Hematology Flashcards
Hematopoiesis
Occurs in 5 days
O2 level stimulates kidney to secrete erythropoitin, which leads to erythroblast formation, which forms reticulocytes (immature RBCs)
If rapid erythropoiesis is necessary may release reticulocytes and nucleated RBCs
After maturity, cells live about 120 days
When RBCs get destroyed, the side effect is bilirubin: if you have a mature liver, you won’t get yellow and the body will get rid of it no problem.
RBC Function
95% of cell mass is hemoglobin
Have no nucleus
Flexible and disk shaped to facilitate absorption and release of gases
Transport of gases through diffusion
Main function-transport of O2 between lungs
Also aids in buffer system
Transport: food, oxygen, carbon dioxide
RBC Needs
Iron stores and metabolism
Vitamin B12 & Folic Acid metabolism
Destruction
Destroyed at 120 days, old RBC just takes up room and is not longer functioning
If disease is destroying RBC, will give Epigen (erythropoietin)
WBC
Total Amount = 5,000-10,000
60-70% are granulocytes
30-40% are lymphocytes
Granulocytes
Agranulocytes
Lymphocytes: fight germs
WBC Function
Protect against bacterial invasion and other foreign entities
Neutrophils – fast arrival for short lived phagocytosis. don’t live long, eat germs
Monocytes – long term phagocytosis as macrophages, also digest old RBC (spleen). long term eating germs, digest old RBC.
Lymphocytes-produces substances that attack foriegn material that kill directly or that enhance phagocytic cells (T) . B cells differentiate into plasma cells which produce immunoglobulins. attack bacteria.
Eosinophils- allergic reactions (neutralizes histamine) and phagocytosis of parasites
Basophils produce and store histamine which when released provokes an allergic reaction. Controls histamines
Other Components
Platelets (thrombocytes) – granular fragments
- Produced in marrow also
- Regulated by the hormone thrombopoitin
- Function: Control bleeding
- Collect & activate at the site of injury forming a plug
- Releases substances that activate coagulation factors
- Nurture and maintain the lining of the vessels
Plasma and plasma proteins
- 90% = water, rest = plasma proteins, clotting factors, nutrients enzymes, waste and gases
- Serum
- Proteins – albumin, globulins: alpha and beta (alpha and beta, transport), gamma (immune system)
Reticuloendothelial System- inflammation
Monocytes derived cells live within the tissues
Liver spleen,lymph node and lungs
Protect against foreign invaders- phagocytosis
Stimulate the inflammatory process
Hemostasis
Primary- formation of platelet plug- vessels constrict
Secondary- inactivated coagulation factors are activated on the surface of the plug – end result is fibrin anchoring to plug forming a clot
Hemostasis Disorders
Clinical manifestations:
Occasionally none
Bleeding
- Mucosa/skin
- Hemorrhage frank/insidious
- Prolonged bleeding for venipuncture sites
- With TTP, increased range of PCs due to clots in system
Diagnostics
Labs
- Platelet counts. Peripheral smears, pt,ptt, RBC morphology
- Bone marrow exams
- look at platelets, morphology (endosis) of the cells.
Spontaneous ecchymosis: bruising without a cause (heparin, Plavix)
Acquired Coagulation Disorders
Liver Disease: Prolonged PT, peptic ulcers, esophageal baresis- vomit blood (use blakemore tube)
Vitamin K Deficiency: babies, sometimes gut does not help manufacture
Complications of Anticoagulant Therapy: warfarin (blood draws frequently)
Disseminated Intravascular Coagulation (DIC): can get this with anything, clotting cascade gets messed up causing mini clots, if you get a bleed, can’t join together to form a big clot. Give heparin to stop the clotting cascade. Then give plasma or clotting factors.
Hemostasis Disorders
Thrombocytopenia – platelets below 150,000
- decreased production of platelets within the bone marrow (aplasticanemia) (could be: alcoholism, malabsorption of B12 (elderly has this, need intrinsic factor, doesn’t always work)
- increased destruction of platelets, (caused by certain drugs, cancers, septicemia)
- increased consumption of platelets (large bleed)
Etiology
- Inherited
- Acquired: Immune- (ITP) Immune Thrombocytopenia, Purpura – most common
- Acquired: Non-immune – due to shortened circulation, turbulent blood flow (causes damage), decreased production (Caused by Drugs, Infections, Alcoholism/marrow suppression, Malignancies, Radiation, Invasive tumors, Fibrosis), will see a lot of pticiai, bruising, bleeding gums, super heavy period all of the time, brain bleeds
- avoid rough activity. Can do swimming (no diving), patient needs to be aware of any bruising or bleeding
Acquired Immune: Immune Thrombocytopenic Purpura
- Normal function of platelets – shortened life
- Platelets coated with antibodies
- Platelets recognized by spleen as foreign material & Destroyed by macrophages
- Marrow cannot keep supply
to demand
Acute- most common and in kids. Usually 1-6 weeks after a viral infection (measles or chickenpox, or the shots), self limiting
Chronic- due to autoimmune problems, or a drug reaction
Acquired – Nonimmune- Thrombotic Thrombocytopenia Purpura (TTP)- RARE
- Absence of anticlotting plasma enzyme leads to
enhanced agglutination of platelets form micro-clots
that deposit in capillaries, decreasing # in system
***Medical Emergency – clotting/bleeding at same time
micro-clots will form and go to the brain, heart, kidney, may have headache, confusion, coma, disrhythmias, kidney failure.
When giving platelets: special tubing (shorter so we don’t lose any)
Acquired – Nonimmune- Heparin induced Thrombocyopenia and Thrombosis Syndrome (HITTS)
- Microclotting with reduction of circulating platelets
- Immune-mediated response to heparin = antibodies = removal = decreased platelets & platelet/fibrin clots
- Heparin neutralized- NO HEPARIN
When giving platelets: special tubing (shorter so we don’t lose any)
Other Acquired- non immune
in stage renal disease multiple miloma (bone cancer): will have abnormal proteins that interfere with platelet function cardiopulmonary bypass: destroys platelets
