PAT401 Exam Questions & Answers
risk factors of leukaemia for children
prenatal x-ray, postnatal radiation, cigarette smoke exposure, exposure to pesticides and toxins
pre or during pregnancy, genetic mutations, conditions, monozygotic siblings
risk factors of leukaemia for adults
chemical exposure, chemotherapy, ionizing radiation, viral infections
four types of leukaemia
acute myelogenous, acute lymphocytic, chronic myelogenous, chronic lymphocytic
acute myelogenous leukaemia AKA
acute myeloblastic leukaemia
AML is more common in
adults
rate of AML
aggressive, fast growing with a 24% survival rate
what is AML
acute myelogenous leukaemia, overproduction and abnormal proliferation of myeloblasts
primary cell in AML
precursor myeloid cells
overproduction of myeloblasts
acute myelogenous / myeloblastic leukaemia
acute lymphocytic leukaemia AKA
acute lymphoblastic leukaemia
ALL is most common in
children
disorders involving erythrocytes?
,insufficient or excessive numbers of RBC in circulation or normal levels with abnormal
components
disorders involving leukocytes
increased numbers of WBC in response to infections or disorders like leukaemia or decreased
WBC
increased wbc
Leukocytosis
decreased WBC
leukopenia
disorders involving platelets
increase or decrease clotting in at least one of the 3 major components of the clotting process,
seen in many diseases
normal erythrocyte value
4.2-6.1 x 10^12/L
hematocrit
percentage of blood volume occupied by red blood cells
hematocrit value
0.40-0.54 g/L
hemoglobin
protein in red blood cells that carries oxygen for delivery to cells
hemoglobin normal value
7.4 - 11.2 mmol/L
what is sickle cell disease
blood disorder that causes the change in the structure of the hemoglobin, making RBC sickled
triggers of the sickling of cells
decreased PO2 of the blood, increased hydrogen ion concentration in the blood causing
acidosis, increased plasma osmolarity with decreased volume and temp
,decreased PO2 in blood
hypoxemia
increased hydrogen ions in blood
low pH, acidic
what is the abnormal hemoglobin in RBC during SCD
hemoglobin S or sickle hemoglobin (HbS)
severest form of SCD
sickle cell anemia
polymerization in sickle cell disease
sickled RBC stiffen and stretch into elongated shape, go from flexible and beneficial to inflexible
inflexibility of RBC in SCD causes
hypoxia and damage to tissues
does presence of sickle cell trait cause sickling
no because pt also produces the normal HbF and HbA which do not cause sickling
HbF
fetal hemoglobin
HbA
adult hemoglobin
HbF is present for
120 days, thus anemia persists
hemoglobin structural alterations in SCD are stimulated by
deoxygenation
deoxygenation in SCD stimulates
hemoglobin structural alterations
mutation of HbS
HbA --> point mutation to HbS
, how does HbS cause hemolysis
normal RBC has deoxygenation causing an influx of Ca and outflow of K and H2O, causing
extensive membrane damage, irreversible sickled cell, and hemolysis
hemolysis
destruction of red blood cells
what happens if HbS causes deoxygenation ONLY
influx of Ca, efflux of K and H2O, membrane damage, sickled cell, hemolysis
how does HbS cause microvascular occlusion
deoxygenated RBC becomes oxygenated again, dehydration and membrane damage, prolonged
transit times, occlusion
oxygenation of deoxygenated RBC can cause what
either microvascular occlusion or another cycle of deoxygenation
what happens when HbS deoxygenation becomes oxygenated
deoxygenation, damage to membrane, prolonged transit, occlusion
abnormal HbS in RBC causes what triggers
hypoxemia, decreased pH, low temp, decreased plasma volume
how does sickling of RBC occur
persistent hypoxemia from HbS, reducing of PO2 in circulation, sickling
how may sickled cells become normal
reversal of hypoxemia, reoxygenation, rehydration causing them to regain shape and resume
function
two ways sickling can increase
slow blood flow, hypoxemia OR low pH decreased hemoglobin affinity to O2, decreasing PO2
what do sickled cells do to vessels
clog
HbS to sickling
risk factors of leukaemia for children
prenatal x-ray, postnatal radiation, cigarette smoke exposure, exposure to pesticides and toxins
pre or during pregnancy, genetic mutations, conditions, monozygotic siblings
risk factors of leukaemia for adults
chemical exposure, chemotherapy, ionizing radiation, viral infections
four types of leukaemia
acute myelogenous, acute lymphocytic, chronic myelogenous, chronic lymphocytic
acute myelogenous leukaemia AKA
acute myeloblastic leukaemia
AML is more common in
adults
rate of AML
aggressive, fast growing with a 24% survival rate
what is AML
acute myelogenous leukaemia, overproduction and abnormal proliferation of myeloblasts
primary cell in AML
precursor myeloid cells
overproduction of myeloblasts
acute myelogenous / myeloblastic leukaemia
acute lymphocytic leukaemia AKA
acute lymphoblastic leukaemia
ALL is most common in
children
disorders involving erythrocytes?
,insufficient or excessive numbers of RBC in circulation or normal levels with abnormal
components
disorders involving leukocytes
increased numbers of WBC in response to infections or disorders like leukaemia or decreased
WBC
increased wbc
Leukocytosis
decreased WBC
leukopenia
disorders involving platelets
increase or decrease clotting in at least one of the 3 major components of the clotting process,
seen in many diseases
normal erythrocyte value
4.2-6.1 x 10^12/L
hematocrit
percentage of blood volume occupied by red blood cells
hematocrit value
0.40-0.54 g/L
hemoglobin
protein in red blood cells that carries oxygen for delivery to cells
hemoglobin normal value
7.4 - 11.2 mmol/L
what is sickle cell disease
blood disorder that causes the change in the structure of the hemoglobin, making RBC sickled
triggers of the sickling of cells
decreased PO2 of the blood, increased hydrogen ion concentration in the blood causing
acidosis, increased plasma osmolarity with decreased volume and temp
,decreased PO2 in blood
hypoxemia
increased hydrogen ions in blood
low pH, acidic
what is the abnormal hemoglobin in RBC during SCD
hemoglobin S or sickle hemoglobin (HbS)
severest form of SCD
sickle cell anemia
polymerization in sickle cell disease
sickled RBC stiffen and stretch into elongated shape, go from flexible and beneficial to inflexible
inflexibility of RBC in SCD causes
hypoxia and damage to tissues
does presence of sickle cell trait cause sickling
no because pt also produces the normal HbF and HbA which do not cause sickling
HbF
fetal hemoglobin
HbA
adult hemoglobin
HbF is present for
120 days, thus anemia persists
hemoglobin structural alterations in SCD are stimulated by
deoxygenation
deoxygenation in SCD stimulates
hemoglobin structural alterations
mutation of HbS
HbA --> point mutation to HbS
, how does HbS cause hemolysis
normal RBC has deoxygenation causing an influx of Ca and outflow of K and H2O, causing
extensive membrane damage, irreversible sickled cell, and hemolysis
hemolysis
destruction of red blood cells
what happens if HbS causes deoxygenation ONLY
influx of Ca, efflux of K and H2O, membrane damage, sickled cell, hemolysis
how does HbS cause microvascular occlusion
deoxygenated RBC becomes oxygenated again, dehydration and membrane damage, prolonged
transit times, occlusion
oxygenation of deoxygenated RBC can cause what
either microvascular occlusion or another cycle of deoxygenation
what happens when HbS deoxygenation becomes oxygenated
deoxygenation, damage to membrane, prolonged transit, occlusion
abnormal HbS in RBC causes what triggers
hypoxemia, decreased pH, low temp, decreased plasma volume
how does sickling of RBC occur
persistent hypoxemia from HbS, reducing of PO2 in circulation, sickling
how may sickled cells become normal
reversal of hypoxemia, reoxygenation, rehydration causing them to regain shape and resume
function
two ways sickling can increase
slow blood flow, hypoxemia OR low pH decreased hemoglobin affinity to O2, decreasing PO2
what do sickled cells do to vessels
clog
HbS to sickling
