Professional Documents
Culture Documents
ANATOMY
1. Define the following terms. (p 396)
A. Anisocytosis _______________________________________________________________
B. Poikilocytosis ______________________________________________________________
C. Reticulocyte _______________________________________________________________
4. List the types of white blood cells in order of decreasing prevalence. (p 396) _________________
______________________________________________________________________________
______________________________________________________________________________
6. CD14 is a cell surface marker for which cell type? (p 397) ________________________________
______________________________________________________________________________
______________________________________________________________________________
9. B lymphocytes are produced in the _______________ (bone marrow/thymus) and mature in the
_______________ (bone marrow/thymus). T lymphocytes are produced in the _______________
(bone marrow/thymus) and mature in the _______________ (bone marrow/thymus). (p 398)
10. What type of cell has an off-center nucleus, abundant RER, and a clock-face chromatin distribution?
(p 399) _________________________________________________________________________
PHYSIOLOGY
11. Why are Rh-negative mothers given anti-D IgG? (p 400) __________________________________
______________________________________________________________________________
12. In the chart, check which coagulation factors are in the intrinsic vs. the extrinsic coagulation
pathways. (p 401)
II
VII
VIII
IX
XI
XII
13. Which factors are vitamin K dependent? How does warfarin inhibit the activation of these factors?
(p 402) _________________________________________________________________________
______________________________________________________________________________
14. Describe the four steps of primary hemostasis and platelet plug formation. (p 403) ____________
______________________________________________________________________________
______________________________________________________________________________
PATHOLOGY
15. Identify each cell type and its associated pathology. (pp 404-405)
A. B. C. D. E. F.
A. _______________________________ D. ______________________________
B. _______________________________ E. ______________________________
C. _______________________________ F. ______________________________
16. In α-thalassemia, what is the condition called when all four α-globin genes are deleted? When three
are deleted? When two are deleted? When one is deleted? (p 406) __________________________
______________________________________________________________________________
17. What clinical manifestations do folate deficiency and vitamin B12 deficiency have in common? What
______________________________________________________________________________
______________________________________________________________________________
19. Match the intrinsic hemolytic normocytic anemia with its characteristic. (p 410)
20. Which autoimmune hemolytic anemias are warm and which are cold? (p 411) ________________
______________________________________________________________________________
21. Indicate whether the lab findings in the chart are elevated, decreased, or normal. (p 412)
Anemia of Pregnancy/
Iron Hemo-
Lab Value Chronic
Deficiency chromatosis
Disease OCPs
Ferritin
Serum iron
Transferrin
% Transferrin
22. In lead poisoning what enzymes are affected and what substrates are accumulated? (p 413) ____
______________________________________________________________________________
23. What are the “5 P’s” of acute intermittent porphyria? (p 413) _____________________________
______________________________________________________________________________
______________________________________________________________________________
24. Indicate whether the lab findings in the chart are elevated, decreased, or normal. (pp 414-416)
Platelet Bleeding
Disorder PT PTT
Count Time
DIC
Glanzmann thrombasthenia
Hemophilia
TTP
Vitamin K deficiency
______________________________________________________________________________
________________________________________
________________________________________
________________________________________
27. Match the disease with the genetic translocation most closely associated with it. (pp 418, 420)
28. What will serum protein electrophoresis reveal in a patient with multiple myeloma? What will be seen
in the urine? (p 419) _________________________________________________________
29. What are the four major groups of leukemia? Which type is at risk for DIC upon initiation of treatment
and why? (p 420) ________________________________________________________________
_______________________________________________________________________________
_______________________________________________________________________________
30. Indicate whether the lab findings in the chart are elevated, decreased, or normal. (p 421)
Chronic
Myeloproliferative Platelets RBCs WBCs
Disorder
CML
Essential
thrombocytosis
Myelofibrosis
Polycythemia vera
PHARMACOLOGY
31. What is the mechanism of action of heparin? How is overdose treated? (p 423) ______________
______________________________________________________________________________
32. What is the mechanism of action of warfarin? How is overdose treated? (p 424) _____________
______________________________________________________________________________
34. Match the patient with the drug he or she is most likely taking. (pp 427-428)
cystitis
_____ F. Patient with testicular cancer has PFTs consistent with restrictive lung disease
Answers
ANATOMY
1. A. Anisocytosis: Cells vary in size.
6. Macrophages.
PHYSIOLOGY
11. To prevent the development of anti-Rh IgG, which can cause erythroblastosis fetalis in a subsequent
fetus.
12.
I √
II √
V √
VII √
VIII √
IX √
X √
XI √
XII √
13. Factors II, VII, IX, X, and proteins C and S. Warfarin inhibits the enzyme vitamin K epoxide reductase,
which is necessary to convert vitamin K to its reduced form so that it can go on to activate these
factors.
3. Adhesion: Platelets bind vWF via the GpIb receptor and release ADP/Ca2+.
4. Activation: ADP binds the ADP receptor, and GpIIb/IIIa is expressed. Aggregation: Fibrinogen
binds GpIIb/IIIa and links platelets.
PATHOLOGY
15. A = Degmacyte (bite cell): G6PD deficiency. B = Ringed sideroblast: sideroblastic anemia. C =
Schistocyte: microangiopathic hemolytic anemia (DIC, TTP, HUS). D = Dacrocyte (teardrop cell):
bone marrow infiltration (eg myelofibrosis). E = Target cell: HbC disease, asplenia, liver disease,
thalassemia. F = Heinz bodies: G6PD deficiency.
16. Four deletions: Hb Barts; three deletions: HbH disease; two deletions: α-thalassemia minor; one
deletion: α-thalassemia minima.17.Both folic acid and vitamin B12 deficiency can cause
megaloblastic anemia. Only vitamin B12 deficiency, however, is associated with neurologic
symptoms, such as subacute combined degeneration. Also B12 deficiency is associated with
increased methylmalonic acid, unlike folic acid deficiency.
18. Idiopathic, radiation and drug exposure, viral agents, and Fanconi anemia.
20. Warm (IgG): SLE, chronic lymphocytic leukemia, and certain drug reactions.
Cold (IgM): chronic lymphocytic leukemia, Mycoplasma pneumoniae infection, and infectious
mononucleosis.
21.
Anemia of Pregnancy/
Iron Hemo-
Lab Value Chronic
Deficiency choromatosis
Disease OCPs
Ferritin ↑ ↓ normal ↑
Transferrin ↓ ↑ ↑ ↓
% Transferrin normal ↓↓ ↓ ↑↑
22. Enzymes: Ferrochelatase and ALA dehydratase. Substrates: Protoporphyrin and ALA (blood)
23. Painful abdomen, Port wine-colored urine, Polyneuropathy, Psychological disturbances, and
Precipitated by drugs (eg, cytochrome P-450 inducers), alcohol, and starvation.
24.
Platelet Bleeding
Disorder PT PTT
Count Time
DIC ↓ ↑ ↑ ↑
28. An M-spike, representing a monoclonal antibody; Ig light chains (Bence Jones proteins).
29. AML, ALL, CML, and CLL. AML can be associated with DIC upon initiation of treatment because the
leukemia cells contain Auer rods composed of the enzyme peroxidase, which is released into the
bloodstream when treatment causes cells to lyse.
30.
Chronic
Myeloproliferative Platelets RBCs WBCs
Disorder
CML ↑ ↓ ↑
Essential
↑ — —
thrombocytosis
Polycythemia vera ↑ ↑ ↑
PHARMACOLOGY
31. Heparin activates antithrombin, decreasing thrombin and Xa. Treat heparin overdose with protamine
sulfate.
32. Warfarin interferes with normal synthesis and γ-carboxylation of vitamin K-dependent clotting factors.
Treat warfarin overdose with vitamin K, fresh frozen plasma, or PCC.
33. A-5, B-1, C-9, D-8, E-3, F-2, G-4, H-7, I-6, J-10.