Exam V - Heme Flashcards

1
Q

Life cycle of the RBC, including its’ breakdown and byproducts, and related processes for increasing its’ count

A

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)

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2
Q

Compare and contrast terms used to define increased and decreased levels of WBCs, RBCs, platelets

A

WBCs:
-leukocytosis/leukopenia

RBCs:
-polycythemia/anemia

Platelets:
-thrombocytosis/thrombocytopenia

in general: “-cytosis”, “-philia” = increase and “-penia” = decrease

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3
Q

Pathophysiology of eosinophilia and basophilia.

A

Eosinophila:
-Type 1 hypersensitivity reaction/parasitic infection –> release of ECT from mast cells –> high eosinophils

Basophilia:
-Inflammatory/hypersensitivity reaction –> high basophils

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4
Q

Describe thrombus, it’s pathophysiology

A

Virchow’s triad –> stationary clot formation

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5
Q

Describe general signs and symptoms of anemia

A

Hypoxemia leads to: tachycardia, fatigue, weakness, dypsnea, pallor, SoB, dizzy, headache, glossitis
Manifestations occur when HgB ~7/8

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6
Q

Compare and contrast types and etiologies of anemia (pernicious, folate, iron)

A

-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

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7
Q

Describe pathophysiology and clinical manifestations of Infectious mononucleosis (IM)

A

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

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8
Q

Describe pathophysiology and clinical manifestations of leukemia in general ways (acute vs chronic etc)

A

Patho: uncontrolled malignant leukocyte proliferation
Acute (ALL, AML): fever, anorexia, neuro
Chronic (CML, CLL): insidious–infection, fever, weight loss, spleen and liver enlargement

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9
Q

Explain potential triggers, pathophysiology, clinical manifestations of DIC

A

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

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10
Q

Describe pathophysiology of hemolytic disease of the fetus and newborn (HDFN)

A

patho: maternal antibodies in blood (parent has diff blood type than fetus & sufficient blood transfer) –> IgG binds w/ fetal erythrocytes –> widespread hemolysis –> anemia

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11
Q

Describe pathophysiology, genetic inheritance, clinical manifestations of sickle cell disease

A

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)

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12
Q

Discuss triggers that worsen sickling of RBCs in sickle cell disease

A

Hypoxemia/dehydration:
-low pH
-Low temp
-decreased plasma volume

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13
Q

Describe pathophysiology of ITP, triggers

A

autoimmune platelet destruction
Patho: autoantibodies bind to platelet PM –> splenic/lymph phagocytes sequester/destroy them
Triggered by drugs, infection, lymphoma…

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14
Q

Describe Hemophilia A vs B and the related deficiency

A

A:
B:

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