Heme Flashcards
Iron Deficiency Anemia cause
↓ iron -> impaired hemoglobin production -> bone marrow pumps out small and pale RBC -> ↓ O2 to tissue -> ↑ BM activation -> ↑ poikilocytosis (shape) and anisocytosis (size) -> defective mitochondrial enzymes
Chronic bleeding (cancer, menses, h pylori, hookworms, etc)
Malnutrition
Absorption disorders
Gastrectomy/surgery
Pregnancy, childhood
Iron Deficency Anemia diagnosis
- Serum iron level decreased
- Total iron-binding capacity increased
- Percentage transferrin saturation decreased
- Serum ferritin level decreased or normal
- Platelet count increased
- Reticulocyte count decreased
- FEP increased
- Peripheral blood smear
- Mentzer index >13
- Microcytic hypochromic RBC
- Basophilic stippling
- Howell-jolly bodies (if severe)
Iron Deficiency Anemia comp
Plummer-Vinson syndrome (triad of IDA, esophageal webs, dysphagia)
Glossitis
Iron Deficiency Anemia clinical
Fatigue, conjunctival pallor, palpitation, pica, spoon nails (koilonychia), SOB, hair loss
a-Thalassemia cause
Cis or trans deletion on chromosome that results in absent/reduced alpha globin chains
a-globin gene deletions on chromo 16, decreased a-globin synthesis
autosomal recessive
a-Thalassemia RF
Cis deletion - Asian populations
Trans deletion - African populations
areas of high incidence of malaria
a-Thalassemia comp
chronic tissue hypoxia, leg ulcers, high output heart failure, hypermetabolic state, gallstones, bone marrow hyperplasia, bone marrow widens structural malformations, iron deposition in liver, myocardium, pancreas, and kidney
a-Thalassemia sx
Feeling tired or weak
Shortness of breath
Paleness
Dizziness and fainting
Headaches
Pale skin or yellowing of the skin and eyes (jaundice)
A large abdomen from a spleen or liver that is larger than normal
Changes or problems with bones in the face
Dark urine
Poor appetite
Intellectual or developmental disabilities
Lead Poisoning-Related Anemia RF
contaminated water, lead paint, industrial emissions (smelters, refiners, battery manufacturing, recycling) , lead-glazed ceramics
Lead Poisoning-Related Anemia comp
developmental delays, learning difficulties, chronic kidney disease, HTN, low libido, infertility, SIADH,
Lead Poisoning-Related Anemia clinical
fatigue, dyspnea, activity intolerance, abdominal pain, headache, difficulty concentrating, muscle/joint pain, confusion, ataxia
Lead anemia DX
heavy metal testing
CBC
Lead Poisoning-Related Anemia clinical
fatigue, dyspnea, activity intolerance, abdominal pain, headache, difficulty concentrating, muscle/joint pain, confusion, ataxia
Beta Thalassemia cause
mutation in beta globins
1: carrier
2: mild anemia
Beta Thalassemia comp
chronic tissue hypoxia, leg ulcers, high output heart failure, hypermetabolic state, gallstones, bone marrow hyperplasia, bone marrow widens structural malformations, iron deposition in liver, myocardium, pancreas, and kidney
Beta Thalassemia RF
FH, Mediterranean, middle eastern, southeast Asian, African genetic descent
Alpha thalassemia diagnosis
Microcytic
Basophilic stippling
Heinz’s bodies
Serum iron increased or normal
TIBC decreased or normal
Percentage saturation increased
Ferritin increased or normal
Reticulocyte increased or decreased
Serum LDH increased or normal
Haptoglobin decreased
Mentzer Index (Ratio of MCV/RBC) <13
Beta Thalassemia DX
- CBC
- microcytic anemia
- target cells
- inc RBCS
- Hemoglobin electrophoresis with hemoglobin F and A2 quantitation
- Mentzer index <13
Autoimmune Hemolytic Anemia path
Warm: IgG to Rh on RBC at normal body temp, antibody fixes complement + binds to RBC membrane -> antibody-coated RBCs destroyed extravascular by macrophages in spleen, liver
Cold: IgM, I, i, P
antibodies activate direct complement system attack, intravascular, complement-mediated
Autoimmune Hemolytic Anemia RF
immune deficiencies, malignancies, certain drugs, measles, varicella, mycoplasma, H. influenza, lymphoproliferative disorders, autoimmune disorders, exposure to cold
Autoimmune Hemolytic Anemia comp
venous thromboembolism, cholelithiasis, renal insufficiency, cardiac comp (older)
Autoimmune Hemolytic Anemia clinical
pallor, fatigue, activity intolerance, bounding pulses, tachycardia, pulmonary congestion,
cold: hemoglobinuria, jaundice, pain in legs and back, anemia, acrocyanosis, Raynaud’s, anemia after infx
Autoimmune hemolytic anemia dx
- High ferritin
- TIBC normal
- Reticulocyte count low
- CBC
- Normocytic/microcytic
- Normochromic/ hypochromic
- Low serum iron
Glucose-6-Phosphate Dehydrogenase Deficiency path
inadequate G6PD, GSH -> oxidative stress -> build-up of free radicals, peroxides -> precipitation of hemoglobin -> disruption of cell membrane -> ↑ cellular rigidity -> extravascular hemolysis, accelerated removal of damaged RBCs by reticuloendothelial system in spleen; intravascular hemolysis may also occur
G6PD deficiency dx
- total serum bilirubin
- CMP
- rapid fluorescent spot test
- quantitative spectrophotometric analysis
- reticulocyte count
- serum aminotransferase
- lactate dehydrogenase
- A peripheral blood smear may show signs of hemolysis such as schistocytes.
Glucose-6-Phosphate Dehydrogenase Deficiency clinical
pallor, jaundice, dark urine, abdominal/back pain, renal insufficiency,
Hemolytic Disease of the Newborn path
fetomaternal hemorrhage exposes maternal circulation to antigens present on fetal RBCs -> maternal sensitization -> formation of maternal IgG antibodies against fetal RBCs -> IgG antibodies small enough to cross placenta -> antibody attachment to fetal cells -> agglutination -> microcirculatory impairment -> hemolysis, destruction of RBCs by macrophages in reticuloendothelial system
Hemolytic Disease of the Newborn comp
Acute bilirubin encephalopathy, cerebral palsy, auditory dysfunction, paralysis of upward gaze, and permanent intellectual dysfunction
Hemolytic Disease of the Newborn clinical
anemia and hyperbilirubinemia, which may present as lethargy, jaundice, conjunctival icterus, pallor, hepatosplenomegaly, tachycardia or bradycardia, increased oxygen requirement, and/or apnea
Hemolytic Disease of Newborn dx
maternal RBC antibodies (agglutination in an indirect antibody test) and/or a positive direct antibody test (DAT) in the infant’s serum
Hereditary Spherocytosis path
mutation of genes encoding for proteins that secure RBC membrane skeleton to plasma membrane -> membrane destabilization -> rigidity, resistance to deformability -> hemolysis
Hereditary Spherocytosis comp
transient aplastic crisis caused by parvovirus B19
megaloblastic anemia
neonatal icterus, non-immune hydrops fetalis
Hereditary Spherocytosis clinical
Mild: anemia, splenomegaly, jaundice, modest reticulocytosis, normal hemoglobin, adolescents/adults
Moderate: anemia, reticulocytosis, hyperbilirubinemia, infants/children
Severe: anemia, hyperbilirubinemia, splenomegaly,
Hereditary Spherocytosis RF
northern European descent
Hereditary spherocytosis dx
Diagnosis is considered positive in patients who present Coombs-negative hemolysis with increased mean corpuscular hemoglobin concentration (MCHC), positive history for hereditary spherocytosis and spherocytes on microscopy, or by a positive result in a specialized test such as osmotic fragility, eosin-5-maleimide (EMA), or acidified glycerol lysis test (AGLT)
Sickle cell anemia path
point mutation of beta globin gene -> produces hemoglobin S -> RBC polymerize, deform into sickle/crescent-shaped forms when deoxygenated
Sickle cell anemia RF
areas where there are mosquitoes that carry malaria
Sickle cell anemia comp
ischemia/infraction, stroke, transient ischemic attack, seizures, MI, dysrhythmias, cardiomyopathy, HF, thromboembolism, leg ulcers, sudden death, acute chest syndrome, pulmonary HTN, priapism, pregnancy complications, osteoporosis, proliferative retinopathy, retinal detachment, multiorgan failure
Sickle cell anemia clinical
fatigue, activity intolerance, exertional dyspnea, hypersplenism, pain, vaso-occlusion, dactylitis, increased risk of infx,
Sickle Cell anemia dx
- “Sickle” shaped RBC with pointed ends on peripheral smear
- TIBC deceased
- Transferrin decreased
- electrophoresis
Anemia of chronic disease cause
infx, cancer, diabetes, autoimmune,
Anemia of chronic disease path
systemic inflammation -> ↑ circulation cytokines, IL-1, IL-6, TNF alpha, IFN beta, IFN gamma -> ↑ hepcidin secretion by liver -> ↓ iron absorption from GI tract, ↓ iron sequestration in reticuloendothelial system -> ↓ iron available for erythropoiesis -> ↓ secretion erythropoietin -> ↓ erythrocyte lifespan
Anemia of chronic disease labs
- normochromic normocytic
- low serum iron
- high ferritin
- TIBC normal
- Reticulocyte count low
Aplastic anemia cause
Fanconi anemia, Shwachman-Diamond syndrome, SLE, graft-versus-host disease, paroxysmal nocturnal hemoglobinuria, chemotherapy, carbamazepine, phenytoin, indomethacin, sulfonamides, Epstein-Barr, HIV, hepatitis, herpes, solvents, benzene, pesticides, radiation, idiopathic
Aplastic anemia path
bone marrow hypoplasia/aplasia, hematopoietic cell loss -> ↓ production of cell lineages -> peripheral pancytopenia
Aplastic anemia clinical
shorter lifespan, ↑ infx, neutropenia-related sepsis, gingival nares, ecchymosis, petechiae, heavy menstrual flow, occult blood in stool, intracranial hemorrhage, pallor, fatigue, dyspnea, activity intolerance, cardiorespiratory compromise
Aplastic anemia dx
- Normocytic
- Normochromic
- Serum iron elevated
- Reticulocytes count decreased
- Bone marrow aspiration
Megaloblastic anemia cause
cobalamin and/or folate deficiency due to diet, malabsorption, medications, surgery, pancreatic insufficiency, alcoholism
Megaloblastic anemia path
impaired DNA synthesis during erythropoiesis -> uncoordinated maturation of cytoplasm and nuclei in erythroblasts -> abnormally large RBCs + deflective cells w/ fragile membranes -> RBC die prematurely -> anemia
Megaloblastic anemia RF
alcohol use, old age, strict diets,
Megaloblastic anemia clinical
fatigue, activity intolerance, pallor, tachycardia, bounding pulse, jaundice, splenomegaly, glossitis
megoblastic anemia dx
- Macrocytic
- Ferritin increased
- B12 decreased
- Folate decreased
- Bilirubin increased
- Peripheral smear- neutrophil 5 or more segments
sideroblastic anemia cause
X-linked/autosomal recessive/mitochondrial inheritance, myelodysplastic syndromes, myeloproliferative neoplasms, excessive alcohol, isoniazid, chloramphenicol, copper deficiency, zinc overload
sideroblastic anemia path
impaired erythropoiesis, hemoglobin synthesis -> reduced iron in RBCs + defective RBCs undergo apoptosis w/in bone marrow + fewer functional RBCs in circulation -> anemia
sideroblastic anemia RF
genetics, alcohol, diet
sideroblastic anemia comp
iron overload, hemochromatosis, erythroid hyperplasia of bone marrow, increased risk of infx, acute leukemia, infx fatal
sideroblastic anemia clinical
fatigue, dyspnea, palpitations, pallor, mild jaundice, hepatosplenomegaly, cardiac arrhythmias, HF
Sideroblastic anemia dx
- Microcytic/ normocytic
- Hypochromic
- Basophilic stippling
- Ferritin elevated
- Serum iron elevated
- Transferrin saturation elevated
Polycythemia Vera path
JAK2V617F mutation
hematopoietic stem cell -> ↑ RBCs, platelets, basophils, eosinophils -> ↑ blood viscosity, ↑ total blood volume -> may evolve into spent phase
Polycythemia Vera RF
radiation, age, genetics
Polycythemia Vera comp
HTN, Budd-Chiari syndrome, DVT, arterial thrombosis, MI, gout, AML
Polycythemia Vera clinical
headache, fatigue, dizziness, dyspnea, plethora, cyanosis, pruritus, gastric ulcers, DVT, MI, portal vein thrombosis, hyperemic and inflamed extremities, bleeding gums, epistaxis, ecchymoses, GI bleed, hepatosplenomegaly, HTN
Polycythemia Vera dx
- Increased RBC
- Increased Hgb
- High platelets
- High WBCs
- High LDH
- Panmyelosis in the BM
- Low EPO level
- Positive JAK2 mutation
- May also have increased platelets and granulocytes
Disseminated Intravascular Coagulation cause
DIC TEAR
Delivery TEAR: obstetric
Infection
Cancer: prostate, pancreas, lung, stomach
Toxemia of pregnancy
Emboli
Abruptio placentae
Retain fetus products
preeclampsia, obstetric hemorrhage, retained dead fetus, critical illness, mucin-secreting adenocarcinoma, acute promyelocytic leukemia, infx/sepsis (gram - bacteria), massive tissue injury, intravascular hemolysis, shock, snakebites
Disseminated Intravascular Coagulation path
release of procoagulants, tissue factors, bacterial components, enzymes/major endothelial injury -> excessive activation of coagulation cascade -> thrombosis of small/medium blood vessels -> activation of fibrinolysis to resolve clots -> fibrin degradation products released into circulation -> interfere w/ platelet aggregation, clot formation
Disseminated Intravascular Coagulation RF
sepsis, cancer, blood transfusion reaction, pancreatitis, liver disease, surgery, anesthesia,
Disseminated Intravascular Coagulation comp
thromboembolism, tissue hypoxia, infraction, hypoxia of kidney, liver, lung, brain
Disseminated Intravascular Coagulation dx
- alow platelet count
- elevated D-dimer concentration
- decreased fibrinogen concentration
- prolongation of clotting times such as prothrombin time (PT)
Hemophilia A cause
X-linked recessive mutation F8 gene
Hemophilia A path
quantitative/qualitative deficiency of factor VII -> insufficient activation of the intrinsic pathway -> defect in common coagulation pathway -> increased tendency for bleeding
Hemophilia A RF
male
Hemophilia A comp
intracerebral hemorrhage, stroke
Hemophilia A clinical
asymptomatic
easy bruising, prolonged bleeding, hematomas, muscle hematomas, hemophilic pseudotumor, GI bleeding, hematuria, severe epistaxis, joint irregularity and disability,
Hemophilia A dx
high aPPT
normal PT
platelet count normal
Hemophilia B cause
mutation of F9 on X chromosome
Hemophilia B path
qualitative/quantitative deficiency of coagulation factor IX -> insufficient activation of intrinsic coagulation pathway -> impaired hemostasis
Hemophilia B comp
intracerebral hemorrhage, stroke
Hemophilia B RF
genetics, male
Hemophillia B dx
high aPPT
normal PT
platelet count normal
Hemophilia B clinical
bleeding sponatenously or after trauma
Von Willebrand Disease def
defective platelet function w/ normal platelet count
Von Willebrand Disease cause
autosomal dominant/recessive
Von Willebrand Disease path
quantitative/qualitative deficiency of vWF -> impaired platelet aggregation, adhesion, dysfunction of factor VII -> deficiency in coagulation cascade -> bleeding tendency
Von Willebrand Disease RF
genetics
Von Willebrand Disease comp
severe bleeding, pregnancy probs
Von Willebrand Disease clinical
asymptomatic
surgery/trauma bring on
spontaneous epistaxis, easy bruising, excessive bleeding from wounds, bleeding gums, menorrhagia, GI bleeding, internal/joint bleeding
Immune Thrombocytopenic Purpura def
autoimmune condition where body makes antibodies to thrombocytes/platelets
Immune Thrombocytopenic Purpura cause
Acute: children after viral infx
Chronic: females of reproductive age, no underlying trigger, or by hepatitis C, HIV, lupus
Immune Thrombocytopenic Purpura path
IgG antibodies from the spleen -> bind to GPIIb/IIIa on platelet -> target for destruction of platelets in spleen
Immune Thrombocytopenic Purpura clinical
asymptomatic
purpura (red/purple spots small)
Immune Thrombocytopenic Purpura RF
women, no vaccination,
Immune Thrombocytopenic Purpura comp
hemorrhage
Immune Thrombocytopenic Purpura clinical
asymptomatic
purpura (red/purple spots small)
epistaxis
Vitamin K Deficiency def
lack of Vit K
Vitamin K Deficiency cause
exclusive breastfeeding, medication, lack of Vit K1 prophylaxis at birth, malabsorption, low intake, diseases of SM intestine, liver, gallbladder, pancreas
Vitamin K Deficiency path
↓ phylloquinone ( vit K) -> ↓ bile salts make fat soluble vitamin soluble -> ↓ incorporation into GI micelles -> ↓ absorbed by small intestine -> ↓ integrated into chylomicrons -> ↓ transported to portal circulation -> ↓ liver use to synthesize coagulation factors, other essential proteins
Vitamin K Deficiency RF
infants: no K1 prophylaxis, immature liver, low K stores, sterile gut, maternal ingestion of coumarin-like anticoagulants/some anticonvulsants/antibiotics,
adults: prolonged diarrhea, antibiotics, low intake, TPN administration
Vitamin K Deficiency comp
intracranial hemorrhage, impaired bone mineralization, vascular calcium deposits
Vitamin K Deficiency clinical
low bone density signs, gingival bleeding, epistaxis, easy bruising, hematuria, melena, umbilical stump/circumcision site bleeding, vomiting, seizures
Acute Lymphoblastic Leukemia (ALL) def
uncontrolled proliferation of partially developed white blood cells/lymphoblasts, cancer
Acute Lymphoblastic Leukemia (ALL) cause
B cell: translocation (12,21) and (9,22) Philadelphia chromosome
T cell: NOTCH1 mutation
abnormal chromosome number
Acute Lymphoblastic Leukemia (ALL) path
mutations -> loss ability to differentiate into mature blood cells -> stuck in blast cells -> don’t function effectively and divide uncontrollably -> other cells get crowded out -> leading to anemia, thrombocytopenia, and leukopenia -> blast cells spill into blood travel to thymus, lymph nodes, liver, spleen to enlarge
Acute Lymphoblastic Leukemia (ALL) RF
young age
down syndrome
radiation exposure
alkylating chemotherapy
Acute Lymphoblastic Leukemia (ALL) comp
intracranial hemorrhage
Acute Lymphoblastic Leukemia (ALL) clinical
Fever, fatigue, SOB, pallor, bruising, petechiae, epistaxis, Bone pain, Hepatosplenomegaly, lymphadenopathy, easy bleeding, inc infx, thymus enlargement
Acute Myeloblastic Leukemia (AML)
def
uncontrolled proliferation of myeloblasts, cancer
Acute Myeloblastic Leukemia (AML) cause
chromosomal translocations (15, 17), myelodysplastic syndrome
Acute Myeloblastic Leukemia (AML) path
mutations -> loss ability to differentiate into mature blood cells -> stuck in blast cells -> don’t function effectively and divide uncontrollably -> other cells get crowded out -> leading to anemia, thrombocytopenia, and leukopenia -> blast cells spill into blood travel to thymus, lymph nodes, liver, spleen to enlarge
Acute Myeloblastic Leukemia (AML) RF
down syndrome
radiation
alkylating chemotherapy
Acute Myeloblastic Leukemia (AML) comp
DIC
Acute Myeloblastic Leukemia (AML) clinical
easy bleeding, inc infx, Fever, fatigue, SOB, pallor, bruising, petechiae, epistaxis, Bone pain, swelling of gums
Chronic Myelogenous Leukemia (CML) def
cancer rapid proliferation of mature granulocytes/precursors
Chronic Myelogenous Leukemia cause
Philadelphia chromosome t(9,22) BCR-ABL gene
trisomy of chromosome
doubling of Philadelphia chromosome
Chronic Myelogenous Leukemia path
mutation -> tyrosine kinase is one -> rapid division of myeloid cells -> spill into blood -> liver spleen cause to swell
Chronic Myelogenous Leukemia RF
adult age, radiation, benzene
Chronic Myelogenous Leukemia comp
Recurrent infections, bleeding
Chronic Myelogenous Leukemia clinical
chronic: asymptomatic, fatigue, weight loss, fever,
accelerated phase: pallor, SOB, splenomegaly, hepatomegaly, lymphadenopathy, recurrent infx, bleeding, petechiae, ecchymoses,
blast crisis: bone pain, fever, anemia, significant splenomegaly, inc bleeding, basophilia
Chronic Lymphocytic Leukemia def
cancer, proliferation of mature, functionally abnormal B lymphocytes in bone marrow and don’t die
Chronic Lymphocytic Leukemia path
mutation -> interfere w/ B cell receptors -> activate tyrosine kinase (bruton’s tyrosine kinase and other) -> prevent maturation and slow death - move to lymph nodes
Chronic Lymphocytic Leukemia clinical
fatigue, SOB, pallor, bruising, petechiae, epistaxis, fever, pneumonia, sepsis, lymphadenopathy
Burkitt’s Lymphoma def
B lymphocyte tumor
Burkitt’s Lymphoma cause
chromosomal translocation t(8,14)
Burkitt’s Lymphoma path
translocation -> Myc gene moved adjacent to IgH promoter sequence -> upregulation of Myc gene -> Myc gene simulates cell growth, metabolism -> increased cell division
Burkitt’s Lymphoma RF
EBV infection, Africa
Burkitt’s Lymphoma clinical
“Starry sky” appearance
Burkitt’s Lymphoma clinical
“Starry sky” appearance (b-cells w/ no cytoplasm and tingible-body macrophages w/ dead neoplastic cells)
extranodal involvement at jaw (Africa) or ileocecal junction
Subtypes of Classical Hodgkin Lymphoma
nodular sclerosis: most common, nodules surrounded by collagen, lacunar cell
mixed cellularity: b lymphocytes, plasma cells, eosinophils, lymphocytes, neutrophils, histocytes, immunocompromised
lymphocyte-rich: lymphocytes surrounding Reed-Sternberg cells, best prognosis
lymphocyte-depleted: lack of normal lymphocytes, abundance of Reed-Sternberg cells, immunocompromised
Hodgkin Lymphoma cause
mutation in DNA
Hodgkin Lymphoma path
mutation -> cell growth and division
Hodgkin Lymphoma RF
20, 60s< EBV
Hodgkin Lymphoma comp
second cancer
Hodgkin Lymphoma clinical
spread to nearby lymph nodes in a contiguous manner
swollen lymph nodes that are painless, rubbery, non-erythematous, nontender including cervical
supraclavicular and axillary
fever, weight loss, night sweats
Reed-Sternberg cells (binucleated neoplastic B cells)
Non-Hodgkin Lymphoma def
cancer of the B or T cells
Non-Hodgkin Lymphoma cause
chromosomal translocation (14, 18) BCL2 gene, BCL-6 and BCL-2 mutation, Human T-Lymphotropic Virus, chromosomal translocation (11, 14) BCL1 gene
Non-Hodgkin Lymphoma path
mutations -> uncontrolled cell division
Non-Hodgkin Lymphoma RF
old age, smoking, FH,
Non-Hodgkin Lymphoma comp
metastases, respiratory problems
Non-Hodgkin Lymphoma clinical
swollen lymph nodes that are painless, rubbery, non-erythematous, nontender in bone marrow, GI tract, spinal cord, fever, weight loss night sweats
Mantel cell Lymphoma RF
male
Marginal Zone Lymphoma RF
older people, H. pylori, hepatitis C
Follicular Lymphoma clinical
waxing/waning lymphadenopathy
Diffuse Large B-cell lymphoma def
b cell lymphoma, aggressive growth of b cells, most common in adults
Diffuse Large B-cell lymphoma cause
BCL-6 and BCL-2 mutation
Mantel cell Lymphoma cause
chromosomal translocation (11, 14) BCL1 gene
Adult T-cell Lymphoma def
proliferation of T cell
Adult T-cell Lymphoma cause
Human T-Lymphotropic Virus
Adult T-cell Lymphoma path
Human T-Lymphotropic Virus RNA -> DNA -> incorporates into T cell DNA -> cancer
Adult T-cell Lymphoma clinical
severe hypercalcemia, bone lesions
Mycosis Fungoides clinical
patch or plaque like lesions that look like fungal infection, Pautrier micro abscesses in the epidermis
Lymphoplasmacytic Lymphoma
bone marrow, lymph nodes, spleen, Waldenstrom macroglobulinemia
Adult T-cell Lymphoma cause
Human T-Lymphotropic Virus
Adult T-cell Lymphoma clinical
severe hypercalcemia, bone lesions
Mycosis Fungoides clinical
patch or plaque like lesions that look like fungal infection, Pautrier micro abscesses in the epidermis, erythroderma
Subtypes of Non-Hodgkin Lymphoma B cell
Lymphoplasmacytic Lymphoma Marginal Zone Lymphoma Mantel cell Lymphoma Diffuse Large B-cell lymphoma Follicular Lymphoma
Subtypes of Non-Hodgkin Lymphoma T cell
Mycosis Fungoides
Adult T-cell Lymphoma
Multiple Myeloma def
cancer of plasms cells in bone marrow
Multiple Myeloma cause
t(14, 11), t( 14,6), deletion of gene TP53 tumor suppressor on chromosome 17
Multiple Myeloma RF
alcohol consumption, obesity, radiation, FH
Multiple Myeloma comp
amyloidosis, renal failure, death, UTIs, pneumonia, hyper-viscosity syndrome
Multiple Myeloma path
bone marrow cells, myeloma cells secrete cytokines, IL6, NF-kB -> promote proliferation, survival myeloma cells -> bone resoprtion, monoclonal free light chains, inhibited hematopoiesis, and IL1beta, TNFalpha -> bone lesions, renal disease, anemia, and high calcium
Multiple Myeloma clinical
CRAB (calcium, renal disease, anemia, bone lesions)
confusion, somnolence, constipation, N, thirst, fatigue, pallor, fever, infections, bleeding, bone lesions, pain, fractures, spinal cord compression, paresthesia, Bence Jones, Tamm-Horsfall proteins
Babesiosis def
infection of RBC by Babesia microti, ducani, or divergems
Babesiosis cause
Ixodes scapularis tick, contaminated blood transfusion
Babesiosis def
infection of RBC by Babesia microti, ducani, or divergems
Babesiosis RF
endemic area, May-September, blood transfusions, >50, male, asplenia, malignancy, HIV/AIDS, immunosuppressive drugs, coinfection w/ Borrelia and/or Anaplasma, premature birth
Babesiosis comp
CHF, noncardiac pulmonary edema, acute respiratory distress syndrome, splenic infarct, splenic rupture, septic shock, MI, disseminated intravascular coagulation, death
Babesiosis clinical
asymptomatic, fatigue, fever, chills, headache, myalgia, arthralgia, anorexia, N, cough, hypotension, poor prefusion, pulmonary edema, acute renal failure, disseminated intravascular coagulation
Babesiosis clinical
asymptomatic, fatigue, fever, chills, swears, headache, myalgia, arthralgia, anorexia, N, cough, hypotension, poor prefusion, pulmonary edema, acute renal failure, disseminated intravascular coagulation
maltese cross
Plasmodium species (Malaria) def
single cell parasites that get spread by mosquitoes
Plasmodium species (Malaria) cause
P. falciparum, P. vivax, P. malariae, P. ovale, P. knowlesi
Plasmodium species (Malaria) cause
P. falciparum (few days), P. vivax, P. malariae (few weeks), P. ovale, P. knowlesi
Plasmodium species (Malaria) path
P-infected female anopheles mosquito hunts for a blood meal in evening -> Plasmodium is in a sporozoite stage in salivary gland -> mosquito’s proboscis piece skin sporozoites spill into bloodstream -> liver start asexual reproduction called schizogony -> over 1-2 weeks P. falciparum, malariae, knowlesi multiply asexually & mature to merozoites -> 1 mon-years P. ovale and vivax go dormant -> merozoites bind to duffy receptor on all different stages of RBC –> asexual reproduction 2-3 days -> trophozoite -> late trophozoite -> hemozoin/schizont -> replication -> release into RBC -> some turn into gametocytes and taken up by mosquitos -> mature and fuse into a zygote in gut -> ookinete -> oocyst rupture releasing sporozoites -> into salivary gland
Plasmodium species (Malaria) clinical
paroxysm of fevers P. falciparum (variable), P. vivax (48 h), P. malariae (72), P. ovale (48), P. knowlesi (24 h)
Plasmodium species (Malaria) comp
death, organ failure, cerebral malaria (altered mental status, seizure, coma), diarrhea, jaundice, vomiting, liver failure
Plasmodium species (Malaria) clinical
paroxysm of fevers P. falciparum (variable, worst infx), P. vivax (48 h), P. malariae (72), P. ovale (48), P. knowlesi (24 h)
fatigue, headaches, jaundice, splenomegaly,
Susan just headed for fiji
Schistosomiasis def
parasitic flatworms that cause damage in the mesenteries of the bladder
Schistosomiasis cause
Schistosoma haematobium, S. japonicum, and S. mansoni
Schistosomiasis path
Schistosoma eggs are eleminated in feces or urine into water -> eggs hatch and release miracidia -> miracidia penetrate snail tissue -> sporocyst develop in snail -> free-swimming cercariae released from snail into water -> cercariea penetrates skin -> cerciarea loses tails during penetration and becomes shcistocomulae -> migration to liver through circulation -> adult form -> migration to mesenteric venules/vesical venous plex -> egg deposit -> inflammation -> fibrosis
Schistosomiasis RF
male, rural areas, contact w/ fresh water bodies in endemic areas
Schistosomiasis comp
bacteremia, infertility, intestinal obstruction, nephrotic syndrome, renal failure, cardiomegaly, acute myelopathy
Schistosomiasis clinical
Acute: pruritic papular/urticarial rash of legs/feet, fever, urticaria, chills, arthralgia, myalgia, headaches, angioedema, dry cough, abdominal pain, diarrhea
chronic: abdominal pain, poor appetite, diarrhea, hepatosplenomegaly, portal HTN, ascites, dyspnea, cor pulmonale, hematuria, pyuria, dysuria, frequency, seizures, sensory/motor impairment, cerebellar syndrome
Plasma cell Microscopic Anatomy
clock face chromatin distribution and eccentric nucleus,
Plasma cell Origins
spleen and lymph node
Plasma cell Maturation
bone marrow
Plasma cell function
large amounts of antibody specific to particular antigens
Plasma cell regulation
transcription factors
Plasma cell synthesis
antigen-activated B in spleen and lymph node -> plasmablast -> plasma cells
Plasma cell degradation
2-3 days
How does hepcidin effect iron levels in body?
inhibits ferroportin-1
