Microcytic Anemia - Answers Due to DECREASED production of Hb. If Hb is LOW one way RBC has to
maintain [Hb] is by dividing an extra time.
-Hb is made of HEME (IRON AND PROTOPORPHYRIN) and GLOBIN
Lack of Fe - Answers is the most common nutritional deficiency in the world. (1/3 of the world has this
deficiency). Fe: Consumed in heme (meat-derived) and non-heme (vegetables).
Anemia of chronic disease - Answers Most common type of anemia in hospitalized patients. (Chronic
inflammation)
Hepcidin sequesters Fe in storage sites, blocks Fe exportation from the enterocyte and limits Fe transfer
from macrophages to erythroid precursors.
Macrocytic Anemia - Answers • Most commonly due to Folate or Vitamin B12 deficiency. (Megaloblastic
Anemia)
• Microcytic: Extra Division
• Macrocytic: 1 less division occurs (cells are larger)
• Folate and B12 are necessary for DNA synthesis. Lack of any of them impairs synthesis of DNA
Precursors. Megaloblastic anemia, Hypersegmented neutrophils.
Vitamin B12 deficiency - Answers Animal derived protein (meat, eggs). It takes years to Develop it due to
a large hepatic stores of B12.
Pernicious Anemia - Answers Autoimmune destruction (Type II hypersensitivity) of the parietal cells,
leading to Intrinsic factor deficiency
Sickle cell anemia - Answers • Autosomal recessive mutation in β chain of Hb. Normal glutamic acid
(hydrophilic) is replaced with Valine (hydrophobic). It arises when 2 abnormal β genes are present.
• This type of anemia results in more than 90% of Hb S in RBCs.
• The problem is that HB S polymerizes when deoxygenated. Polymers aggregate into needle like
structures resulting in sickle cells. The risk for sickling increases when: Hypoxemia, Dehydration and
acidosis are present
, Hemostasis - Answers Integrity of the blood vessel is necessary to carry blood to tissues. Damage to the
wall is repaired by hemostasis, which involves formation of a thrombus (clot) at the site of vessel injury.
Primary hemostasis - Answers forms a weak platelet plug and is mediated by interaction between
platelets and the vessel wall.
Secondary hemostasis - Answers stabilizes the platelet plug and is mediated by the coagulation cascade.
PRIMARY HEMOSTASIS - Answers Step 1: Transient vasoconstriction of damaged vessel. Mediated by
reflex neural stimulation and endothelin release from endothelial cells
PRIMARY HEMOSTASIS - Answers Step 2: Platelet ADHESION to the surface of disrupted vessel. Von
Willebrand factor (vWF) binds exposed subendothelial collagen. Platelets bind vWF using the GPlb
receptor. vWF is derived from the Weibel-Palade bodies of endothelial cells and a-granules of platelets
PRIMARY HEMOSTASIS - Answers Step 3: Platelet DEGRANULATION. Adhesion induces shape change in
platelets and degranulation with release of multiple mediators. ADP is released from platelet dense
granules;
PRIMARY HEMOSTASIS - Answers Step 4: Platelet AGGREGATION. Platelets aggregate at the site of injury
via GPIIb/IIla using fibrinogen (from plasma) as a linking molecule; results in formation of platelet plug.
Platelet plug is weak; coagulation cascade (secondary hemostasis) stabilizes it.
SECONDARY HEMOSTASIS - Answers Stabilizes the weak platelet plug via the coagulation cascade.
Coagulation cascade generates thrombin, which converts fibrinogen in the platelet plug to fibrin. Fibrin
is then cross-linked, yielding a stable platelet-fibrin thrombus.
Factors of the coagulation cascade are produced by the liver in an inactive state. Activation requires:
1. Exposure to an activating substance (Tissue thromboplastin activates factor VII (extrinsic
pathway);Subendothelial collagen activates factor XII (intrinsic pathway)
2. Phospholipid surface of platelets
3. Calcium (derived from platelet dense granules)
-HEMOPHILIA A - Answers Genetic factor VIII (FVIII) deficiency .X-linked recessive (predominantly affects
males). Can arise from a new mutation (de novo) without any family history. Presents with deep tissue,
joint, and postsurgical bleeding. Clinical severity depends on the degree of deficiency.
VON WILLEBRAND DISEASE - Answers -Genetic vWF deficiency. Most common inherited coagulation
disorder. Multiple subtypes exist, causing quantitative and qualitative defects; the most common type is
autosomal dominant with decreased vWF levels. Presents with mild mucosal and skin bleeding; low vWF
impairs platelet adhesion however, deep tissue, joint, and postsurgical bleeding are usually not seen
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