Heme Flashcards

1
Q

Iron Deficiency Anemia cause

A

↓ 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

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2
Q

Iron Deficency Anemia diagnosis

A
  • 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)
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3
Q

Iron Deficiency Anemia comp

A

Plummer-Vinson syndrome (triad of IDA, esophageal webs, dysphagia)
Glossitis

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4
Q

Iron Deficiency Anemia clinical

A

Fatigue, conjunctival pallor, palpitation, pica, spoon nails (koilonychia), SOB, hair loss

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5
Q

a-Thalassemia cause

A

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

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6
Q

a-Thalassemia RF

A

Cis deletion - Asian populations
Trans deletion - African populations
areas of high incidence of malaria

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7
Q

a-Thalassemia comp

A

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

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8
Q

a-Thalassemia sx

A

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

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9
Q

Lead Poisoning-Related Anemia RF

A

contaminated water, lead paint, industrial emissions (smelters, refiners, battery manufacturing, recycling) , lead-glazed ceramics

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10
Q

Lead Poisoning-Related Anemia comp

A

developmental delays, learning difficulties, chronic kidney disease, HTN, low libido, infertility, SIADH,

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11
Q

Lead Poisoning-Related Anemia clinical

A

fatigue, dyspnea, activity intolerance, abdominal pain, headache, difficulty concentrating, muscle/joint pain, confusion, ataxia

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12
Q

Lead anemia DX

A

heavy metal testing
CBC

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13
Q

Lead Poisoning-Related Anemia clinical

A

fatigue, dyspnea, activity intolerance, abdominal pain, headache, difficulty concentrating, muscle/joint pain, confusion, ataxia

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14
Q

Beta Thalassemia cause

A

mutation in beta globins

1: carrier
2: mild anemia

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15
Q

Beta Thalassemia comp

A

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

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16
Q

Beta Thalassemia RF

A

FH, Mediterranean, middle eastern, southeast Asian, African genetic descent

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17
Q

Alpha thalassemia diagnosis

A

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

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18
Q

Beta Thalassemia DX

A
  • CBC
    • microcytic anemia
    • target cells
    • inc RBCS
  • Hemoglobin electrophoresis with hemoglobin F and A2 quantitation
  • Mentzer index <13
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19
Q

Autoimmune Hemolytic Anemia path

A

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

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20
Q

Autoimmune Hemolytic Anemia RF

A

immune deficiencies, malignancies, certain drugs, measles, varicella, mycoplasma, H. influenza, lymphoproliferative disorders, autoimmune disorders, exposure to cold

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21
Q

Autoimmune Hemolytic Anemia comp

A

venous thromboembolism, cholelithiasis, renal insufficiency, cardiac comp (older)

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22
Q

Autoimmune Hemolytic Anemia clinical

A

pallor, fatigue, activity intolerance, bounding pulses, tachycardia, pulmonary congestion,

cold: hemoglobinuria, jaundice, pain in legs and back, anemia, acrocyanosis, Raynaud’s, anemia after infx

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23
Q

Autoimmune hemolytic anemia dx

A
  • High ferritin
  • TIBC normal
  • Reticulocyte count low
  • CBC
    • Normocytic/microcytic
    • Normochromic/ hypochromic
    • Low serum iron
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24
Q

Glucose-6-Phosphate Dehydrogenase Deficiency path

A

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

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25
Q

G6PD deficiency dx

A
  • 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.
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26
Q

Glucose-6-Phosphate Dehydrogenase Deficiency clinical

A

pallor, jaundice, dark urine, abdominal/back pain, renal insufficiency,

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27
Q

Hemolytic Disease of the Newborn path

A

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

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28
Q

Hemolytic Disease of the Newborn comp

A

Acute bilirubin encephalopathy, cerebral palsy, auditory dysfunction, paralysis of upward gaze, and permanent intellectual dysfunction

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29
Q

Hemolytic Disease of the Newborn clinical

A

anemia and hyperbilirubinemia, which may present as lethargy, jaundice, conjunctival icterus, pallor, hepatosplenomegaly, tachycardia or bradycardia, increased oxygen requirement, and/or apnea

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30
Q

Hemolytic Disease of Newborn dx

A

maternal RBC antibodies (agglutination in an indirect antibody test) and/or a positive direct antibody test (DAT) in the infant’s serum

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31
Q

Hereditary Spherocytosis path

A

mutation of genes encoding for proteins that secure RBC membrane skeleton to plasma membrane -> membrane destabilization -> rigidity, resistance to deformability -> hemolysis

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32
Q

Hereditary Spherocytosis comp

A

transient aplastic crisis caused by parvovirus B19
megaloblastic anemia
neonatal icterus, non-immune hydrops fetalis

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33
Q

Hereditary Spherocytosis clinical

A

Mild: anemia, splenomegaly, jaundice, modest reticulocytosis, normal hemoglobin, adolescents/adults

Moderate: anemia, reticulocytosis, hyperbilirubinemia, infants/children

Severe: anemia, hyperbilirubinemia, splenomegaly,

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34
Q

Hereditary Spherocytosis RF

A

northern European descent

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35
Q

Hereditary spherocytosis dx

A

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)

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36
Q

Sickle cell anemia path

A

point mutation of beta globin gene -> produces hemoglobin S -> RBC polymerize, deform into sickle/crescent-shaped forms when deoxygenated

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37
Q

Sickle cell anemia RF

A

areas where there are mosquitoes that carry malaria

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38
Q

Sickle cell anemia comp

A

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

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39
Q

Sickle cell anemia clinical

A

fatigue, activity intolerance, exertional dyspnea, hypersplenism, pain, vaso-occlusion, dactylitis, increased risk of infx,

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40
Q

Sickle Cell anemia dx

A
  • “Sickle” shaped RBC with pointed ends on peripheral smear
  • TIBC deceased
  • Transferrin decreased
  • electrophoresis
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41
Q

Anemia of chronic disease cause

A

infx, cancer, diabetes, autoimmune,

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42
Q

Anemia of chronic disease path

A

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

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43
Q

Anemia of chronic disease labs

A
  • normochromic normocytic
  • low serum iron
  • high ferritin
  • TIBC normal
  • Reticulocyte count low
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44
Q

Aplastic anemia cause

A

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

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45
Q

Aplastic anemia path

A

bone marrow hypoplasia/aplasia, hematopoietic cell loss -> ↓ production of cell lineages -> peripheral pancytopenia

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46
Q

Aplastic anemia clinical

A

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

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47
Q

Aplastic anemia dx

A
  • Normocytic
  • Normochromic
  • Serum iron elevated
  • Reticulocytes count decreased
  • Bone marrow aspiration
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48
Q

Megaloblastic anemia cause

A

cobalamin and/or folate deficiency due to diet, malabsorption, medications, surgery, pancreatic insufficiency, alcoholism

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49
Q

Megaloblastic anemia path

A

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

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50
Q

Megaloblastic anemia RF

A

alcohol use, old age, strict diets,

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51
Q

Megaloblastic anemia clinical

A

fatigue, activity intolerance, pallor, tachycardia, bounding pulse, jaundice, splenomegaly, glossitis

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52
Q

megoblastic anemia dx

A
  • Macrocytic
  • Ferritin increased
  • B12 decreased
  • Folate decreased
  • Bilirubin increased
  • Peripheral smear- neutrophil 5 or more segments
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53
Q

sideroblastic anemia cause

A

X-linked/autosomal recessive/mitochondrial inheritance, myelodysplastic syndromes, myeloproliferative neoplasms, excessive alcohol, isoniazid, chloramphenicol, copper deficiency, zinc overload

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54
Q

sideroblastic anemia path

A

impaired erythropoiesis, hemoglobin synthesis -> reduced iron in RBCs + defective RBCs undergo apoptosis w/in bone marrow + fewer functional RBCs in circulation -> anemia

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55
Q

sideroblastic anemia RF

A

genetics, alcohol, diet

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56
Q

sideroblastic anemia comp

A

iron overload, hemochromatosis, erythroid hyperplasia of bone marrow, increased risk of infx, acute leukemia, infx fatal

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57
Q

sideroblastic anemia clinical

A

fatigue, dyspnea, palpitations, pallor, mild jaundice, hepatosplenomegaly, cardiac arrhythmias, HF

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58
Q

Sideroblastic anemia dx

A
  • Microcytic/ normocytic
  • Hypochromic
  • Basophilic stippling
  • Ferritin elevated
  • Serum iron elevated
  • Transferrin saturation elevated
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59
Q

Polycythemia Vera path

A

JAK2V617F mutation
hematopoietic stem cell -> ↑ RBCs, platelets, basophils, eosinophils -> ↑ blood viscosity, ↑ total blood volume -> may evolve into spent phase

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60
Q

Polycythemia Vera RF

A

radiation, age, genetics

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61
Q

Polycythemia Vera comp

A

HTN, Budd-Chiari syndrome, DVT, arterial thrombosis, MI, gout, AML

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62
Q

Polycythemia Vera clinical

A

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

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63
Q

Polycythemia Vera dx

A
  • 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
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64
Q

Disseminated Intravascular Coagulation cause

A

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

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65
Q

Disseminated Intravascular Coagulation path

A

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

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66
Q

Disseminated Intravascular Coagulation RF

A

sepsis, cancer, blood transfusion reaction, pancreatitis, liver disease, surgery, anesthesia,

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67
Q

Disseminated Intravascular Coagulation comp

A

thromboembolism, tissue hypoxia, infraction, hypoxia of kidney, liver, lung, brain

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68
Q

Disseminated Intravascular Coagulation dx

A
  • alow platelet count
  • elevated D-dimer concentration
  • decreased fibrinogen concentration
  • prolongation of clotting times such as prothrombin time (PT)
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69
Q

Hemophilia A cause

A

X-linked recessive mutation F8 gene

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70
Q

Hemophilia A path

A

quantitative/qualitative deficiency of factor VII -> insufficient activation of the intrinsic pathway -> defect in common coagulation pathway -> increased tendency for bleeding

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71
Q

Hemophilia A RF

A

male

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72
Q

Hemophilia A comp

A

intracerebral hemorrhage, stroke

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73
Q

Hemophilia A clinical

A

asymptomatic
easy bruising, prolonged bleeding, hematomas, muscle hematomas, hemophilic pseudotumor, GI bleeding, hematuria, severe epistaxis, joint irregularity and disability,

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74
Q

Hemophilia A dx

A

high aPPT
normal PT
platelet count normal

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75
Q

Hemophilia B cause

A

mutation of F9 on X chromosome

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76
Q

Hemophilia B path

A

qualitative/quantitative deficiency of coagulation factor IX -> insufficient activation of intrinsic coagulation pathway -> impaired hemostasis

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77
Q

Hemophilia B comp

A

intracerebral hemorrhage, stroke

78
Q

Hemophilia B RF

A

genetics, male

79
Q

Hemophillia B dx

A

high aPPT
normal PT
platelet count normal

80
Q

Hemophilia B clinical

A

bleeding sponatenously or after trauma

81
Q

Von Willebrand Disease def

A

defective platelet function w/ normal platelet count

82
Q

Von Willebrand Disease cause

A

autosomal dominant/recessive

83
Q

Von Willebrand Disease path

A

quantitative/qualitative deficiency of vWF -> impaired platelet aggregation, adhesion, dysfunction of factor VII -> deficiency in coagulation cascade -> bleeding tendency

84
Q

Von Willebrand Disease RF

A

genetics

85
Q

Von Willebrand Disease comp

A

severe bleeding, pregnancy probs

86
Q

Von Willebrand Disease clinical

A

asymptomatic
surgery/trauma bring on
spontaneous epistaxis, easy bruising, excessive bleeding from wounds, bleeding gums, menorrhagia, GI bleeding, internal/joint bleeding

87
Q

Immune Thrombocytopenic Purpura def

A

autoimmune condition where body makes antibodies to thrombocytes/platelets

88
Q

Immune Thrombocytopenic Purpura cause

A

Acute: children after viral infx
Chronic: females of reproductive age, no underlying trigger, or by hepatitis C, HIV, lupus

89
Q

Immune Thrombocytopenic Purpura path

A

IgG antibodies from the spleen -> bind to GPIIb/IIIa on platelet -> target for destruction of platelets in spleen

90
Q

Immune Thrombocytopenic Purpura clinical

A

asymptomatic

purpura (red/purple spots small)

91
Q

Immune Thrombocytopenic Purpura RF

A

women, no vaccination,

92
Q

Immune Thrombocytopenic Purpura comp

A

hemorrhage

93
Q

Immune Thrombocytopenic Purpura clinical

A

asymptomatic
purpura (red/purple spots small)
epistaxis

94
Q

Vitamin K Deficiency def

A

lack of Vit K

95
Q

Vitamin K Deficiency cause

A

exclusive breastfeeding, medication, lack of Vit K1 prophylaxis at birth, malabsorption, low intake, diseases of SM intestine, liver, gallbladder, pancreas

96
Q

Vitamin K Deficiency path

A

↓ 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

97
Q

Vitamin K Deficiency RF

A

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

98
Q

Vitamin K Deficiency comp

A

intracranial hemorrhage, impaired bone mineralization, vascular calcium deposits

99
Q

Vitamin K Deficiency clinical

A

low bone density signs, gingival bleeding, epistaxis, easy bruising, hematuria, melena, umbilical stump/circumcision site bleeding, vomiting, seizures

100
Q

Acute Lymphoblastic Leukemia (ALL) def

A

uncontrolled proliferation of partially developed white blood cells/lymphoblasts, cancer

101
Q

Acute Lymphoblastic Leukemia (ALL) cause

A

B cell: translocation (12,21) and (9,22) Philadelphia chromosome
T cell: NOTCH1 mutation
abnormal chromosome number

102
Q

Acute Lymphoblastic Leukemia (ALL) path

A

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

103
Q

Acute Lymphoblastic Leukemia (ALL) RF

A

young age
down syndrome
radiation exposure
alkylating chemotherapy

104
Q

Acute Lymphoblastic Leukemia (ALL) comp

A

intracranial hemorrhage

105
Q

Acute Lymphoblastic Leukemia (ALL) clinical

A

Fever, fatigue, SOB, pallor, bruising, petechiae, epistaxis, Bone pain, Hepatosplenomegaly, lymphadenopathy, easy bleeding, inc infx, thymus enlargement

106
Q

Acute Myeloblastic Leukemia (AML)

def

A

uncontrolled proliferation of myeloblasts, cancer

107
Q

Acute Myeloblastic Leukemia (AML) cause

A

chromosomal translocations (15, 17), myelodysplastic syndrome

108
Q

Acute Myeloblastic Leukemia (AML) path

A

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

109
Q

Acute Myeloblastic Leukemia (AML) RF

A

down syndrome
radiation
alkylating chemotherapy

110
Q

Acute Myeloblastic Leukemia (AML) comp

A

DIC

111
Q

Acute Myeloblastic Leukemia (AML) clinical

A

easy bleeding, inc infx, Fever, fatigue, SOB, pallor, bruising, petechiae, epistaxis, Bone pain, swelling of gums

112
Q

Chronic Myelogenous Leukemia (CML) def

A

cancer rapid proliferation of mature granulocytes/precursors

113
Q

Chronic Myelogenous Leukemia cause

A

Philadelphia chromosome t(9,22) BCR-ABL gene
trisomy of chromosome
doubling of Philadelphia chromosome

114
Q

Chronic Myelogenous Leukemia path

A

mutation -> tyrosine kinase is one -> rapid division of myeloid cells -> spill into blood -> liver spleen cause to swell

115
Q

Chronic Myelogenous Leukemia RF

A

adult age, radiation, benzene

116
Q

Chronic Myelogenous Leukemia comp

A

Recurrent infections, bleeding

117
Q

Chronic Myelogenous Leukemia clinical

A

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

118
Q

Chronic Lymphocytic Leukemia def

A

cancer, proliferation of mature, functionally abnormal B lymphocytes in bone marrow and don’t die

119
Q

Chronic Lymphocytic Leukemia path

A

mutation -> interfere w/ B cell receptors -> activate tyrosine kinase (bruton’s tyrosine kinase and other) -> prevent maturation and slow death - move to lymph nodes

120
Q

Chronic Lymphocytic Leukemia clinical

A

fatigue, SOB, pallor, bruising, petechiae, epistaxis, fever, pneumonia, sepsis, lymphadenopathy

121
Q

Burkitt’s Lymphoma def

A

B lymphocyte tumor

122
Q

Burkitt’s Lymphoma cause

A

chromosomal translocation t(8,14)

123
Q

Burkitt’s Lymphoma path

A

translocation -> Myc gene moved adjacent to IgH promoter sequence -> upregulation of Myc gene -> Myc gene simulates cell growth, metabolism -> increased cell division

124
Q

Burkitt’s Lymphoma RF

A

EBV infection, Africa

125
Q

Burkitt’s Lymphoma clinical

A

“Starry sky” appearance

126
Q

Burkitt’s Lymphoma clinical

A

“Starry sky” appearance (b-cells w/ no cytoplasm and tingible-body macrophages w/ dead neoplastic cells)
extranodal involvement at jaw (Africa) or ileocecal junction

127
Q

Subtypes of Classical Hodgkin Lymphoma

A

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

128
Q

Hodgkin Lymphoma cause

A

mutation in DNA

129
Q

Hodgkin Lymphoma path

A

mutation -> cell growth and division

130
Q

Hodgkin Lymphoma RF

A

20, 60s< EBV

131
Q

Hodgkin Lymphoma comp

A

second cancer

132
Q

Hodgkin Lymphoma clinical

A

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)

133
Q

Non-Hodgkin Lymphoma def

A

cancer of the B or T cells

134
Q

Non-Hodgkin Lymphoma cause

A

chromosomal translocation (14, 18) BCL2 gene, BCL-6 and BCL-2 mutation, Human T-Lymphotropic Virus, chromosomal translocation (11, 14) BCL1 gene

135
Q

Non-Hodgkin Lymphoma path

A

mutations -> uncontrolled cell division

136
Q

Non-Hodgkin Lymphoma RF

A

old age, smoking, FH,

137
Q

Non-Hodgkin Lymphoma comp

A

metastases, respiratory problems

138
Q

Non-Hodgkin Lymphoma clinical

A

swollen lymph nodes that are painless, rubbery, non-erythematous, nontender in bone marrow, GI tract, spinal cord, fever, weight loss night sweats

139
Q

Mantel cell Lymphoma RF

A

male

140
Q

Marginal Zone Lymphoma RF

A

older people, H. pylori, hepatitis C

141
Q

Follicular Lymphoma clinical

A

waxing/waning lymphadenopathy

142
Q

Diffuse Large B-cell lymphoma def

A

b cell lymphoma, aggressive growth of b cells, most common in adults

143
Q

Diffuse Large B-cell lymphoma cause

A

BCL-6 and BCL-2 mutation

144
Q

Mantel cell Lymphoma cause

A

chromosomal translocation (11, 14) BCL1 gene

145
Q

Adult T-cell Lymphoma def

A

proliferation of T cell

146
Q

Adult T-cell Lymphoma cause

A

Human T-Lymphotropic Virus

147
Q

Adult T-cell Lymphoma path

A

Human T-Lymphotropic Virus RNA -> DNA -> incorporates into T cell DNA -> cancer

148
Q

Adult T-cell Lymphoma clinical

A

severe hypercalcemia, bone lesions

149
Q

Mycosis Fungoides clinical

A

patch or plaque like lesions that look like fungal infection, Pautrier micro abscesses in the epidermis

150
Q

Lymphoplasmacytic Lymphoma

A

bone marrow, lymph nodes, spleen, Waldenstrom macroglobulinemia

151
Q

Adult T-cell Lymphoma cause

A

Human T-Lymphotropic Virus

152
Q

Adult T-cell Lymphoma clinical

A

severe hypercalcemia, bone lesions

153
Q

Mycosis Fungoides clinical

A

patch or plaque like lesions that look like fungal infection, Pautrier micro abscesses in the epidermis, erythroderma

154
Q

Subtypes of Non-Hodgkin Lymphoma B cell

A
Lymphoplasmacytic Lymphoma
Marginal Zone Lymphoma
Mantel cell Lymphoma
Diffuse Large B-cell lymphoma
Follicular Lymphoma
155
Q

Subtypes of Non-Hodgkin Lymphoma T cell

A

Mycosis Fungoides

Adult T-cell Lymphoma

156
Q

Multiple Myeloma def

A

cancer of plasms cells in bone marrow

157
Q

Multiple Myeloma cause

A

t(14, 11), t( 14,6), deletion of gene TP53 tumor suppressor on chromosome 17

158
Q

Multiple Myeloma RF

A

alcohol consumption, obesity, radiation, FH

159
Q

Multiple Myeloma comp

A

amyloidosis, renal failure, death, UTIs, pneumonia, hyper-viscosity syndrome

160
Q

Multiple Myeloma path

A

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

161
Q

Multiple Myeloma clinical

A

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

162
Q

Babesiosis def

A

infection of RBC by Babesia microti, ducani, or divergems

163
Q

Babesiosis cause

A

Ixodes scapularis tick, contaminated blood transfusion

164
Q

Babesiosis def

A

infection of RBC by Babesia microti, ducani, or divergems

165
Q

Babesiosis RF

A

endemic area, May-September, blood transfusions, >50, male, asplenia, malignancy, HIV/AIDS, immunosuppressive drugs, coinfection w/ Borrelia and/or Anaplasma, premature birth

166
Q

Babesiosis comp

A

CHF, noncardiac pulmonary edema, acute respiratory distress syndrome, splenic infarct, splenic rupture, septic shock, MI, disseminated intravascular coagulation, death

167
Q

Babesiosis clinical

A

asymptomatic, fatigue, fever, chills, headache, myalgia, arthralgia, anorexia, N, cough, hypotension, poor prefusion, pulmonary edema, acute renal failure, disseminated intravascular coagulation

168
Q

Babesiosis clinical

A

asymptomatic, fatigue, fever, chills, swears, headache, myalgia, arthralgia, anorexia, N, cough, hypotension, poor prefusion, pulmonary edema, acute renal failure, disseminated intravascular coagulation
maltese cross

169
Q

Plasmodium species (Malaria) def

A

single cell parasites that get spread by mosquitoes

170
Q

Plasmodium species (Malaria) cause

A

P. falciparum, P. vivax, P. malariae, P. ovale, P. knowlesi

171
Q

Plasmodium species (Malaria) cause

A

P. falciparum (few days), P. vivax, P. malariae (few weeks), P. ovale, P. knowlesi

172
Q

Plasmodium species (Malaria) path

A

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

173
Q

Plasmodium species (Malaria) clinical

A

paroxysm of fevers P. falciparum (variable), P. vivax (48 h), P. malariae (72), P. ovale (48), P. knowlesi (24 h)

174
Q

Plasmodium species (Malaria) comp

A

death, organ failure, cerebral malaria (altered mental status, seizure, coma), diarrhea, jaundice, vomiting, liver failure

175
Q

Plasmodium species (Malaria) clinical

A

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

176
Q

Schistosomiasis def

A

parasitic flatworms that cause damage in the mesenteries of the bladder

177
Q

Schistosomiasis cause

A

Schistosoma haematobium, S. japonicum, and S. mansoni

178
Q

Schistosomiasis path

A

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

179
Q

Schistosomiasis RF

A

male, rural areas, contact w/ fresh water bodies in endemic areas

180
Q

Schistosomiasis comp

A

bacteremia, infertility, intestinal obstruction, nephrotic syndrome, renal failure, cardiomegaly, acute myelopathy

181
Q

Schistosomiasis clinical

A

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

182
Q

Plasma cell Microscopic Anatomy

A

clock face chromatin distribution and eccentric nucleus,

183
Q

Plasma cell Origins

A

spleen and lymph node

184
Q

Plasma cell Maturation

A

bone marrow

185
Q

Plasma cell function

A

large amounts of antibody specific to particular antigens

186
Q

Plasma cell regulation

A

transcription factors

187
Q

Plasma cell synthesis

A

antigen-activated B in spleen and lymph node -> plasmablast -> plasma cells

188
Q

Plasma cell degradation

A

2-3 days

189
Q

How does hepcidin effect iron levels in body?

A

inhibits ferroportin-1

190
Q
A