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Heme/Onc Flashcards

1
Q

Hemoglobin Types

  • A
  • A2
  • F
A
  • A: 2 alpha and 2 beta chains
  • A2: 2 alpha and 2 delta
  • F: 2 alpha and 2 gamma
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2
Q

Timeline of hemoglobin erythropoesis

- sinificance

A
  • yolk sac, liver, spleen, bone marrow

- if bone marrow cant't keep up with need then liver and spleen help to make RBC

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3
Q

Blood types: antigen, antibodies

  • A
  • B
  • AB
  • O
A
  • A antigen, B antibodies
  • B antigen, A antibodies
  • A and B antigens, no antibodies
  • No antigens, A and B antigens
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4
Q

Hemolytic disease of the newborn

  • interaction
  • mechanism
  • sxs
  • tx
A
  • Rh - mother and Rh + mom
  • first pregnancy the mother is exposed to Rh + blood and forms Rh antibody, next Rh+ pregnancy the antibodies cross placenta and attack baby
  • jaundice, kernicterus, hydrops fetalis
  • anti-D IgG to Rh - mother during 3rd trimester to prevent maternal antibody formation
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5
Q

ABO hemolytic disease of the newborn

  • interaction
  • mechanism
  • sxs
  • tx
A
  • Type O mother with type A/B fetus
  • pre-existing maternal anti-A or B igG
  • mild jaundice -> can happen with 1st pregnancy
  • phototherapy or exchange transfusion
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6
Q

Hematopoesis

  • myeloid cell
  • lymphoid cell
A
  • RBC, platelets, neutrophil, basophil, eosinophil, monocyte

- Bcell, Tcell, NK cells

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7
Q

Responders to infections

  • neutrophils/ macrophages
  • CD8+ / B cells
  • eosinophils
  • basophils and mast cells
A
  • bacterial
  • viral
  • helminths
  • allergies
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8
Q

Primary hemostasis

  • function
  • steps
A
  • platelet plug
  • injury -> collagen exposed -> vWF binds to collagen -> platelt binds vWF -> platelet changes shape and releases ADP -> GPIIa/IIIb exposed -> fibrinogen binds and helps connect platelets to each other
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9
Q

Secondary hemostasis

  • function
  • extrinsic
  • intrinsic
  • classical
A
  • fibrin mesh over platelets to stabilize the platelet plug
  • 3 + 7 -> 7A + 10 -> 10a
  • 12+11 -> 11A + 9 -> 9a +8a +10 -> 10a
  • 10a+5a+2 (prothrombin) -> 2a (thrombin) +1 (fibrinogen) -> 1a (fibrin)
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10
Q

Vit K

  • factors impacted
  • what needs to happen
A
  • 2, 7, 9, 10, C and S

- vit K must be in reduced state through vit K epoxide reductase to activate the factors

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11
Q

RBC types (look like and why do they occur)

  • Spur cell
  • Dacrocyte
  • Bite
  • Burr cell
  • Elliptocyte
  • Macro-ovalocytes
  • Schistocytes
  • Spherocytes
  • Target cells
A
  • spiny cell, cholesterol dysregulation
  • teardrop, myelofibrosis
  • chunks taken out of RBC, G6PD deficiency
  • small uniform projections from RBC, end stage renal dx/ pyruvate kinase deficiency
  • hereditary elliptocytosis
  • megaloblastic anemia
  • fragmented RBC, hemolytic anemia, DIC, mechanical hemolysis
  • small spherical cells w/o central pallor, hereditary
  • small, spherical w/ central pallor, Thalassemia, asplenia
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12
Q

RBC inclusions: looks like, caused by

  • basophilic stippling
  • heinz bodies
  • howell-jolly
  • pappenheimer
A
  • aggregation of ribosomal precipitates w/ lead poisoning, myelodysplastic syndromes
  • Hb denature and precipitates, G6Pd deficiency
  • Basophilic nuclear remnant in RBC normally removed by spleen, in patients with spleen problems
  • basophilic remnants with iron caused by lead poisoning
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13
Q

Microcytic anemias (what is it, why)

  • iron def
  • alpha thal; types
  • beta thal; types, tx
  • lead poisoning
  • sideroblastic: causes
A
  • decrease in iron, malnutrition or malabsorption
  • alpha globin gene deletion -> decrease in alpha globin synthesis, Minima (aa/a- ; silent carrier)/ Minor (aa/–; mild anemia) / Hemoglobin H (a-/–; moderate anemia)/ Hemoglobin Barts (–/–; hydrops fetalis)
  • point mutation that results in decreased beta chain synthesis; minor (heterozygote -> chain underproduced, high HgbA2), major(homozygote -> chain not produced, need blood transfusions)
  • lead inhibits heme synthesis,
  • genetic: defect in ALA synthase, acquired: myelodysplastic, reversible: EtOH, vit B6 deficiency
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14
Q

Macrocytic anemia

  • folate deficiency; what does it do, labs
  • Vit B 12 deficiency; labs, causes
  • orotic aciduria; what is it, why, dx, tx
  • Diamond Black-fan: what is it
A
  • impaired DNA synthesis bc of decrease absorption or increase in excretion, elevated homocysteine
  • increase homocysteine and methylmaolic acid w/ neuro deficits; pernicious, malabsorption, pancreatic insuff
  • unable to convert orotic acid to UMP, autosomal recessive; orotic acid in urine; UMP supplementation
  • rapid onset anemia w/i 1st yr bc intrinsic deficit in erythroid precursor cells
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15
Q

Non-hemolytic, normocytic

  • anemia of chronic dx: why, labs
  • aplastic anemia: what is it, causes, dx
A
  • increase in inflammation increases hepcidin release so iron trapped in cells and shed; decreased iron but increased ferritin
  • failure or destruction of hematopoetic stem cells, fanconi/viral/ radiation, decreased reticulocytes w/ high EPO
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16
Q

Intrinsic hemolytic, normocytic

  • hereditary spherocytosis: what is it, dx
  • G6PD deficiency: what is it, RBC
  • pyruvate kinase def: what happens, occurs in
  • paroxsymal nocturnal hemoglobinuria: what is it, associated w/
  • sickle cell: caused by,
A
  • defect in proteins interacting with RBC membrane, increase in fragility w/ osmotic fragility test
  • decrease in NADPH -> decreased reduced glutathione -> increase in oxidative stress; bite cells
  • decrease in ATP -> rigid RBC -> hemolysis; hemolytic anemia in a newborn
  • complement attacks RBC, associated with aplastic anemia
  • point mutation, low O2/ high altitude/ acidosis causes sickling
17
Q

Extrinsic hemolytic, normocytic

  • AI hemolytic anemia: kinds, when are they seen, what kind of antibody
  • Microangiopathic anemia: what is it
  • Macroangiopathic anemia
A
  • warm: seen in SLE/CLL , IgG; cold: acute anemia w/ cold temp, IgM
  • RBC damaged whenpassing through obstructed/narrowed vessel
  • heart valve or stenosis causes anemia
18
Q

Acute intermittent porphyria

  • what is it
  • enzyme
  • sxs
A
  • decrease in heme synthesis
  • porphobilinogen deaminase, build up of porphinobilinogen
  • painful abdomen, port wine urine, poly neuropathy, psych disturbance, worse w/ drugs, EtOH, starvation
19
Q

Coagulation disorders

  • PT
  • PTT
A
  • extrinsic problem

- intrinsic problem

20
Q

Hemophilias

  • A: factor, genetics
  • B: factor, genetics
  • C: factor, genetics
  • sxs
  • dx
  • tx
A
  • factor VIII, x-linked
  • factor IX, x-linked
  • factor XI, AR
  • hemearthrosis, easy bruising, bleeding after trauma
  • bleeding time normal
  • desmopressin and factor VIII concentrate
21
Q

von Willebrand Dx

  • what is it
  • genetics
  • dx
  • tx
A
  • decrease in vWF -> platelts cant adhere to exposed collagen
  • auto dom
  • increase in bleeding time, and PTT (involved with VIII), no platelet aggregation with ristocetin
  • desmopressin
22
Q

Thrombotic thrombocytopenic pupura

  • what is it
  • why
  • epi
  • tx
A
  • deficiency of ADAMTS13 -> decrease degradation of multimers -> increase platelet adhesion and aggregation
  • platelets form clots (throbocytopenia) -> rip apart RBC (anemia) , AKI, fever and neuro sxs
  • females
  • plasmapharesis
23
Q

Hemolytic uremic syndrome

  • caused by
  • presentation
  • epi
  • tx
A
  • caused by shiga toxin (and shiga like)
  • thrombocytopenia, anemia, AKI, bloody diarrhea
  • children
  • plasmapharesis, steroids
24
Q

Hypercoagulable states

  • anti-thrombin def: what is it, effects
  • factor V leiden: what is it, tx
  • Protein C/S deficiency, effect
A
  • inherited deficiency of antithrombin, diminshes increase in PTT following heparin admin
  • mutant factor V that is resistant to degradation by protein C, heparin
  • decreased ability to inactivate factors 5a and 8a
25
Q

Hodgkin lymphoma

  • characterized by
  • Nodular sclerosis
  • lymph rich
  • mixed
  • lymph depleted
A
  • single group LN, reed sternberg cells
  • cells surrounded by collagen, most common
  • best prognosis
  • seen in immunocompromised
  • decrease is reactive lymph with lots of tumor cells; seen in immuncompromised
26
Q

Non-hodgkin lymphoma

  • characterized by
  • Burkitt: epi, genetics, histo, associated w/, AA
  • Diffuse large B cell: epi, genetic, prognosis
  • Follicular: epi, genetics, sxs, prognosis
  • Mantle cell: epi, genetics, prognosis
  • Marginal zone: epi, genetics, prognosis, sxs
  • Primary central nervous system: importance
  • Adult T cell: associated with, sxs
  • Mycosis fungoides: sxs, cells
A
  • multiple LN, majority are B cells
  • Burkitt: young, T(8 c-myc:14), starry sky w/ tingible bodies, EBV, endemic form w/ jaw lesions
  • Diffuse: older adults, chrom 18- BCL2, most common type, aggressive
  • Follicular: adults, T(14:18) BCL2, indolent course, waxing and waning lypnadenopathy
  • Mantle: adult male, T(11:14) cyclin D, aggressive
  • Marginal: adult, T (11:18) cyclin D and BCL 2, indolent, chronic inflammation/gastritis
  • Primary central nervous: adult, AIDS defining illness
  • Adult T: IV drug users, cutaneous lesions
  • Mycosis: adults, skin patches and plaques, characterized by atypical CD4+
27
Q

Multiple myeloma

  • what is it
  • produces
  • histo
  • presentation
A
  • malignant plasma cell, derived from one plasma cell that wouldnt stop replicating
  • IgG and IgA, Ig light chain
  • lots of plasma cells with clock face
  • bone lytic lesion/ back pain -> hyper Ca
28
Q

Acute lymphoblastic leukemia

  • epi
  • blood and marrow
  • Dx
  • mets
  • associated w/
  • translocation
A
  • children
  • lots of lymphoblasts
  • TdT + (marker of pre-T and B cells), CD10+ (pre B cell)
  • CNS, testes
  • downs
  • 12:21 -> better prognosis
29
Q

Chronic lymphoblastic leukemia

  • epi
  • sxs
  • Dx
  • richter transformation
A
  • older than 60 yrs, most common
  • asymptomatic
  • CD 20+, 23+, 5+; smudge cells
  • CLL to aggressive lymphoma
30
Q

Acute myelogenous leukemia

  • epi
  • made up of
  • micro
  • risks
  • translocation
  • tx
A
  • 65 yrs old
  • myeloblasts
  • auer rods, myeloperoxidase +
  • chemotherapy, radiation, downs
  • T 15:17
  • vit A
31
Q

Chronic myelogenous leukemia

  • epi
  • genetics
  • whats wrong
  • turn into
  • labs
  • tx
A
  • older
  • phili chrom (9:22)- BCR ABL
  • dysregulated production of mature and maturing grnaulocytes
  • can turn into AML
  • lots of PMNS w/ low leukocyte alk phos; infection will have lots of PMNs with high leukocyte alk phos
  • imatinib
32
Q

Polycythemia vera

  • what is it
  • sxs
  • dx
  • tx
A
  • increase in RBC
  • itching after hot shower; serve, burning pain and red-blue discoloration cause by blood clots in extremities
  • decrease in EPO
  • phlebotomy and hydroxy urea
33
Q

Essential thrombocytopenia

  • what is it
  • sxs
  • dx
A
  • too many platelets
  • bleeding and thrombosis
  • lots of misformed platelets and megakaryocytes
34
Q

Myelofibrosis

- what is it

A
  • fibrosis of bone marrow -> leads to dry bone marrow tap

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