Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
54 Cards in this Set
- Front
- Back
incorrect statement about RBCs
a) large nucleus b) no mitochondria c) biconcave d) live 120 days |
large nucleus is incorrect-
Mature RBCs are anucleus |
|
what is the primary function of RBC
a) Carry CO2 attached to Hb b) Immune Response c) Clotting ability d) Carry O2 via Hb |
Carry O2 via Hb
|
|
T/F
in adult life the LV and SP are essential for producing RBCs |
F
Fetal life- yolk sac, LV, SP Adult- Bone Marrow |
|
RBCs first appear in the blood as
a) erythrocyte b) proerythroblasts c) reticulocyte d) none |
reticulocyte- matures w in 1-2 days
|
|
T/F
RBCs create ATP via their mitochondria |
F- RBCs do not have mitochondria- instead use glycolytic pathway
|
|
Which of the following is not used in the destruction of RBCs
a) LV b) SP c) Marrow d) lymphnode e) all are used |
All
Sp is primary organ |
|
T/F
the Fe+ attached to the Hb is recycled during RBC destruction |
True
Fe, AA, Globin chains are recycled the rest is converted to bilirubin |
|
T/F
bilirubin is insoluble in plasma |
T
|
|
describe the pathway of bilirubin
|
insoluble
enters LV-conjugated to soluble form stored in GB bile released into intestines and blood intestines excrete form in stools blood enters KD- urobilinogen elim in urine |
|
T/F
O2 bind to adult Hb easier than fetal Hb |
F
|
|
RBCs entering the LU are
Saturated or Unsaturated? |
unsaturated >4 O2 attached
|
|
define anemia
|
lo number of circulating RBCs and/or Hb levels
|
|
upon receiving blood test results your female px has
Hct: 35%, RBCs: 3M/mm3 [Hb]: 11g/dl is she anemic? |
yes
Normal Female Levels Hematocrit Female 37-47% RBC# 3.6-5 [Hb] 12-15g/dl |
|
Your male px was feeling fatigued so you ordered a blood work up. results were
Hct 42% RBCs 5 [Hb] 15g/dl is he anemic? |
no
Normal Male levels Hct 40-50% RBC# 4.5-5.5 [Hb]14-16 |
|
The general manifestations of Anemia are similar to that of
a) ischemia b) hypoxia c) ca++ xu d) none |
hypoxia
|
|
list manifestations of anemia
|
pallor
dizzy fatigue/weakness dyspnea angina cramps palpitations, ht murmur, ventricular hypertrophy bone pain, sternal tenderness |
|
list the lab tests used to determine anemia
|
RBC count- decrease
Reticulocyte Count- increase Hb- decrease Hct- decrease |
|
List the types of anemia
|
hemolytic
nutritional blood loss aplastic chronic disease |
|
____amount of blood loss can cause anemia
|
20%
either acute or chronic |
|
Hemolytic Anemia
a) premature destruction of RBCs b) loss of 20% blood c) reduction of platelets d) rheumatoid arthritis |
premature destruction of RBCs
|
|
list the types of hemolytic anemia
|
spherocytosis
sickle cell thalassemia G6PD xu |
|
list the types of nutritional anemia
|
Fe xu
B12 xu Folic Acid xu |
|
Your px comes to you because they experience recurring gallstones, with a full inspection you find that their spleen is enlarged upon palpation, and they have a mild form of jaundice
what is the diagnosis a) Thalaseemia b) Iron xu c) Spherocytosis d) G6PD xu |
spherocytosis- autosomal dominant trait w xu of membrane protein causing deformity of RBC
|
|
What is the treatment for spherocytosis
a) blood transfusion b) spleenectomy c) there is no cure d) Fe supplement |
spleenectomy
blood transfusion- aplastic anemia no cure- sickle cell- pain management only |
|
Which of the following is not an autosomal dominant trait
a) spherocytosis b) thalassemia c) sickle cell d) G6DP |
sickle cell = autosomal recessive- defective beta chain of Hb
G6DP = x linked dominant- lack of NADPH prdctn |
|
T/F
sickle cell causes painful aggregation of Hb whenever O2 is hi |
F
Hypoxia/lo O2 causes aggregation prevention = avoid sickling episode, lo O2, infection, cold, exertion, acidosis, dehydration |
|
Which of the following can cause sickling episodes
a) infection b) acidosis c) dehydration d) all e) none of the above |
All
anything that causes hypoxia |
|
which is not a manifestation of sickle cell
a) organ infarct b) hyperbilirubinemai c) bone marrow expansion d) stroke d) |
bone marrow expansion = thalassemia
|
|
what is the cause of thalassemia
a) absence of alpha chain b) absence of beta chain c) imbalance of globin chain prdctn d) all |
all are possible causes
|
|
Coombs test is used for
a) Thalassemia, b) G6DP c) Aplastic Anemia d) Acquired hemolytic Anemia |
Acquired Hemolytic Anemia
lab tests Thalassemia- monitor Hb G6DP assay Aplastic- bone marrow biopsy |
|
Which is not a manifestation of Thalassemia
a) hemolysis post infection b) growth retardation c) hepatomegaly d) b, c |
hemolysis following infection, malarial drugs, sulfonomides/aspirin
Thalassemia CM also spleenomegaly bone marrow expansion thinning of cortical bone |
|
list the treatments for Fe Xu anemia
|
control blood loss
increase dietary Fe Fe supplement |
|
Fe is stored in
a) Sp b) Lv c) Kd d) none |
LV
|
|
a lo MC and MCHC is indicative of
a) Aplastic Anemia b) B12 xu c) Sickle Cell d) Fe xu |
Fe xu
also: hypochromic microcytic RBCs |
|
T/F
the RBCs of a person with Fe Xu anemia will be pale and small compared to normal RBCs |
True
Hypochromic Microcytic RBCs |
|
T/F
Folic Acid Xu can cause neuropathy |
F
B12-> neuropathy due to demyelination |
|
Megaloblastic Anemia is the lab result of
a) Fe xu b) B12 xu c) Folic Acid xu d) a,b e) b,c f) all |
B12, Folic Acid
|
|
The following are characteristics of Aplastic Anemia except
a) reduced RBCs b) reduced WBCs c) reduced Platelets d) none |
Aplastic Anemia= reduction in all 3
|
|
list the manifestations of Aplastic Anemia
|
anemia (RBC)
hemorrhage (WBC) infection (Platelets) |
|
Which is not a treatment of Aplastic Anemia
a) avoid toxic agent b) avoid cold c) marrow transplant d) blood transfusion |
cold- sickle cell
|
|
Abnormally hi number of RBCs
|
polycythemia
|
|
list the types of polycythemia
|
relative
polycythemia vera secondary |
|
true statement about relative polycythemia
a) compensatory response b) dysfunction of the bone marrow c) treat by increasing vascular volume d) none |
treat by increasing vascular volume
bc due to loss of plasma volume- (liquid solid imbalance s/a dehydration, burns) |
|
Incorrect statement about primary polycythemia
a) xs proliferation of pluirpotent cells b) due to increase in erythropoiten c) TIAs d) tx via reducing blood viscosity |
due to increase in erythropoiten = secondary polycythemia
|
|
lab test for plolycythemia vera would indicate all of the following except
a) hi RBC count b) hi Hb c) hi Hct d) all would be present |
all
|
|
list the manifestations of polycythemia vera
|
HA
itch dusky red appearance angina deep vein thrombosis TIA HBP |
|
what is the treatment plan for secondary polycythemia?
|
relieve hypoxia
(polycyth ver- tx- reduce viscosity) (relative polycyth- tx- increase vascular fluid) |
|
Neonate Physiologic anemia occurs
a) at birth b) 2-3 day of life c) 1 week d) 2 months |
2 months
|
|
Neonate physiologic jaundice occurs
a) at birth b) 2-3 day of life c) 1 week d) 2 months |
2-3 day
self limited by 1 week |
|
Neonate pathologic jaundice occurs
a) at birth b) 2-3 day of life c) 1 week d) 2 months |
at birth or 1 week later
treated with phototherapy manifestation= kernicterus |
|
list the causes of pathologic jaundice in a neonate
|
hemolytic disease- erythroblastosis fetalis
hypoxia infections acidosis drugs |
|
T/F
erythroblastosis fetalis occurs when the infant is Rh- and the mother is Rh+ |
F-
infant = Rh+ mother = Rh- occurs with the 2nd child |
|
list the manifestations of a blood transfusion reaction
|
flushed face
uticaria chills, fever nausea cramping ab pain tachycardia hypotension dyspnea |
|
T/F
When the incorrect blood is used in a transfusion the donor's RBCs are attacked by the recipients antibodies |
True
will recipient blood destroy donor blood? |