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Systems Path 2 Test 1 > Chapter 11 > Flashcards

Chapter 11 Flashcards

1
Q

DIC

A

disseminating intravascular coagulation

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2
Q

what is thrombocytopenia?

A

reduction in platelets

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3
Q

where does hematopoiesis? Adults? Children?

A

A. Pelvis, cranium, vertebral bodies, sternum, ribs Kids: Marrow of loong bones, tibia, femur. Extramedullary hematopoiesis—-spleen, liver, lymph noes, thymus

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4
Q

simply put, what will hyperplasia of RBC stem cells cause?

A

increased erythropoiesis

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5
Q

what is a reticulocyte?

A

immature RBC—1% of all RBC’s mature after 1 day of circulation

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6
Q

reticulocytopenia……

A

decreased reticulocytes—- less than 0.5% = marrow failure

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7
Q

prevalence of anemia in U.S.?

A

4% of men and 8% of women

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8
Q

causes of anemia

A

blood loss, inc RBC destructionm, dec RBC production, malaria?

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9
Q

anemia causes tissue hypoxia, how does kid respond?

A

kidneys increase erythropoietin (EPO) increases eythropoiesis up to 8x

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10
Q

presentation of anemia

A

pallor,m fatigue, weakness/lassitude (cloudy) dec growth, osseous abnorm, cachexia

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11
Q

what can hemolytic anemia do?

A

Hb–> bilirubin–> jaundice/gallstone

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12
Q

types of anemia cellular color

A

Microcytic, normocytic, macrocytic hypochromic, normochromic, hyperchromic

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13
Q

hemorrhagic anemia, where do you lose the blood

A

G.I/ gynecologic pathology. Normocytic/normochromis RBCs

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14
Q

how does body respond to hemorrhagic anemia

A

inc EPO `3 days inc plasma ~7days inc reticulocytes

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15
Q

Chronic hemorrhagic anemia can cuase IDA

A

Iron deficiency anemia duh

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16
Q

how much blood loss for hypovolemic shock?

A

20%

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17
Q

Accelerated RBC destruction

A

hemolytic anemia

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18
Q

how does body adapt to hemolytic anemia?

A

Inc. erythropoiesis, reticulocytes, extramedullary hematopoiesis (liver, spleen)

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19
Q

with hemolytic anemia, does IDA appear?

A

no, the iron is recycled wuite efficiently

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20
Q

Hereditary: abnormal RBC membranes, enzymes deficiency, disordered Hb synthesis

A

Intracorpuscular defects (inside the RBC) dont for get hereditary!

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21
Q

antibodies, RBC trauma, infxns (malaria) Acquired!

A

extracorpuscular

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22
Q

Where does hemolysis occur? Inside peripheral circulation (vessels) Trauma : physical or biochemical damaged heart valve, toxins, heat

A

intravasuclar hemolysis releases hemoglobin inc Hb in urine = hemogloblinuria Inc bilkirubin = jaundice & gallstones

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23
Q

Extravascualr hemolysis happens where? What are we gonna see?

A

spleen or liver. RBC damage, antibody opsonization splenomegaly, jaundice

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24
Q

abnormal RBC membrane = inc fragility autosomal dominant mutation

A

Hereditary spherocytosis

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25
Q

Hereditary sphercytosis severity? more about RBCs

A

anemia MC is moderate decreased elasticity look at more under hereditary spherocytosis—you werent paying attendtion anyway

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26
Q

B-globin mutation, autsomal recessive Chronic hemolytic anemia

A

Sickle cell anemia sickle hemoglobin (HbS)

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27
Q

HbS who gets it

A

8% african amercans are heterozygous - Carriers translates to 3.5 mil 1 in 600 are homozygous = sickle cell anemia

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28
Q

sickling occurs where? common at areas of stasis–Bone Marrow

A

decrease in oxygen, may cause microvascular thrombi

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29
Q

here is a ton of things for sickle cell

A

thrombosis, fever, malaise, chronic low level pain priapism 4 hr erection, splenomegaly/infarction, gallstones Dec growth, osseous distortion

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30
Q

Sickle cell syndromes: lung infxns ort PE produces pulmonary stasis- red O2- thrombosis

A

Acute Chest syndrome

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31
Q

more syndromes assoc with sickle cell

A

stroke, infxn/septicemia, hypoxia induced fatty changes

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32
Q

what can happen to sine in homozygous sickle cell anemia? 10 % of sickle cell anemia

A

“lincoln log vertebra”… H-shaped vertebra

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33
Q

what ahppens in thalassemia

A

alpha or B globin genes mutated B is B mutation —chromosome 11 alpha is alpha—- chromosome 16

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34
Q

autosomal recessive, abnomral hemoglobin production microcytic, hypochromic

A

Thalassemia—beta couldnt fill the blood cell up with stuff

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35
Q

the mutation of thalassemia will cause an excess of the other globin chain, what does this do?

A

damages RBCs—hemolysis damages erythroblasts 2 alpha, 2 beta—but cant make beta—excessive alpha

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36
Q

the decreased beta globin chain synthesis of beta-thalassemia will cause what

A

unpaired alpha-globin—hemolysis death of erythroblast—decrease of erythropoiesis

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37
Q

beta thallaseemia minor affects 1 allele

A

subtle hemolysis—aysmptomatic

38
Q

beta-thalassemia major —2 alleles

A

severe hemolysis, severe anemia extramedullary hematopoiesis, splenomegaly —stunted growth —-bone marrow expansion/distortion

39
Q

beta thalassemia is know as beta thalassemia ‘trait’ affects?

A

asympt or mild, normal life span, microcytic/microchromic Tx: may not be encessary –monitoring –occasional transfusion monitor serum ferritin—iron chelation

40
Q

beta thalassemia major Dx:

A

clinical features—severe anemia, stunted growth, skeletal deform, splenomegaly, poikilocytes

41
Q

Tx of major?

A

repeated transfusion and iron chelation —dec anemia symptons & deformities —extends life into 20s…ouch =(

42
Q

more stuff of Major *hair on end”—calvarium xray “lace-like trabeculation”—deformed hands

A

eventual iron overlaod—“:hematochromatosis” lethal dilated cardiomyopathy—liver damage, failure

43
Q

alpha thalassemia, what are we gonna see

A

typically less severe than B thalassemia abnormal Hb—-HBH slight red o2 capacity ineffective erythropoiesis highly variable, 4 alpha globin genes

44
Q

G6PD defeciency—x-linked

A

needed to mkae glutathione–antioxidant protects rbcs against oxidative stress—p

45
Q

G6PD is asympt until exposed to stress

A

infections or fava beans (favism)

46
Q

acute onset of

A

fatigue,pallor, splenomegaly, back/abdominal pain, hemosiderinuria(dark urine)

47
Q

risks of G6PD

A

males. africans 10% of AAs areas of endemic malaria

48
Q

tx?

A

depends on severity identify/terminate oxidative stress blood transfusion, partial splenectomy

49
Q

paroxysmal Nocturnal hemoglobinuria (PNH)

A

dark urine upon waking

50
Q

the mutation is a PIGA mutation = deactivates complement inhibitors

A

RBCs have inc complement fixation acceleration with drop pH= sleeping complement mediated hemolysis at night

51
Q

features of PNH

A

chronic low level anemia (MC) inc risk for venous thrombosis

52
Q

Tx of PNH

A

antibodies that inhibit the MAC marrow transplant (curative)

53
Q

folate or Vit B12 deficiency— B9 cobalamin

A

required for DNA replication megaloblastic anemia

54
Q

what happens in megaloblastic anemia

A

inadequate dna rep, then production of megaloblasts macrocytes- macrocytic adn hyperchromic

55
Q

pancytopenia for megaloblastic anemia—finish you bum

A

finish

56
Q

rare, poor diet… increased metabolism –elderly, pregnant,m alcoholism, celiac

A

folate def. anemia folic acid denatured 10-15 mins after cooking

57
Q

features of folate def. anemia

A

insidious, fatigue, weakness, sore tongue —no neurologic dys

58
Q

Dx. of folate def anemia

A

macrocytes in peripheral blood, dec., serum folate, normal vit b12

59
Q

`pernicious anemia

A

vit b12 def anemia. —DNA synthesis and maintenance of neuronal tissue PNS and spinal cord

60
Q

whom might get pernicious anemia

A

strict vegans but MC is chronic malab

61
Q

what are the chronic malabs that interfere with b12

A

autoimmune gastritis = dec intrinsic factor post gastrectomy

62
Q

features of vit b123 anemia

A

fatigue, pallor, weakness, dyspnea demyelination of PNS& CNS (cord) -numbness, tingling, burning —dec proprioception & ataxia

63
Q

Dx of vit B12 deficiency

A

macrocytes dec serum vit b12 and normal folate

64
Q

tx of vit b12 def

A

injection vit b12 neurologic recovery is unlikely

65
Q

anemia of chronic disease—-think about the name

A

inflamm = dec erythropoiesis MC among hospitalized

66
Q

features of anemia of chronic disease

A

dec iron binding capacity inc iron storage in the marrow inc serum ferritin

67
Q

suppression of myeloid stem cells “bone marrow failure”: hypoceluular, inc fat pancytopenia—rbc wbc platelets

A

aplastic anemia

68
Q

greater than 1/2 of aplastic anemia is idiopathic alos what

A

myelotoxic agents: ADRs, toxins, viral infxn such as EBV, CMV, VZV worse diagnosis

69
Q

autoimmune portion of aplastic anemia

A

autoreactive T cells that attack marrow

70
Q

features of aplastic anemia

A

reticulocytopenia- weakness pallor dyspnea thrombocytopoenia = dec platelets— petechiae granulocytopenia: infxn, fever, chills splenomegaly not there

71
Q

Tx of immunosuppressive meds

A

80 % respond transfusions, marrow transplant best prognosis if less than 40 years and no Hx of transfusions

72
Q

extensive marrow infiltration

A

myelophthisic anemia

73
Q

these inflitrate the bone marrow causing myelophthisic anemia

A

mets to bone MC granulomatous disease—TB, Bridges-Good syndrome lipid storage disease—Niemann PIck Type C

74
Q

features of myelophthisic anemia

A

anemia, thrombocytopenia Dacrocytes—tear shaped RBCs

75
Q

Tx of myelophthisic anemia

A

address underlying cond. then maybe a transplant?

76
Q

Epstein BArr virus

A

HHV 4

Infectious mono

77
Q

HHV 4

A

mono

50% of exposed will become infected

20-50% will shed the virus

78
Q

Nonspecific response to infxn, red skin

A

Reactive lymphadenitis

79
Q

Bartonella henselae

A

cat scratch fever

bacterial

90% of the time its children

2weeks after scratch, lasts 2-4 months

Irregular stellate necrotizing granulomas

cervical and axillary lymph nodes

80
Q

go back to stuff before this

A

go back to stuff you missed. ya big dumb

81
Q

next topic is lymphoid neoplasms

A

problems with T cell and B cells

big prob is b cells—class switching

82
Q

lymphatic mets would go to

A

liver, spleen, marrow, peripheral circulation

83
Q

leukemia

lymphoma

A

involves marrow or blood

involve lymphatic tissues

84
Q

acute leukemias

onset is sudden and stormy

what other features with marrow suppression

A

anemia, fatigue is MC feature

neutropenia (fever), thrombocytopenia (bleeding)

marrow expansion (bone pain)

lymphadenopathy,

hepatosplenomegaly

85
Q

why marrow suppression?

A

results from transformed lymphoblasts “blasts” on marrow biopsy

86
Q

Acute lymphoblastic leukemia

A

acute tumors of lymphoblasts

arrested maturation of B cells or T cells

87
Q

types of acute lymphoblastic leukemia

A

Pre-B cell tumors (MC): marow/peripheral blood

Pre-& Cell tumors: thymus

88
Q

who gets ALL

A

children, young adults

80% of pediatric leukemias

MC dx at age 4, later with T cell age 15-20

89
Q

Chronic Lymphocytic Leukemia

A

B cells, cancer combined with immunosuppression

MC leukemia of adulthood, avg age, 60, males 2x

indolent, initially asymptomatic, gradual prog.

CLL > 4,000 lymphocytes per microL

S(small)LL < 4,000 lymphocytes per microL

90
Q

CLL what happens

A

tumor cells displace marrow: pancytopenia

anemia, fatigue, cachexia, hepatosplenomegaly generaized lymphadenopathy

Systems Path 2 Test 1 (3 decks)

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