Exam 2: Hematological Disorders Flashcards
Anemia
A decrease in RBCs or hemoglobin, or both
-cytic (size of cells - MCV)
-chromic (hemoglobin content aka color - MCH)
Etiology: 1. Excessive loss of RBCs, 2. Destruction of RBCs (hemolysis), 3. Defective RBC production, 4. Inadequate RBC production due to bone marrow
Epidemiology of anemia
women childbearing age and elderly adults, gastrointestinal bleeding, pregnancy, postnatal period, lactation, GI bleeding, peptic ulcer, intestinal polyps, hemorrhoids, cancer, vegetarians who don’t supplement with iron rich foods, most common anemia worldwide. Excessive aspirin intake.
Clinical Manifestations/Signs & Symptoms of anemia
(caused by decreased oxygen supply from RBCs) angina, tachycardia, palpitations, dizziness, dyspnea, SOB (especially w/activity), tachypnea, fatigue, HA, faintness, MSK weakness, exercise intolerance, pallor
Patho of anemia
Normal Process: MCV is normal (cell size is normal), MCHC is normal (normal color), hematocrit is normal, hemoglobin is normal, RBCs are normal. RBCs are able to carry sufficient oxygen to perfuse the body.
Disease Process: Different anemias have different impacts on above labs, but hematocrit, hemoglobin, and RBCs will be low (except for hemorrhagic). RBCs are not able to carry sufficient oxygen to perfuse the body.
Normocytic-Normochromic anemia
Excessive loss of RBCs (hemorrhagic)
Patho: MCV is normal, MCHC is normal -> cells are ok, but total blood volume is depleted
Clinical manifestations: similar to dehydration -> hypotension, tachy, oliguria, LOC
Hemolytic anemia
Destruction of RBCs (hemolysis)
Etiology: acquired (destruction of RBCs from antibodies): drug reactions, transfusion reactions, ABO or Rh factor incompatibility of mother or fetus; inherited: sickle cell, thalassemia
Patho: premature destruction of RBCs, but cause can be different
Clinical Manifestations: acquired - fever, chills, angina, bronchospasm, angioedema
Iron-deficiency anemia
Microcytic hypochromic
Defective RBC production (missing key parts for RBC synthesis -> iron or vit B12 or folic acid)
Patho: MCV is low, MCHC is low -> body is unable to synthesize hemoglobin and leads to small amount in RBCs
Megaloblastic (Macrocytic) anemia
Defective RBC production (missing key parts for RBC synthesis -> iron or vit B12 or folic acid)
(vit B12 or folic acid deficiency)
Patho: MCV & MCH are high, MCHC is normal
Epidemiology: Pregnant or lactating, alcohol abusers, at risk elderly, vegetarian, gastric bypass surgery, Celiac’s disease or IBS, dietary deficiency, chronic inflammation
Clinical manifestations: same as all anemia, but can have neuro damage also
Pernicious anemia
Defective RBC production (missing key parts for RBC synthesis -> iron or vit B12 or folic acid)
(vit B12 deficiency)
Etiology: atrophic gastritis, no intrinsic factor for B12 so unable to absorb
Aplastic anemia
Inadequate RBC production due to bone marrow
Etiology: cancer, sepsis, or radiation exposure
Patho: No bone marrow function - all blood cells impacted, not just RBCs
Clinical manifestations: same as anemia, petechial, bleeding, infection
Bleeding disorders
Etiology: Factor depletion, ↓production, ↓platelets, ↑consumption, Liver dysfunction, Vitamin K deficiencies
Clinical Manifestations/Signs & Symptoms: epistaxis, petechiae and purpura, bleeding gums, abnormal vaginal bleeding, decreased platelets (note <20,000 can cause spontaneous bleeding), blood tests that look at PT/INR/PTT and other clotting factors, and/or splenomegaly
Diagnosis: CBC/PT/INR/PTT
Immune thrombocytopenic purpura (ITP)
Autoimmune after a virus, antibodies destroy platelets, children
Thrombotic thrombocytopenic purpura (TTP)
Inherited or acquired, deficient ADAMTS13 enzyme needed to prevent clots from forming -> more likely to clot
Heparin Induced thrombocytopenia (HIT)
Immune reaction when given heparin, PF4-heparin complex (positive feedback) -> platelets are activated and start making clots
TTP & HIT
-> low platelet count because all platelets being used in other clots and none for bleeding elsewhere can cause excessive bleeding
Disseminated Intravascular Coagulation (DIC)
Exaggerated immune reaction to illness/trauma/other issues where coagulation and fibrinolysis
become abnormally (and often massively) activated, leading to ongoing coagulation and fibrinolysis. Bleeding and clotting at the same time from decreased platelet count
Hemophilia
Causes bleeding: joints/anywhere
X-linked recessive
Primarily affects males
Women who carry the trait for disease do not suffer from the bleeding problems
Hemophilia A
Caused by a lack of factor VIII
More common than B
Hemophilia B:
Caused by a lack of factor IX
Hematologic Cancers
Normal Process: Normal hematopoiesis.
Disease Process: Nonfunctional, cancerous WBCs proliferate and overwhelm the bone marrow and other lymphoid tissue. The cancerous WBCs increase to excess numbers and they crowd and suppress development of the other blood cells in the bone marrow
Heme Cancers Clinical Manifestations/Signs & Symptoms:
S/S: anemic symptoms - (fatigue, weakness, pallor),leukopenia (increased susceptibility to infection), thrombocytopenia (increased susceptibility to bleeding and bruising) and bone pain (caused by proliferating cancerous blood cells that put pressure in marrow of bones)
Diagnosis: Enlarged lymph nodes, splenomegaly, or both, ↑WBCs, Bone marrow biopsy for leukemia, Lymph node biopsy for lymphomas, Philadelphia chromosome defect
Leukemia acute vs chronic
Acute = blasts (immature WBCs), sharp onset, children
Chronic = cytes (mature WBCs), slow onset sometimes asymp., adults
ALL
Acute Lymphocytic Leukemia
T or B cells
Most common in children
T or B Lymphoblasts cannot mature, so immature lymphoblasts overwhelm and no room for healthy blood cells
AML
Acute myeloid leukemia
Myeloids
Most common in adults
Myeloid cells cannot differentiate and mature, so overwhelm and no room for healthy cells
CLL
Chronic lymphocytic leukemia
B cells can’t differentiate, release mutated, none, or low levels of Ig
Older adults w/ environmental exposures that were caught on routine exams
CML
Chronic myeloid leukemia
Overproduction of mature myeloid cells
Multiple myeloma
Abnormal and excessive plasma cells in bone marrow, chromosomal on 13 and 14
CRABI
C=hypercalcemia due to bone demineralization
R= renal failure due to proteins damaging the kidneys
A= anemia due to decreased production of RBCs
B= bone pain due to fractures or bone lesions
I= infection due to the immune dysfunction.
Lymphoma
Solid tumors
Hodgkin’s
Reed Sternberg (B) cells - owl eyes
Enlarged painless lymph nodes
Multiple node involvement
Intermittent fever without signs of infection, Fatigue, Weight loss
Non-Hodgkin’s
Abnormal B or T cell, NK cell neoplasms
Lack Reed Sternberg cells
Localized or generalized lymphadenopathy
Overall survival not as good compared to HL
Painless nodes that enlarged
