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BMS200 > wk 11, lec 3 > Flashcards

wk 11, lec 3 Flashcards

1
Q

what is the different between iron deficiency anemia and anemias of inflamamtion

A

o Similar CBC
o Different iron handling

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2
Q

causes of anemias of inflammation

A

infection (TB, HIV), autoimmune (RA, lupus), IBD, malignancies

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3
Q

what suppress erythropoeisi in anemias of inflammation

A
  • Cytokines suppress erythropoiesis
    o Decrease erythropoeitein production
    o Iron sequestration
    o Effect early myeloid progenitors
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4
Q

rheumatoid arthritis and neoplasm and bacterial infection do what cytokines in anemias of inflmmation

A
  • RA: IL-1 and IFN-y
  • Neoplasm and infection: TNF and IFN-B
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5
Q

what is suppressed in anemias of inflammation

A
  • Suppress EPO release: IL-1 and TNF-alpha
  • Suppress RBC precursors; IFNs
    o IFN release is also stimulated by TNFa and IL-1
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6
Q

how do anemias of inflammation sequester iron away from bone marroe

A

Il-1 and TNFa stimulate IL-6  increase hepcidin production  decrease iron availability for hematopoiesis

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7
Q

what is the function of hepcidin

A
  • Decrease absorption in intestines
  • Decrease transfer of iron from transferrin to hepatocytes
  • Decrease liberation of iron from reticuloendothelial system (i.e. iron that’s rescued from degraded RBCs in the spleen)
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8
Q

symptoms of anemia’s of inflammation

A
  • Symptoms of underlying dieases i.e. fatigue
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9
Q

labs of anemia’s of inflammation

A
  • Labs vary depending on causes
    o Increased iron sequestration  smaller RBCs
    o Decreased marrow production but close to normal iron availability- RBCs normocytic or mildly microcytic
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10
Q

anemia of chronic kidney disease is what type of anemai

A
  • Hypoproliferative anemia (inadequate production of RBCs)
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11
Q

Anemia of chronic kidney disease (CKD) does what to EPO and RBCs? what do the RBCs look like?

A
  • Decreased EPO and reduced RBC survival
  • RBCs are normocytic and normochromic
    o Decreased reticulocyte counts
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12
Q

how to treat Anemia of chronic kidney disease (CKD)

A

EPO (bc its decreased)

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13
Q

symptoms of Anemia of chronic kidney disease (CKD)

A
  • Symptoms: fatigue, exercise intolerance
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14
Q

which markers are lower in early iron store depletion

A

marrow iron stores, serum ferritin, TIBC

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15
Q

iron deficient erythropoises has what abnormal

A

abnormal serum iron (SI) and % transferrin saturation

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16
Q

what are some types of anemias of abnormal RBC (Hb) synthesis

A
  • Sickle cell anemia
  • Thalassemia (alpha and beta)
  • Genetic metabolic or cytoskeletal disorders
    o G-6-PD deficiency
    o Hereditary spherocytosis
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17
Q

what is the most common anemia from cytoskeletal elements defects

A

Hereditary spherocytosis

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18
Q

who is Hereditary spherocytosis most common in

A

europeans

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19
Q

type of mutation in Hereditary spherocytosis

A

nnkyrin + anion exchanger 1 (AE1) (band 3)

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20
Q

mutation in Hereditary spherocytosis

A

o Autosomal dominant mutation in ankyrin (anchors spectrin and actin to cell membrane), anion exchanger 1 (AE1) (band 3) (fluid exchange across RBC and anchors cytoskeleton)

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21
Q

mild vs severe hereditary spherocytosis

A
  • Severe: early in life, transfusions for anemia; splenomegaly, jaundice, enlarged spleen
  • Mild: later in life; gallstones, splenomegaly, jaundice
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22
Q

RBC size, effect on RDW and MCHC in hereditary spherocytosis

A
  • Normocytic anemia with increased RDW and MCHC
    o Spherocytes cant deform therefore die early
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23
Q

Hereditary Spherocytosis (HS)

A

is an inherited disorder of the red blood cells (RBCs) that leads to the production of abnormally shaped RBCs, known as spherocytes. These spherical RBCs are more prone to hemolysis (destruction) and are less flexible than normal, biconcave-shaped RBCs.

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24
Q

what is G-6-PD a source of

A
  • Source of NADPH and to reduce glutathione

(pentose phosphate pathway; protect RBC from oxidative stress)

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25
Q

what does G-6-PD deficiency protect against?

A

malaria

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26
Q

when do you get symptoms in G-6-PD deficiency

A
  • Symptoms when RBCs get oxidative stress – i.e. medications, intravascular inflammation, fava beans
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27
Q

what happened in G-6-PD deficiency

A
  • Reduced enzyme activity, reduced NADPH production, no glutathione for ROS
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28
Q

who does G-6-PD deficiency effect more

A

men because x linked

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29
Q

clinical features of G-6-PD deficiency attacks

A
  • Attacks:
    o Malaise, weak, ab/back pain, jaundice, hyperbilirubinuria
    o Anemia: reduced Hb, anisocytosis, spherocytes, bite cells
    o Elevate lactate dehydrogenase and reduce haptoglobin (iron scavenger to sequester free Hb)
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30
Q

G-6-PD deficiency is what type of anemia

A
  • Hemolytic anemia precipitated by oxidative insults to RBCs

(premature destruction of RBCs)

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31
Q

what does the Embden-meyerhof pathway (glycolysis) generate for RBCs?

A

ATP and NADH

  • Embden-meyerhof pathway (glycolysis) generates ATP
  • Generate NADH for hemoglobin to stay in reduced state
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32
Q

what does the Hexose monophosphate shunt make for RBC metabolism

A

NADPH

  • Hexose monophosphate shunt makes NADPH to reduce glutathoione (protect against oxidant stress)
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33
Q

what enzyme effects oxygens affinity for hemoglobin

A
  • 2, 3 bisphosphoglycerate levels for oxygen affinity of hemoglobin
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34
Q

what is the most deficient enzyme in - Embden-meyerhof pathway (glycolysis)

A

: glucose 6 phosphate dehydrogenase (G6PD)

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35
Q

what are thalamssemias

A
  • Mutation that reduce synthesis of adult hemoglobin – HbA
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36
Q

which hemoglobin chain is typically impacted in thalassemias

A

o Absent or reduced beta-globin chains (chromosome 11)
 Non sense mutations or effect splicing

o Less commonly absent alpha-globin (chromosome 16)

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37
Q

who do thalassemias impact the most

A

o Mediterranean, middle east, Africa, India

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38
Q

what is beta thalassemia

A
  • RBCs with reduced hemoglobin, deficient beta chain
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39
Q

how does beta thalassemias effect erythrocytes and RBC production

A
  • Abnormal erythrocyte shape (get phagocytosed)
    o Poor RBC production (ineffective erythropoiesis) and increased RBC destruction (hemolysis)
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40
Q

what other systems are effected by beta thalassemia

A

liver, spleen, heart, bony marrow

  • Bony abnormalities to keep up with RBC production
  • extramedullary hematopoiesis in spleen and liver (enlarged)
  • blood transfusion and increased iron absorption cause iron overload (damage heart and liver)
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41
Q

how can you get secondary hemochromatosis in beta thalasemia

A

transfusion and increased iron absorption cause iron overload (damage heart and liver)

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42
Q

clinic features in beta thalassemias major vs minor

A
  • Clinical features of beta thalassemia major
    o Present when adult hemoglobin should replace fetal hemoglobin
    o Anemia, bony deformities, hepatosplenomegaly, jaundice, stunted growth
    o Iron overload in heart and liver
    o Without transfusion- poor survival rate
  • Clinical features of beta thalamssemia minor
    o Minor anemia, asymptomatic, good prognosis
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43
Q

minor vs intermedia vs major beta thalassemias

A

minor: microcytic anemia, low MCV

intermedia: occasional transfusions

major: splenomegaly, anemia, bone deformities, need blood transfusions, splenectomy

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44
Q

alpha thalasemia is

A
  • Reduced or absent alpha chains (4 in normal)
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45
Q

alpha thalamssemia is similar to beta…

A
  • Identical clinical picture to beta-thalassemia minor if 2 alpha chains missing
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46
Q

HbH (hemoglobin h) disease of alpha thalassemias

A

3 alpha chains missing; resembles beta-thalassemia intermedia

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47
Q

hydrops fetalis of alpha thalassemias

A

4 missing alpha chains
o Hb are beta chain tetramers, poor oxygen, anemia, need transfusions, fatal

48
Q

types of alpha thalassemias

A

can have 1-4 alleles affected

49
Q

what is sickle cell disease a type of

A
  • Hemoglobinopathy
50
Q

who does sickle cell disease effect the most

A

-10% heterozygous in Africans

51
Q

what is the change in the beta chain in hemoglobin in sickle cell disease ?

A
  • Replaced glutamate with valine at codon 6 in beta-globin gene
52
Q

why are sickle cells shaped differetnly

A
  • Replaced glutamate with valine at codon 6 in beta-globin gene
    o Sickle shape from polymerization and crystal formation during deoxygenation
53
Q

heterozygous for sickle cell disease benefits

A

resistant to malaria

54
Q

what does sickle cell anemia protect against

A

o Malarial parasites decrease O2 in RBCs  sickling  remove cell and parasite in spleen
o Reduced PfEMP-1 that increases sticking and infarct

55
Q

what does sickling cause

A
  • Sickling causes micro-infarcts
    o In hypoxia, inflammation and low pH
     Prolonged transit time  occlusion in blood vessel
56
Q

type of anemia in sickle cell disease

A

hemolytic anemia

57
Q

clinical features in sickle cell disease

A

o Hemolytic anemia
o Worse in crises: hypoxia (in bones, lungs, spleen, brain, liver, penis), hypovolemia and shock
o Hypoxia impairs growth and kidney failure
o Micro-infarcts impair cognition, heart failure, spleen

58
Q

what makes sickle cell worse

A

hypoxia

59
Q

prognosis of sickle cell anemia

A

o 90% survive beyond age 20, 50% beyond age 50
o Hydroxyurea increases fetal hemoglobin and reduces sickling

60
Q

type of malaria that most common and causes most death

A
  • P. falciparum most common and causes most deaths

o Invades rapidly, not dormant, no relapses

61
Q

how do you get malaria

A
  • Female anopheles mosquitoes
  • P. falciparum
62
Q

life cycle in malaria

A
  1. Mosquito blood meal; inject human with plasmodial sporozoites via its saliva glands
  2. The parasite is carries to the liver and invades hepatic parenchymal cells and then reproduces asexually
    a. P. vivax and p. ovale can be dormant “hypnozoites” for a while
  3. Infected liver cells burst and discharge motile merozoites into blood stream
  4. Merozoites invade RBCs and become trophozoites
    a. Consumes RBC hemoglobin and occupies most of cell
    b. When RBC ruptures can infect new RBCs
  5. When become dense in blood = symptoms
    - Can transmit to another person when become sexual gametocytes and reproduce during another blood meal
    - Infection of human host is asexual though
63
Q

what does the malaria do to RBCs

A

costume RBC hemoglobin and occupy cell space

64
Q

what does malaria induce the expression of in RBCs? how does this effect blood flow?

A
  • Induce RBCs to express parasitic protein PfEMP1
    o Attaches RBCs to receptor of capillaries and veins  blocks them and interferes with blood flow (esp in brain)
65
Q

mild vs severe malaria

A
  • Mild: fever, headache, ab pain, muscle aches
  • Severe: >2% erythrocyte infestation  anemia, convulsion, hypoglycemia, jaundice, renal failure, pulmonary edema
    o Cerebral malaria: coma, obtundation, delirium
    o Retinal hemorrhages, papilledema, neck stiffness, death
    o Acidosis
66
Q

types of neoplasms of blood cells

A
  • Lymphoid neoplasms
    o Hodgkins’s lymphoma
    o Non-Hodgkin’s lymphoma (NHL)
    o Lymphocytic leukemia
  • Myeloid neoplasms
    o Acute myelogenous leukemias
    o Chronic myeloproliferative disorders
67
Q

what is leukemia

A
  • Tumors in bone marrow  bone marrow suppression, immature cells in peripheral blood smear
68
Q

what is lymphoma

A
  • In lymphatic tissue (sometimes solid organs)
  • Can invade bone marrow

can overlap in clinical presentation with leukemia ; type of cell in tumour important, not location

69
Q

what is important differentiation between leukemia and lymphoma

A

type of cell in tumour important, not location

  • Lymphoma: Involves lymphocytes (a type of white blood cell).
  • Leukemia: Involves abnormal white blood cells (can be myeloid or lymphoid).
70
Q

what is the locations of leukemia and lymphoma

A

leukemia in bone marrow

lymphoma in lymph then can go to bone marrow or solid organs

  • Lymphoma: Starts in the lymphatic system and forms solid tumors in lymph nodes or organs.
  • Leukemia: Starts in the bone marrow and primarily affects circulating blood cells, causing abnormal white blood cell proliferation.
71
Q

acute lymphoblastic leukemia/lymphoma

A
  • Lymphoblasts with condensed nuclear chromatin, small nucleoili, scant agranula cytoplasm
72
Q

acute myeloid leukemia without maturation

A
  • Myeloblasts have delicate nuclear chromatin, prominent nucleoili and fine axurophilic granules in cytoplasm
73
Q

Acute lymphoblastic leukemia/lymphoma vs Acute myeloid leukemia without maturation

A

ALL is a leukemia/lymphoma of lymphoid cells (B or T cells), while AML-WM is a leukemia of myeloid cells that is characterized by a lack of maturation.

74
Q

what type of cells do lymphoid neoplasms happen in?

A
  • B cell precursors
    o Malignancy via antibody class switching or recombination events to increase antibody affinity
75
Q

location in body of Hodgkin vs non Hodgkin lymphoma

A
  • Non-hodgkin lymphoma more widespread
  • Hodkin lymphoma more localized along lymph nodes
76
Q

lymphs in lymphomas

A

100% hodgkins and 2/3 NHL have enlarged lymphs (other 1/3 NHL is solid organ)
o Later can involve bone marrow and cause pancytopenia

77
Q

findings on blood smear in leukemia and where they can invade

A

pancytopenia (decrease blood cell size) and malignant cell in peripheral blood smear
o Can later invade lymph (enlarge), skin, CNS

78
Q

what are the main white cell malignancies

A

B cell neoplasms bc of antibody rearrangement

79
Q

causes of white cell malignancies

A
  • Chronic inflammation (lymphocytic mitosis and lymphoma)
    o Celiac, chronic gastritis
  • Viral infection
    o i.e. EBV associated with Hodgkin and NHL
    o i.e. HIV – NHL
80
Q

B cell neoplasms

which 2 enzymes

A

o enzymes (AID = activation-induced cytosine deaminase and recombinases/RAGs) create breaks in antibody genes for:

 Class switching (mostly AID)
 Hypermutation to aid antibody affinity (mostly recombinases but also AID)

81
Q

chromosomal translocation in B cell neoplasms

A

o Chromosomal translocations  decrease apoptosis, increase growth

82
Q

white cell malignancies - how is cell division increased?

A
  • Increase cell division (MYC, RTK, Ras, MAPK, PI-3K)
  • Disrupt apoptotic pathways
  • Halt normal differentiation
83
Q

acute lymphoblastic leukemia (ALL) is from what type of cells

A
  • From precursor B and T cells (85% B cell)
84
Q

acute lymphoblastic leukemia (ALL) is similar to

A
  • Similar presentation to acute myelogenous leukemia but different response to treatment
85
Q

acute lymphoblastic leukemia (ALL) involves

A

solid organs

86
Q

what is the most common childhood cancer

A

acute lymphoblastic leukemia (ALL)

87
Q

acute lymphoblastic leukemia (ALL) pathophysiology

A
  • Immature leukemic blast cells are blocked in differentiation
    o <10 mutations
    o Accumulate immature non functional blast cells:
     Crowd out normal cells and bone marrow fails
     Encourage self renewal in bone marrow
88
Q

symptoms and sings in acute lymphoblastic leukemia (ALL)

A

o Fatigue, infection (neutropenia), bleeding, bone pain, solid organs metastases (spleen, liver, testes, lymph, meninges)
o Lymphadenopathy, splenomegaly, hepatomegaly,
o CNS: cranial nerve palsy, headache, vomit

89
Q

diagnosis of Acute lymphoblastic leukemia (ALL)? what is the WBC?

A

o Blast cells in bone marrow and peripheral blood smears
o WBC count elevated or depressed
o Chromosomal abnormalities or overexpression of enzymes (hyperdiploidy)

90
Q

prognosis of Acute lymphoblastic leukemia (ALL)

A

o Kids 2-10 yrs do good with treatment bc usually B cell (older kids are bad bc T cell)

91
Q

chronić lymphocytic leukemia (CLL) is the most common leukemia in

A

adults of western world

92
Q

what cells are effected in Chronic lymphocytic leukemia (CLL)

A
  • Tumor in mature B cells, expressing CD 19, CD 20, CD 23

o Mutation in memory cells

o Depress B cell function, induce autoantibodies
 Hypogammaglobulinemia
 Deficient T-cell response

93
Q

symptoms of Chronic lymphocytic leukemia (CLL)

A

o Asymptomatic
o Usually based on elevated lymphocyte count
o Weight loss, fatigue, anorexia
o Lymphadenopathy or splenomegaly
o Susceptible to bacterial infection  die
o Hemolytic anemia and thrombocytopenia from autoantibodies

94
Q

prognosis of Chronic lymphocytic leukemia (CLL)

A

o Slow growing tumor usually

95
Q

non-hodgkins lymphoma is a cancer of what type of cells

A
  • Cancer of mature B, T, and NK cells

o 90% are B cell origin  MYC and BCL6 and BCL2

96
Q

b cell genes effected in non-hodgkins lymphoma

A

MYC and BCL6 and BCL2

97
Q

what’s more common; Hodgkin or non-hodgkin

A

non hodgkin

hodgkin is - 10% of lymphoma cases

98
Q

risks for Non- Hodgkin’s lymphoma

A
  • Risks: agriculture chemicals, EBV, HIV, immunosuppression, autoimmune, Hodgkin’s treatment, relatives with NHL
99
Q

2 subtypes of Non-Hodgkin’s lymphoma-

A

Non-Hodgkin’s lymphoma- diffuse large b-cell lymphoma

Non-Hodgkin’s lymphoma- follicular lymphoma

100
Q

most common subtype of Non-Hodgkin’s lymphoma-

A
  • Most common NHL subtype (1/3)
101
Q

age and progression in Non-Hodgkin’s lymphoma- diffuse large b-cell lymphoma

A
  • Age 64 ; rapid aggressive growth
102
Q

risks of Non-Hodgkin’s lymphoma- diffuse large b-cell lymphoma

A

family, immunodeficneiy, autoimmune (EBV), immunosuppression

103
Q

symptoms Non-Hodgkin’s lymphoma- diffuse large b-cell lymphoma

A

B symptoms (fever, night sweats, weight loss), elevated LDH

104
Q

area affected in Non-Hodgkin’s lymphoma- diffuse large b-cell lymphoma

A
  • Extranodal: Bone marrow involvement and CNS dissemination
    o Also GI, thyroid, liver, skin
105
Q

genes in Non-Hodgkin’s lymphoma- diffuse large b-cell lymphoma

A
  • Genes: BCL2, BCL6, MYC, double hit (2 of these)
106
Q

Non-Hodgkin’s lymphoma- follicular lymphoma symptoms

A
  • Painless lymphadenopathy; epitrochlear nodes and extranodal
107
Q

Non-Hodgkin’s lymphoma- follicular lymphoma imaging

A
  • Imaging: CT, PET
    o Best is follicular lymphoma international prognostic index (FLIPI)
108
Q

Hodgkins lymphoma effects

A

mature b cells

109
Q

what is effected in hodking vs non-hodgkins

A

hodgkin= mature b cells

non= B, T, or NK cells , but usually B cells

110
Q

2 types of Hodgkin’s lymphoma

A
  • 2 types: classical Hodgkin’s lymphoma (cHL) and nodular lymphocyte-predominant Hodgkin’s lymphoma (NLPHL).
    o NLPHL resembles cHL a bit but more so NHL
111
Q

virus in hodgkin lymphoma

A

EBV and HIV

112
Q

what are Reed-sternberg (HRS) cells

A
  • Reed-sternberg (HRS) cells: large cells with abundant cytoplasm and multiple nuclei
    o Diagnostic of cHL
    o Express EBV protein LMP-1
    o Express PD-1
113
Q

what lymphoma is Reed-sternberg (HRS) cells diagnostic over

A

classical Hodgkin’s lymphoma (cHL

114
Q

features of Hodgkin lymphoma

A

o Palpable, nontender lymphadenopathy (early: cervical, supraclavicular, axillary)
o B symptoms: fever, weight loss, night sweats

115
Q

labs in hodgkin lymphoma

A

o CBC with diff, ESR, hepatic and renal labs, HIV and hepatitis testing
o Imaging: PET and CT

BMS200 (43 decks)

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