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
Assessment/Diagnostic Findings
Hematologic Studies
- CBC
- Hemoglobin- iron contained in RBC, Carries oxygen
- Hematocrit- % of RBC
Bone Marrow Aspiration and Biopsy
- Assess the quantity and quality of each type of cell produced in the bone marrow
- Procedure
- Only take very little
Marrow Aspiration
Purpose: Hematopoiesis, cytopathology, Chromasomal study.
Site- Anterior/posterior iliac crest, sternum
Performed by physician under local anesthesia
Needle inserted, stylet removed, 0.2-0.5 ml removed
Needle removed and PRESSURE APPLIED FOR AT LEAST 10 MINUTES TO AVOID BLEEDING
Bone Marrow Transplant:
Kill off bone marrow with drugs like chemotherapy, high doses, so that pt. doesn’t reject immune cells, wait for ***2-3 days keep in reverse isolation .
Give stem cells IV and they will repopulate the marrow and the bone marrow will start to put out healthy cells.
Monitor: fluids, infections, toxicity. Small meals, high protein, low calorie.
PCs: graft vs. host rejection, fatal in 20% of patients. Will see peeling of the hands and feet, call the doctor immediately.
Anemia
Loss of RBCs
Classification
- Decreased production of RBCs (hypoproliferative )
- Increased destruction of RBCs (hemolytic, hemolysis)
Factors to determine cause
- Bone marrow aspiration: to see marrow’s ability to respond to decreased RBCs (only if you are super anemic and can’t find a solution)
- Degree to which young RBCs proliferate in the marrow and how they mature
- Presence/absence of end products of destruction
Low RBC means low oxygen (SOB, find a chair and let them sit) means high H&H
Old people are often anemic because of B12
High bilirubin means you are destroying your RBC too much
KNOW: decreased production, blood loss, increased RBC destruction all cause anemia
Clinical Manifestations
- Many factors enter into the severity of S/S
- Weakness, fatigue, general malaise, pallor are common
- Enlarged liver and spleen
- Sore mouth
- Difficulty swallowing
- Coffee ground emesis
- Bone pain
- Yellow sclera, hemorrhage of the eyes, blurred vision
- Jaundice – also itchy (pruritis)
Cardiac status-
- palpitations,
- high bp,
- Angina
- HF
- Murmurs
- S/S of PAD (peripheral artery disease)
- Heart pumping hard will grown in size (cardiomegaly)
GI status
- Maybe anemic
- Dark stool
- Diarrhea
- Red and smooth tongue
Neuro status: Headaches, vertgo, irritable, depressed, numbness, ataxia, poor coordination, impaired thinking
PC-
Heart failure, paresthesia- numb, tingling sensation , confusion
Management of Anemia
Medical management
- correcting or controlling the cause
- Give: Iron, epigen (AKA procrypt)
- replacement of RBCs- blood transfusion
- Bone marrow transplant if bone marrow is at fault
Nursing interventions
- managing fatigue- limit visitors (also exposes them to more germs)
- maintaining adequate nutrition and perfusion- assess diet (vegetarians may have a B12 problem)
- Family history?
- complying with prescribed therapy- give iron with OJ because it sticks with them better
- monitoring and managing potential complications
Types of Anemia
Iron deficiency anemia Can be due to inadequate intake but mostly to blood loss
- smooth sore tongue -brittle ridged nails -cracked corners of mouth ( angular cherlosis) -small RBC, decreased MCV, decreased serum iron (infection?)-ck for bleeding – SOB
- -Treatment = PO iron (meat and spinach) on empty stomach - 50% loss with meals, Z track injection, eat organic meats & Vit C
Renal anemias due to decreased erythropoitin output, also if on dialysis will have blood loss in the machine so will have iron deficiency anemia, and also looses folic acid in the process
- Short RBC life
- -Treatment = Epogein/Procrit in combo with iron, decreased fatigue and better tolerance of dialysis
- With increased HCT may end up with hypertension so ck HCT frequently may need BP meds
Aplastic anemia due to exposure to radiation benzenes, toxins, DDT
-marrow failure due to damages stem cells PC = Infections
-S/S of anemia, -Enlarged nodes and spleen -purpura
Treatment – Bone Marrow Transplant (BMT), peripheral blood stem cell transplant, Immunosuppressants
Megaloblastic anemia due to decreased folic acid, pernicious anemia (decreased intrinsic factor si cant use B12)
-Jaundice vitiligo, premature grey, smooth red tongue, neuro problems
Treatment = replace folic acid and give B12 shots
Myelodysplastic Syndrome (MDS) – May evolve into leukemia -tired, may bleed, immature blast cells, Infection risk Treatment = chronic transfusions PRECAUTIONS – watch iron levels may need chelation
Thalasemia – mediterranean, SE asia, Africa
-small RBC, short lived hemolysis -Alpha Minor (mild) Beta major – die by age 20-30
Treatment = RBCs watch for Iron over load – chelation may do well with BMT
Glucose 6 phosphate dehydrogenase deficiency – abnormal cell with enzyme deficiency that leads to hemolysis
-African Greek Italian Asian *Jewish (most common) Hemolysis related to stress, high fevers, certain drugs, fava beans
Hereditary Spherocytosis –
-Cell membrane is very thin - RBC changes to a ball shape - destroyed prematurely – jaundice – enlarged spleen
Immune hemolytic – Immunes system recognizes own blood as antigen
Sickle Cell Anemia
Genetic defect – hemolytic- may be born with the trait
Mostly in Mediterranean area
Low O2 causes crystal-like formations - rigid sickle shape
Most of the time begins in the feet, see scars where the clots are that get into the capillaries and kill skin cells
Tangle causing ischemia/infarctions
Sickling takes time so can fix itself when passes thru well oxygenated areas
Cold aggravates the condition as does viscosity, decreased oxygen in the air
PAINFUL BECAUSE OF THE DYING TISSUE
Make sure they have all of their shots up to date and stay away from syphilis
Not iron deficient
S/S
Cells have short life so anemia S/S (tachycardia, murmurs, cardiomegaly etc) Hgb - 7-9, jaundice, enlarged face/head if severe as child
***Treat: Keep warm, raise oxygen, avoid dehydration (dilutes to avoid clots)
Better for these people to live closer to sea level
Sickle Cell Crisis
Sickle crisis –Painful due to death to tissue
Aplastic crisis- infection (parvovirus) yields rapid fall in hemoglobin
Sequestration crisis – pooled sickled cells
Can be deadly
Sickle Cell Acute Chest Syndrome
Blood clots in the chest
S/S = Rapid fall is Hgb, tachycardia, fever, bilateral infiltrates in lungs
Potentially lethal