Exam V - Heme Flashcards
Life cycle of the RBC, including its’ breakdown and byproducts, and related processes for increasing its’ count
Formation and maturation from normoblasts/erythroblasts in long bone marrow –> circulation ( 3 months) –> erythrocyte senescence by MPS in spleen, sometimes liver –> breakdown into hemoglobin (–> bilirubin and amino acids)
-Maturation stimulated by Epo from kidneys (which sense hypoxia)
Compare and contrast terms used to define increased and decreased levels of WBCs, RBCs, platelets
WBCs:
-leukocytosis/leukopenia
RBCs:
-polycythemia/anemia
Platelets:
-thrombocytosis/thrombocytopenia
in general: “-cytosis”, “-philia” = increase and “-penia” = decrease
Pathophysiology of eosinophilia and basophilia.
Eosinophila:
-Type 1 hypersensitivity reaction/parasitic infection –> release of ECT from mast cells –> high eosinophils
Basophilia:
-Inflammatory/hypersensitivity reaction –> high basophils
Describe thrombus, it’s pathophysiology
Virchow’s triad –> stationary clot formation
Describe general signs and symptoms of anemia
Hypoxemia leads to: tachycardia, fatigue, weakness, dypsnea, pallor, SoB, dizzy, headache, glossitis
Manifestations occur when HgB ~7/8
Compare and contrast types and etiologies of anemia (pernicious, folate, iron)
-Pernicious (macrocytic): lack of IF –> B12 deficiency –> damage to myelin sheath –> neuro symptoms
-Folate (macrocytic): folic acid deficiency (dietary issue, alcoholism)
-Iron deficiency (microcytic): most common–dietary deficiency, impaired absorption, blood loss, surgery, eating disorder. Progressive
-S/S: koilonychia (spoon nails), glossitis, angular stomatitis
Describe pathophysiology and clinical manifestations of Infectious mononucleosis (IM)
Patho: EBV –> B lymphocyte infection –> 30-50 day incubation –> flu like symptoms
CM: fever, sore throat, swollen lymph nodes, fatigue, increased lymphocytes, splenomegaly/splenic rupture
Describe pathophysiology and clinical manifestations of leukemia in general ways (acute vs chronic etc)
Patho: uncontrolled malignant leukocyte proliferation
Acute (ALL, AML): fever, anorexia, neuro
Chronic (CML, CLL): insidious–infection, fever, weight loss, spleen and liver enlargement
Explain potential triggers, pathophysiology, clinical manifestations of DIC
Triggers: sepsis, trauma, burn
Patho: exposure to TF –> unregulated thrombin release/fibrin formation AND fibrinolysis/thrombocytopenia –> clotting and hemorrhage at the same time
CM: uncontrolled bleeding from venipunctures/lines, purpura/petechia/hematoma, symmetric cyanosis
Describe pathophysiology of hemolytic disease of the fetus and newborn (HDFN)
patho: maternal antibodies in blood (parent has diff blood type than fetus & sufficient blood transfer) –> IgG binds w/ fetal erythrocytes –> widespread hemolysis –> anemia
Describe pathophysiology, genetic inheritance, clinical manifestations of sickle cell disease
Patho: Abnormal Hb S triggered –> sickling –> clogging of vessels
Genetic: autosomal recessive Hb S from one parent (valine AA replaces glutamic AA), Hb A from other parent
CM: thrombotic crisis (stroke risk, renal risk), aplastic anemia, sequestration crisis (blood in liver/spleen)
Discuss triggers that worsen sickling of RBCs in sickle cell disease
Hypoxemia/dehydration:
-low pH
-Low temp
-decreased plasma volume
Describe pathophysiology of ITP, triggers
autoimmune platelet destruction
Patho: autoantibodies bind to platelet PM –> splenic/lymph phagocytes sequester/destroy them
Triggered by drugs, infection, lymphoma…
Describe Hemophilia A vs B and the related deficiency
A:
B: