Pathophysiology Organ System Essay
HEMATOLOGY ORGAN SYSTEMS
SMALL GROUP ANSWER KEY
Case 1
1. Iron deficiency vs thalassemia vs anemia of chronic disease.
2. Serum iron, TIBC, ferritin.
3. Blood loss, likely GI. A GI evaluation is indicated.
4. Slow response (weeks) to oral iron.
5. Incorrect diagnosis, non-compliance, continued blood loss.
Case 2
1. Anemia of chronic disease vs iron deficiency.
2. Serum iron, TIBC, ferritin.
3. Consistent with ACD, but also iron deficiency with inflammation.
4. Bone marrow iron stain could resolve the possibilities.
5. Trial of oral iron could be considered.
Case 3 1. Macrocytic anemia.
2. B12, folate deficiency, liver disease, reticulocytosis, myelodysplasia.
3. Blood smear, serum B12, red cell folate levels, Schilling …show more content…
Asians with α-thalassemia may carry two deleted a genes on the same chromosome. Blacks with α-thalassemia may carry one deleted a gene on the same chromosome.
Case 8
1. Platelet count.
2. Bone marrow examination will distinguish abnormal platelet production from increased platelet destruction.
3. Platelet aggregation test to identify a qualitative platelet disorder.
Case 9
Intrinsic pathway deficiency vs inhibitor. 2. Without: factor XII, prekallikrein, or HMWK deficiency. With: factors VIII, IX, or XI deficiency.
VIII, IX, then XI. 5. 50% of girls will be carriers; 50% of boys will be hemophiliacs.
Case 10 1. Hemostatically normal vs abnormal. Likely hemostatic disorders with normal screening lab results include vWD and inherited platelet dysfunction. 2. vW studies, platelet aggregation test.
Case 11
DIC vs liver disease. 2. Yes; a positive test indicates DIC. Factor VIII should be low in DIC and increased in liver disease.
No; vitamin K would have minimal clinical impact in this case.
Case 12
IV heparin monitored with PTT tests.
Subtherapeutic heparin PE; supratherapeutic bleeding.
Coumadin monitored with PT tests.
Yes; factor V Leiden, proteins C, S, and antithrombin III
SMALL GROUP ANSWER KEY
Case 1
1. Iron deficiency vs thalassemia vs anemia of chronic disease.
2. Serum iron, TIBC, ferritin.
3. Blood loss, likely GI. A GI evaluation is indicated.
4. Slow response (weeks) to oral iron.
5. Incorrect diagnosis, non-compliance, continued blood loss.
Case 2
1. Anemia of chronic disease vs iron deficiency.
2. Serum iron, TIBC, ferritin.
3. Consistent with ACD, but also iron deficiency with inflammation.
4. Bone marrow iron stain could resolve the possibilities.
5. Trial of oral iron could be considered.
Case 3 1. Macrocytic anemia.
2. B12, folate deficiency, liver disease, reticulocytosis, myelodysplasia.
3. Blood smear, serum B12, red cell folate levels, Schilling …show more content…
Asians with α-thalassemia may carry two deleted a genes on the same chromosome. Blacks with α-thalassemia may carry one deleted a gene on the same chromosome.
Case 8
1. Platelet count.
2. Bone marrow examination will distinguish abnormal platelet production from increased platelet destruction.
3. Platelet aggregation test to identify a qualitative platelet disorder.
Case 9
Intrinsic pathway deficiency vs inhibitor. 2. Without: factor XII, prekallikrein, or HMWK deficiency. With: factors VIII, IX, or XI deficiency.
VIII, IX, then XI. 5. 50% of girls will be carriers; 50% of boys will be hemophiliacs.
Case 10 1. Hemostatically normal vs abnormal. Likely hemostatic disorders with normal screening lab results include vWD and inherited platelet dysfunction. 2. vW studies, platelet aggregation test.
Case 11
DIC vs liver disease. 2. Yes; a positive test indicates DIC. Factor VIII should be low in DIC and increased in liver disease.
No; vitamin K would have minimal clinical impact in this case.
Case 12
IV heparin monitored with PTT tests.
Subtherapeutic heparin PE; supratherapeutic bleeding.
Coumadin monitored with PT tests.
Yes; factor V Leiden, proteins C, S, and antithrombin III