marrow or
the liver and/or spleen of the fetus
Two stages
▪ Mitosis (proliferation)
▪ Maturation (differentiation)
Primary site of hematopoietic stem cells - ANSWER: Bone marrow ("myeloid tissue")
Difference between red and yellow bone marrow - ANSWER: Red marrow produces
RBCs, yellow marrow does not produce RBCs
Active bone marrow sites - ANSWER: pelvic bones
vertebrae
cranium
mandible
sternum
ribs
humerus
femur
Factors that increase hematopoiesis - ANSWER: (1) conversion of yellow bone
marrow, which does not produce blood cells, to hematopoietic red marrow by the
actions of erythropoietin (a hormone that stimulates erythrocyte production)
(2) faster differentiation of progenitor cells
(3) faster proliferation of stem cells into progenitor cells
Erythropoiesis - ANSWER: production of RBCs
Sequence of erythropoiesis - ANSWER: Pluripotent hematopoietic stem cell -->
committed Proerythroblast/Pronormoblast --> Erythroblast/Normoblast (Hgb
synthesis begins) --> Reticulocyte (nucleus is lost; 3 days spent in bone marrow,
about 1 day in blood) --> Erythrocyte
** aprox. 1% of RBCs are reticulocytes **
In each step the quantity of hemoglobin increases and the nucleus decreases in size
Erythropoietin - ANSWER: A hormone produced and released by the kidney that
stimulates the production of red blood cells by the bone marrow
Always present in plasma
,Released in response to low renal oxygenation
- NOT the # of RBCs but rather oxygen delivery
- e RBC production increases within 24 hours; life span 4-12 hours; increased RBC #
in 5 days
- Given to dialysis and chemo patients
Reticulocytes - ANSWER: ▪ Last immature form of erythroblast
▪ Contains polyribosomes (globin synthesis) and mitochondria (heme synthesis)
▪ 24-48 hours after leaving bone marrow for circulation, matures into erythrocyte
- Loses polyribosomes and mitochondria
-Make up 1-2% of RBCs
- Last about 2 days in bone marrow and 1 day in blood continuing to mature
- During time of low HCT time in marrow decreased to as little as 1 day
▪ Reticulocyte count -- Indicates whether new RBCs are being produced; good
indicator of erythropoiesis
Hemoglobin and its structure - ANSWER: Oxygen-carrying protein of the erythrocyte
--> may carry up to 300 hgb molecules
Reversible deformity to be abvle to squeeze through the tiniest of capillaries
Each Hgb molecule has 2 pairs of different globin chains and 4 complexes of iron +
heme
▪ Heme: large, flat, iron-protoporphyrin disk that is synthesized in the mitochondria
and can carry one molecule of oxygen
▪ Each Hgb can carry 4 molecules of oxygen
Heme vs Globin - ANSWER: Heme: Synthesized in mitochondria of reticulocyte
- Carries Oxygen
Globin: Polyribosomes in reticulocytes
- 2 pairs of globin chains on each Hgb molecule
- Combo of pair determines type of globin chain
▪ Most common hgb A: 2 alpha chains and 2 beta chains - hgb F (fetal): 2 alpha, 2
gamma
Red blood cell structure - ANSWER: Sac of Hgb, no nucleus or mitochondria, only
hemoglobin & enzymes surrounded by membrane
-Lack mitochondria, rely on glycolysis for energy --> "aerobic metabolism"
▪ Deficiencies of 2 enzymes result in anemia
,• Pyruvate kinase - necessary for glycolysis - no glycolysis results in RBC damage and
death
• G6PD - involved in protecting the RBC against oxidative stress
Anisocytosis
Poikilocytosis - ANSWER: Variation in RBC size
Variation in RBC shape
Hereditary vs Acquired Hemolysis - ANSWER: Hereditary hemolysis: sickle cell
disease
Acquired hemolysis: immune mechanisms (transfusion reaction), infection (malaria),
drugs (penicillin), liver or kidney disease, toxins (chemicals, venoms)
Normal Labs (RBCs, Hgb, Hct, MCV, MCH) - ANSWER: RBCs 4.2-6.1
Hgb 12-18
Hct 35-50%
MCV: 78-100 (related to size)
MCH: 27-34 (related to hgb content)
Reticulocytes: new RBC formation - low suggest issues in production
Microcytic-Hypochromic Anemias - ANSWER: Characterized by red cells that are
abnormally small and contain reduced amounts of hemoglobin
Iron Deficiency Anemia (IDA)
Sideroblastic
Thalassemia
Iron Deficiency Anemia (IDA) - ANSWER: Type of Microcytic-Hypochromic Anemia
- Most common type of anemia
- Highest risk: older adults, women, infants, poverty
- Associated with cognitive impairment in children
- Causes: inadequate dietary intake; excessive blood loss (GI bleed most common
pathophysiologic cause); chronic parasite infestations; metabolic or functional iron
deficiency; menorrhagia (most common physiologic cause)
** Good sign of malignancy for postmenopausal women and men **
IDA Diagnostic Manifestations - ANSWER: ▪ Low MCV, low MCH
▪ High RDW
▪ Low initial reticulocyte count - elevated once treatment and iron supplementation
begin
, ▪ Ferritin low - #1 test for IDA
▪ Low serum iron; TIBC high - not enough iron to bind transferrin
IDA Clinical Manifestations - ANSWER: ▪ Mild (hgb 10-12): likely no symptoms
▪ Moderate (hgb 7-11): palpitations, dyspnea, exercise intolerance, angular
stomatitis, glossitis, pallor, koilonychia (pitting nails), pica (eating disorder in which a
person eats things not usually considered food)
▪ Severe (hgb <7): postural hypotension, dizziness, weakness, gastritis, paresthesias,
lethargy
▪ Elderly: lethargy and confusion
Sideroblastic Anemia - ANSWER: Type of Microcytic-Hypochromic Anemia
Caused by a defect in mitochondrial heme synthesis
▪ Altered mitochondrial metabolism causes ineffective iron uptake and results in
dysfunctional hemoglobin synthesis --> intracellular iron accumulates
- Can be due to alcohol abuse, lead poisoning
Sideroblastic Anemia Diagnostic Manifestations - ANSWER: - Presence of ringed
sideroblasts in the bone marrow are diagnostic (erythroblasts contain iron granules
that have not been synthesized into hemoglobin)
- Hct 20-30%
- MCV usually normal
- Elevated serum iron ** iron overload** Enlarged spleen and liver
- High transferrin saturation = Low TIBC
Thalassemia - ANSWER: Type of Microcytic-Hypochromic Anemia
Characterized by abnormal formation of hemoglobin resulting from mutation that
causes loss of one or both alpha globin chains or one or both of beta globin chains
-- Abnormal hgb formed results in improper oxygen transport and destructing of
RBCs results in anemia
Autosomal recessive trait
Target cells may be seen
Thalassemia Diagnostic Manifestations - ANSWER: ▪ Hemoglobin electrophoresis =
diagnostic test
▪ Low MCV, low MCH
▪ Ferritin normal to high
▪ Serum iron normal to high
▪ TIBC normal
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