patho Flashcards
▪ Any condition that causes the total number of RBCs, the amount of Hb, or the volume of packed RBCs to decrease.
▪ Caused hypoxia in tissues
▪ General symptoms include dyspnea on exertion, fatigue, dizziness, tinnitus,
headache
▪ Long-term -> pallor, tachycardia, systolic ejection murmur, orthostatic hypotension.
ANEMIAS
IRON DEFICIENCY ANEMIA
▪ Due to chronic blood loss, increased need for blood and oxygen (pregnancy), deficiency intake or poor absorption.
▪ Microcytic, hypochromic (smaller and less color RBCs) anemia
▪ Fatigue, lethargy, pale mucous membranes, low Hb, low RBC, low hematocrit,
small RBCs, low MCV, MCH and MCHC, low serum ferritin and iron.
▪ Long-term def -> in chronic fatigue, low energy, and depression.
▪ Severe def -> gastritis, glossitis, Plummer-Vinson syndrome (dysphagia, esophageal webs)
IRON DEFICIENCY ANEMIA
▪ Vitamin B12 or folic acid deficiency or malabsorption which affects DNA synthesis.
▪ Folic acid deficiency can be caused by alcoholism, pregnancy, intestinal
malabsorption, and folic acid antagonists
▪ Megaloblastic anemia – enlarged abnormal prescursor cells in the bone marrow.
▪ Sx: Fatigue, lethargy, low RBC, low Hb, low hematocrit, large cells (increased MCV, MCH, and normal MCHC), ferritin and iron levels normal, low serum B12, low serum folate, increased serum/urine methylmalonic acid (B12 deficiency), high serum homocysteine levels (folate deficiency), polysegmented neutrophils, pancytopenia
▪ Complications include dementia, depression, glossitis, stomatitis, paranoia, neuropathies, ataxia, hyperreflexia, death
MACROCYTIC ANEMIA
▪ An autoimmune disease that reduces the absorption of food-bound B12 by destroying
intrinsic factor (IF)
▪ Anti-parietal Ab and anti-intrinsic factor Ab
▪Chief cells are damaged resulting in achlorhydria and lack of pepsinogen secretion
▪ Autoimmune atrophic gastritis often results.
▪Complications include recurrent GI infection and the same issues as B12 deficiency
Pernicious anemia
▪ Severe anemia that results from a loss of the precursor cells of RBCs
▪ Results from toxic exposure (drugs, radiation, chemicals) or viral infection.
▪ Bone marrow is hypocellular (< than the normal # of cells) and all cell lines are decreased (peripheral pancytopenia)
APLASTIC ANEMIA
▪ Myeloproliferative disorder that result in the neoplastic clonal proliferation of myeloid stem cells within the marrow.
usually d/t aquired **JAK2 mutation **
▪ Results in an increased number of circulating RBCs, increased hemoglobin, and a moderate increase in circulating granulocytes and platelets.
▪ Splenomegaly and decrease erythropoietin results.
▪ Weakness, fatigue, vertigo, irritability, tinnitus, facial flushing,extremity pain/erythema, blue/black spots on the skin can occur.
POLYCYTHEMIA VERA
▪ Secondary to another condition that causes an increased need for RBCs
▪ High altitude exposure, right-to-left shunts, shock, abnormal Hb
▪ Can also be caused by inappropriate production of erythropoietin by tumors (renal cell carcinoma and hepatocellular carcinoma)
▪ Pheochromocytoma and Cushing’s syndrome can also cause this condition.
▪ High erythropoietin (EPO) result
SECONDARY POLYCYTHEMIA
DISEASES INVOLVING
PRODUCTION OF BLOOD
CELLS
▪ Anemias
▪ Iron deficiency anemia
▪ Macrocytic anemia
▪ Aplastic anemia
▪ Polycythemia vera
▪ Secondary polycythemia
what group of anemias:
▪ Sickle cell anemia
▪ Thalassemias
▪ Hereditary spherocytosis
▪ Glucose-6-phosphate dehydrogenase deficiency
HEMOLYTIC ANEMIAS
▪ Destruction of RBCs
▪ Can cause anemia
▪ Jaundice, hemosiderosis, and usual anemia symptoms
Causes include:
▪ Mechanical trauma to cells
▪ Heart valves, clots
▪ Complement-induced damage
▪ Extravascular hemolysis (within the spleen)
hemolysis
▪ Abnormal hemoglobin (HbS) is produced due to a genetic disease.
▪ People who are heterozygous for the gene are generally asymptomatic.
▪ Those who are homozygous for the defective gene results in deformed RBCs.
▪Can obstruct capillaries and are removed and destroyed by the spleen
▪ Severe hemolytic anemia, chronic leg ulcers, infarcts of the lungs and spleen, vaso-occlusive painful crisis (limbs, back, chest, abdomen), and aplastic crises
SICKLE CELL ANEMIA
THALASSEMIAS
▪ Genetic disorders characterized by deficient production of either of the two globin chains of hemoglobin.
▪ Hypochromic, microcytic anemia
▪ Beta-thalassemias is the most common form in the Mediterranean and US
▪ Majorandminorforms
▪ Defectsinthebetachainofhemoglobin
▪ Major: anemia, splenomegaly, distortion of the facial and long bones, hemosiderosis ▪ Minor: generally asymptomatic
▪ Alpha-thalassemias is most common in Southeast Asia
▪ Resultsfromadefectofoneormoreof4alphahemoglobingenes
▪ The higher the number of deletion the more clinical abnormalities
▪ (Beta/alpha) -thalassemias is the most common form in the Mediterranean and US
▪ Majorandminorforms
Defects in the beta chain of hemoglobin
▪ Major: anemia, splenomegaly, distortion of the facial and long bones, hemosiderosis
▪ Minor: generally asymptomatic
Beta-thalassemias
(Betal/Alpha)-thalassemias is most common in Southeast Asia
▪ Results from a defect of one or more of 4 alpha hemoglobin genes
▪ The higher the number of deletion the more clinical abnormalities
Alpha-thalassemias
▪ Genetic disorders characterized by deficient production of either of the two globin chains of hemoglobin.
▪ Hypochromic, microcytic anemia
THALASSEMIAS
▪ X-linked disorder which causes hemolytic anemia during oxidative stress and is caused by a number of drugs
▪ G6PD is the rate-limiting enzyme for the HMP shunt
It maintains NADPH levels and reduced glutathione
Heinz bodes & bite cells on blood smear
GLUCOSE-6 PHOSPHATE
DEHYDROGENAGE
DEFICIENCY
▪ Genetic defect that causes spherical RBCs that get stuck in the spleen and destroyed
▪ Autosomal dominant
HEREDITARY SPHEROCYTOSIS
Occurs when the mother and fetus have different blood types
▪ Mother is Rh-but baby is Rh+ where the mother generates antibody against the Rhantigens
▪ ABO incompatibility
Hemolysis results in elevated bilirubin levels and jaundice.
▪ Risk of kernicterus, hepatosplenomegaly
No complications occur in the initial pregnancy.
▪ In subsequent pregnancies, maternal antibodies cross the placenta and lyse fetal RBCs which causes anemia, hypoalbuminemia, and possibly high-output heart failure, or fetal death.
Maternal sensitization and antibody production due to Rh incompatibility can be prevented by giving the woman Rh immune globulin.
ERYTHROBLASTOSIS FETALIS
▪ Disseminated intravascular coagulation (DIC)
▪ Hemophilia
▪ Thrombocytopenia
▪ Von Willebrand’s disease
▪ Vitamin K deficiency
CLOTTING ABNORMALITIES
▪ Common hemorrhagic syndrome that occurs after uncontrolled activation of clotting factors and fibrinolytic enzymes throughout small blood vessels.
Triggered by massive tissue damage, sepsis, pregnancy, cancer
▪ Caused by the release of tissue thromboplastin or activation of the intrinsic pathway of
coagulation
▪ Results in prolonged PT, APTT, bleeding and thrombin time
Acute DIC results in fibrin deposition everywhere and platelets and clotting factors are consumed
▪ Fibrin degradation products (D-dimers) inhibit fibrin polymerization and block platelet function.
▪ Outcome is lethal tissue necrosis and bleeding.
Chronic DIC occurs primarily as a result of certain cancers, retained dead fetuses, hemangiomas, and aneurysms.
DISSEMINATED
INTRAVASCULAR
COAGULATION
▪ Blood coagulation disorders (X-linked recessive) due to absence, deficiency, impaired activity of clotting factors which results in prolonged bleeding.
HEMOPHILIA
stages for which blood coagulation cdx:
Mild (5-40% of factor levels)
▪ Asymptomatic or experience prolonged bleeding only after serious injury
Moderate (1-5% normal factor levels)
▪ Prolonged bleeding after injuries and occasional spontaneous bleeding.
Severe (<1% normal factor levels)
▪ Prolonged bleeding even after minor injury, frequent spontaneous bleeding
Hemophilia
Hemophilia A - Factor (VII/VIII) deficiency
▪ Normal bleeding time, platelet count, prothrombin time but prolonged activated partial thromboplastin time
▪ Bleeding occurs in the muscles, subcutaneous tissues, and joints.
Hemophilia B - Factor (IX/X) deficiency
▪ Similar to Hemophilia A
▪ Hemophilia C (Autosomal Recessive) - Factor (XI/XII) deficiency
▪ Hemophilia A - Factor VIII deficiency
▪ Hemophilia B - Factor IX deficiency
▪ Hemophilia C (Autosomal Recessive) - Factor XI deficiency
▪ Reduction in the number of platelets which results from decreased production, sequestration, or increased destruction of platelets.
▪ Decreased production of platelet so ccurs with bone marrow damage, congenital abnormalities, or nutrition deficiencies (B12 and folate).
▪ Petechial cutaneous bleeding and prolonged bleeding time.
▪ Sequestration occurs in splenomegaly → causes platelets to accumulate in the spleen
▪ Increased destruction of platelets occurs in disseminated intravascular coagulation (DIC) or purpura.
THROMBOCYTOPENIA
▪ Platelets require vWF to adhere to the endothelial basement membranes in order to begin clot formation.
▪ vWF is also important in stabilizing factor VIII
▪ vWF is either absent or abnormal in this disease which causes increased
bleeding time (PTT).
▪ Autosomal dominant
▪ Acquired Von Willebrand disease can occur in some autoimmune diseases, aortic
stenosis, Wilm’ s tumor, and hypothyroidism.
▪ Results in impaired platelet adhesion and prolonged bleeding time.
▪ Results in mild prolonged bleeding to severe, hemophilia A-like spontaneously bleeding into joints
VON WILLEBRAND’S DISEASE
▪ Vitamin K is required for the synthesis of factor II (prothrombin), VII, IX, and X (1972)
▪ It negatively affects blood clotting.
▪ Can be caused by malabsorption problems including biliary tract disease, pancreatic diseases, and small intestine diseases.
VITAMIN K DEFICIENCY
▪ Acute or chronic heterogenous neoplastic disorders of WBC (lymphoid or myeloid)
▪ Acute → poorly differentiated blast cells in circulation
▪ Chronic → more differentiated cells
▪ Lymphocytic forms are most often B-cells
▪ Myelogeous forms show non-lymphocytic precursor cells (granulocytes)
LEUKEMIAS
which leukemia:
▪ At least 3 chromosomal translocations
▪ Anemia, fatigue, SOB, easy bleeding and bruising, frequent infections, thrombocytopenia
Acute myelogenous leukemia (AML)
which type of leukemia:
▪ Many chromosomal translocations
▪ Associated with Fanconi anemia, X-linked agammaglobulinemia, severe combined
immunodeficiency
▪ Anemia, fatigue, frequent infections, fever, dyspnea, lymphadenopathy, easy bruising, petechiae,
arthralgias, thrombocytopenia
m/c IN CHILDREN
Acute lymphocytic leukemia (ALL) (MC in children)
which type of leukemia:
▪ Associated with the Philadelphia chromosomal translocation between chromosomes 9 and 22
▪ Asymptomatic leukocytosis initially (high WBC), normal RBC and platelets
▪ Causes malaise, low-grade fever, frequent infections, gout, anemia, splenomegaly, easy bruising
Chronic myelogenous leukemia (CML)
which type of leukemia:
▪ Affects B cells (high WBCs), normal RBC and platelets
▪ Has a very slow progression
▪ Associated with ionizing radiation exposure
▪ Isolated lymphocytosis → anemia or thrombocytopenia, splenomegaly, lymphadenopathy
Chronic lymphocytic leukemia (CLL) (MC leukemia esp. in older men)
▪ Mature B cell lymphoma (CD20 present on most cells)
▪ Reed-Sternberg cells (bi- or multi-nucleated giant cells that are unable to make Abs)
▪ Painless lymphadenopathy is most common, moderate enlargement of the spleen and liver, pruritis, night sweats, fever, leukocytosis, weight loss.
▪ Pel-Ebstrain fever – cyclic high-grade fever
HODGKIN’S LYMPHOMA
▪ B cell lymphoma and T cell lymphoma which are sometimes associated with EBV and HTLV-1 infection
Burkitt’s lymphoma
▪ Rare subtype caused by EBV infection which involves the maxilla or mandible
▪ Lymphadenopathy, tonsilar enlargement, fatigue, anemia, fever, weight loss, night
sweats
▪ GI lymphomas cause diarrhea, abdominal pain, malabsorption, obstruction, perforation, and/or abdominal mass.
▪ Most commonly affects the elderly
NON-HODGKIN’S LYMPHOMA
Malignant neoplasm of plasma cells
▪ Affects 50-60 year old men and women
Bone pain and fractures
▪ punched-out, lytic lesions in the bone caused by activation of osteoclasts
▪ Hypercalcemia (resorbed bone) → confusion and lethargy
▪ Increased bacterial infections
▪ Rouleaux formation of RBC
▪ Increased ESR
▪ Renal failure due to excess proliferation and deposition in the glomeruli of light chains of Ab (Bence Jones proteins)
▪ M-spike (M protein is the most common IgG) ▪ Hyperglobulinemia
MULTIPLE MYELOMA
▪ Infection caused by Babesia microti found in Ixodid ticks
▪ Most are asymptomatic or cause mild fever/flu-like symptoms
▪ Immunocompromised people suffer severe periodic fevers, chills, hemolytic anemia, malaria-like syndrome
▪ Complications include hemolytic anemia, ARDS, multiorgan failure, death
BABESIOSIS
▪ Infection by Plasmodium falciparum, P. malariae, P. ovale, or P, vivas
▪ Female Anopheles mosquitoes transmit the above.
Sporozoites infect hepatocytes and divide to form merozoites within the liver.
▪ These erupt and invade RBCs where they become trophozoites and schizonts before full
maturing to merozoites.
▪ Merozoites erupt from RBCs and erythrocytes are destroyed and hemoglobin is consumed.
▪ Merozoites mature into male and female gametocytes which are consumed by a mosquito.
▪ P. ovale and P. vivax also produce hyponozoites which remain dormant in hepatocyes.
MALARIA
which cdx:
Jaundice, hepatomegaly, splenomegaly, anemia, malarial paroxysm which coincides with the release of merozoites from ruptures RBCs.
▪ Paroxysms starts with malaise, abrupt chills and fever, rapid pulse, polyuria, nausea, headache, profuse sweating
▪ Occurs every 48 hour with P. vivax, P. falciform, and P. ovale and every 72 hours with P. malariae.
▪ Giemsa stain is used to identify the species
▪ Chronic infection with fatigue and lassitude and death can occur (exclusively from P. falciparum infection)
malaria
▪ Infection by Schistosoma spp. of the GI or genitourinary tracts.
▪ Blood flukes (worms)
▪ Urinary bladder, bowel, and liver dysfunction.
▪ Burrows through the skin and enters the blood stream
▪ Causes itching then later fever, hives, headache, cough, weight loss
▪ Complications include pulmonary and portal hypertension.
▪ Eggs induce granuloma formation and fibrosis which is associated with a high incidence of cancer.
SCHISTOSOMIASIS
