patho

Question 1

▪ 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.

Answer 1

ANEMIAS

Question 2

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)

Answer 2

IRON DEFICIENCY ANEMIA

Question 3

▪ 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

Answer 3

MACROCYTIC ANEMIA

Question 4

▪ 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

Answer 4

Pernicious anemia

Question 5

▪ 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)

Answer 5

APLASTIC ANEMIA

Question 6

▪ 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.

Answer 6

POLYCYTHEMIA VERA

Question 7

▪ 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

Answer 7

SECONDARY POLYCYTHEMIA

Question 8

DISEASES INVOLVING
PRODUCTION OF BLOOD
CELLS

Answer 8

▪ Anemias
▪ Iron deficiency anemia
▪ Macrocytic anemia
▪ Aplastic anemia
▪ Polycythemia vera
▪ Secondary polycythemia

Question 9

what group of anemias:
▪ Sickle cell anemia
▪ Thalassemias
▪ Hereditary spherocytosis
▪ Glucose-6-phosphate dehydrogenase deficiency

Answer 9

HEMOLYTIC ANEMIAS

Question 10

▪ 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)

Answer 10

hemolysis

Question 11

▪ 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

Answer 11

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

Question 12

▪ (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

Answer 12

Beta-thalassemias

Question 13

(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

Answer 13

Alpha-thalassemias

Question 14

▪ Genetic disorders characterized by deficient production of either of the two globin chains of hemoglobin.
▪ Hypochromic, microcytic anemia

Answer 14

THALASSEMIAS

Question 15

▪ 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

Answer 15

GLUCOSE-6 PHOSPHATE
DEHYDROGENAGE
DEFICIENCY

Question 16

▪ Genetic defect that causes spherical RBCs that get stuck in the spleen and destroyed
▪ Autosomal dominant

Answer 16

HEREDITARY SPHEROCYTOSIS

Question 17

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.

Answer 17

ERYTHROBLASTOSIS FETALIS

Question 18

▪ Disseminated intravascular coagulation (DIC)
▪ Hemophilia
▪ Thrombocytopenia
▪ Von Willebrand’s disease
▪ Vitamin K deficiency

Answer 18

CLOTTING ABNORMALITIES

Question 19

▪ 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.

Answer 19

DISSEMINATED
INTRAVASCULAR
COAGULATION

Question 20

▪ Blood coagulation disorders (X-linked recessive) due to absence, deficiency, impaired activity of clotting factors which results in prolonged bleeding.

Answer 20

HEMOPHILIA

Question 21

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

Answer 21

Hemophilia

Question 22

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

Answer 22

▪ Hemophilia A - Factor VIII deficiency
▪ Hemophilia B - Factor IX deficiency
▪ Hemophilia C (Autosomal Recessive) - Factor XI deficiency

Question 23

▪ 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.

Answer 23

THROMBOCYTOPENIA

Question 24

▪ 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

Answer 24

VON WILLEBRAND’S DISEASE

Question 25

▪ 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.

Answer 25

VITAMIN K DEFICIENCY

Question 26

▪ 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)

Answer 26

LEUKEMIAS

Question 27

which leukemia:
▪ At least 3 chromosomal translocations
▪ Anemia, fatigue, SOB, easy bleeding and bruising, frequent infections, thrombocytopenia

Answer 27

Acute myelogenous leukemia (AML)

Question 28

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

Answer 28

Acute lymphocytic leukemia (ALL) (MC in children)

Question 29

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

Answer 29

Chronic myelogenous leukemia (CML)

Question 30

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

Answer 30

Chronic lymphocytic leukemia (CLL) (MC leukemia esp. in older men)

Question 31

▪ 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

Answer 31

HODGKIN’S LYMPHOMA

Question 32

▪ 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

Answer 32

NON-HODGKIN’S LYMPHOMA

Question 33

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

Answer 33

MULTIPLE MYELOMA

Question 34

▪ 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

Answer 34

BABESIOSIS

Question 35

▪ 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.

Answer 35

MALARIA

Question 36

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)

Answer 36

malaria

Question 37

▪ 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.

Answer 37

SCHISTOSOMIASIS