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Clinical Medicine > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

granulocytes: what precursor and which cells?

A

myeloid

basophils, eosinophils, neutrophils, mast cells

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2
Q

problem with AIDS patients

A

low CD4 T cell numbers, can’t fight off infections

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3
Q

senescence

A

cells die of old age

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4
Q

immature neutrophils are sent out when and called?

A

when reserve runs out

bands

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5
Q

what do bands indicate

A

acute infection

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6
Q

where does blood cell development begin fetally?

A

embryonic yolk sac

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7
Q

where do adults have BM?

A

axial skeleton, proximal femur and humerus

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8
Q

Where are bone marrow Bx taken from?

A

iliac crest or sternum

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9
Q

diseases that stress marrow capacity

A

marrow fibrosis, myeloproliferative diseases, severe hemolytic anemia (thalassemia major)

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10
Q

what will BM do in response to infection?

A

increase neutrophil production

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11
Q

what will BM do in response to hemorrhage or hypoxia?

A

increase production of erythrocytes

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12
Q

what will happen if BM can’t keep up with the amount of RBCs needed?

A

release premature, reticulocytes

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13
Q

what is a blast?

A

precursor cell to white blood cells in the myeloid and lymphoid cell line

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14
Q

eosinophil characteristics

A

parasites and allergic rxns

have pink granules and C-shaped nucleus

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15
Q

basophil characteristics

A 
allergic rxns (contain histamine), contain anticoagulants,
extremely large granules that obscure the nucleus
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16
Q

neutrophil

A

3-5 lobe nucleus, 1st responder in infections

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17
Q

monocytes

A

large nucleus, large area of cytoplasm

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18
Q

underproduction of mature cells

A

aplastic anemia

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19
Q

overproduction of mature cells

A

myeloproliferative disorders

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20
Q

failed differentiation of mature cells with production of excessive numbers of immature forms

A

myelodysplasia, acute leukemia

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21
Q

what happens in acute leukemia?

A

WBC increases but they are premature and nonfunctional

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22
Q

an example of myeloproliferative disorder

A

COPD

  • ruddy complexion
  • O2 carrying capacity decreases making BM think that the body needs more cells
  • blood becomes “sludgy”
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23
Q

define aplastic anemia

A

failure of hematopoietic stem cells to produce mature RBCs

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24
Q

pathogenesis of aplastic anemia

A

few stem cells present (those that are there can produce little amounts of normal RBCs) other stem cells either can’t produce healthy precursor cells or just slow down and don’t work

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25
Q

characteristics of AA

A

pancytopenia and hypocellular bone marrow

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26
Q

congenital causes of AA (mechanisms)

A

failure of DNA repair proteins or defect in maintenance of telomere lengths

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27
Q

Acquired AA; dose related

A

chemotx (wipes out good and bad) antibiotics such as chloramphenicol and trimethoprimsulfamethoxale

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28
Q

idiosyncratic drugs AA

A

not dose related; gold, chloramphenicol, NSAIDs, cimetidine, sulfonamides, anticonvulsants, antifungals, penicillamine,

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29
Q

toxins that cause AA

A

benzene, insecticides

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30
Q

viral infections AA

A

hepatitis, E-B virus, HIV

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31
Q

immune disease AA

A

host vs graft, hypogammagloburinemia

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32
Q

other causes of AA

A

radiation, pregnancy, paroxysmal nocturnal hemoglobinuria

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33
Q

causes of toxicity to BM in AA; how do they damage?

A

radiation, cancer drugs, chemicals, cytotoxic chemotherapy

damage proliferating stem cells and differentiating SCs by producing DNA damdage

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34
Q

hypothesis of cause of AA

A

host lymphocytes are responsible for destroying normal hematopoiesis
suggested b/c AA can result from viral and immunological disorders
our own Ags are triggering cytotoxic T cells to destroy stem cells

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35
Q

how does AA come on?

A

insidiously

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36
Q

symptoms of AA with erythocytopenia

A

weakness, fatigue, dyspnea, palpitations

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37
Q

symptoms of AA with leukocytopenia

A

recurrent infections

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38
Q

symptoms of AA with thromobocytopenia

A

gingival bleeding, nose bleeds (epistaxis), petechiae, purpura

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39
Q

what will bone marrow bx show in AA

A 
confirm hypocellularity (only 5-15%)
decreased progenitor cells, increased fat
precursor cells morphologically normal but are nonfunctional
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40
Q

DDx of AA

A 
myelodysplastic disease (see dysplastic hematopoietic cells), (acute leukemia
see increased blasts)
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41
Q

AA treatment if mild

A

monitor

42
Q

AA if severe and not treated

A

poor survival rate of 2-6 months if untreated. die from overwhelming infections, need antifungals and antivirals which have bad side effects

43
Q

AA severe (but not severe AA) treatment

A

RBC/platelet transfusions

44
Q

Severe AA reticulocyte count

A

> 1%

45
Q

Severe AA; neutrophil, platelet counts, bone marrow cellularity

A

N < 500 n./microliter (<200 if very severe), P < 20,000 p./microliter, BM cell < 5%

46
Q

treatment of severe AA

A

bone marrow transplant

47
Q

what you need to get a BM transplant

A

HLA compatible donor

48
Q

after BM transplant what do you need?

A

immunosuppressant drugs
antithymocyte globulin (ATC)
cyclosporin (t-cell inhibitor)

49
Q

BM transplant success in ___% of patients with a ___ year survival rate of ___%

A

70-80%; 5 year; 90%

50
Q

side effects of immunosuppression therapy

A

anaphylaxis, serum sickness (violently ill, can be fatal)

51
Q

what diseases are AA pts at his for?

A

myelodysplasia, serum sickness, paroxysmal nocturnal hemoglobinuria

52
Q

myeloproliferative disorders

A

leukocytosis, thrombocytosis, erythrocytosis, splenomegaly, bone marrow hypocellularity

53
Q

pathogenesis of myeloproliferative disorders

A

occurs due to failure of stem cells to respond properly to feedback mechanism, system produces more and more RBCs

54
Q

cause of polycythemia vera

A

increased blood cell mass (amount) due to defect in stem cell’s ability to stop producing RBCs

55
Q

what is first identified in P.V.?

A

elevated Hgb and then increased RBCs

56
Q

normal reasons for increased RBC production?

A

hypoxemia, anemia, hemolysis, acute blood loss

57
Q

signs P.V

A

elevated red cell mass (sludges up blood because more cell mass, less liquid), splenomegaly (spleen is overworking)
thrombocytosis, leukocytosis, elevated leukocyte alkaline phosphatase, elevated serum B12, low serum EPO

58
Q

adverse effects of PV?

A

increased risk of thromboembolic diseases
cerebral, coronary, mesenteric circulation
arterial and venous thrombosis
stokes, MI

59
Q

symptoms of PV

A

headache, visual disturbances, mental disturbances, pruritus after bathing, CVA, TIA, MI, digital pain/emboli with paresthesia (emboli=clots, paresthesia=tingling, dusty digits)
hemorrhagic events-platelets aren’t working properly even tho increased amount
ruddy cyanosis

60
Q

what will peripheral smear PV look like?

A

microcytic

61
Q

bone marrow PV?

A

hypercellular

62
Q

treatment for PV and risk factor

A

intermittent phlebotomy

thrombosis or splenomegaly

63
Q

if phlebotomy doesn’t work for PV what is next? and side effect of this??

A

cytoreductive therapy with allopurinol

hyperuricemia

64
Q

other treatment for PV

A 
low dose chemo (chlorambucil, busulifan)
radioactive phosphorus 
cytotoxic agents
IFN-alpha 
aspirin
65
Q

prognosis of PV

A

transformation to myelofibrosis or myeloid leukemia is 5-20% over 20 yrs

66
Q

unique about RBC sturcture

A

malleable to fit thru small spaces

67
Q

most CO2 stored as? secondarily?

A

carbonic acid, carried unbound by hgb

bound to globular part of hgb molecule

68
Q

bohr effect

A

decrease in amount of oxygen associated with hgb in response to a lowered blood pH resulting from an increase in CO2 in the blood

69
Q

examples of diseases with abnormal hgb

A

sickle cell

thalassemia

70
Q

what is hemolytic anemia

A

more cells go to spleen for destruction than the BM produces

71
Q

2 reasons for anemia

A

decreased production

increased hemolysis

72
Q

MCV

A

size of the RBC

73
Q

example of microcytic anemia

A

Fe deficiency

74
Q

example of macrocytic

A

pernicious anemia

75
Q

MCH

A

how much hgb is in each RBC; determined by color

76
Q

MCHC

A

avg concentration of hgb in RBCs

% of RBC that the hgb makes up

77
Q

hematocrit

A

cellular portion of the blood

78
Q

when bleeding rapidly what occurs in the cardiovasculature

A

HR will go up to increase CO but with decreased BP

79
Q

cardiac index

A

cardiac output per body mass

80
Q

signs of low CI

A

murmur, conjunctiva, mucosa, nails are pale

fatigue, decreased exercise tolerance, dyspnea

81
Q

reticulocyte count in instances where blood loss is occurring

A

increases

82
Q

why does reticulocyte count increase

A

when RBC count decreases, stimulus sent to the kidney to release EPO to send to the BM to produce more RBCs; but RBCs can’t be made so reticulocytes are sent out

83
Q

reticulocyte index

A

reticulocyte count x (pt HCT/normal HCT)

84
Q

what do spherocytes indicate?

A

immune hemolysis

85
Q

schistocytes indicate?

A

microangiopathic hemolysis

86
Q

aniocytosis?

A

big range in size of RBC, large RDW

87
Q

basophilic stippling

A

erythrocytes have small dots at periphery

88
Q

signs of Fe deficiency anemia

A

hypo chromic and microcytic, target cells, elongated

89
Q

what is iron incorporated into?

A

heme

90
Q

what does alcohol abuse cause?

A

enzyme inhibition in heme synthesis

91
Q

what does lead poisoning cause?

A

iron deficiency because lead binds to heme instead

92
Q

what causes thalassemia?

A

failure of globin synthesis

93
Q

how does iron absorption occur?

A

in the proximal small intestine; Fe binds to transferrin to be incorporated into RBC; rest is stored in other places with ferritin

94
Q

other places Fe is stored

A

liver, spleen, bone marrow, muscle

95
Q

TIBC in Fe def

A

total iron binding capacity

high because more spots are available

96
Q

transferrin saturation Fe def

A

percentage of transferrin molecules saturated with iron

low in Fe deficiency

97
Q

ferritin in Fe def, chronic disease and why

A

low in Fe def. because not a lot of iron, so liver stops producing
high in chronic disease because liver sends it out to remove iron so that bacteria don’t use it as a food source

98
Q

bone marrow stores of Fe to confirm dx

A

Fe in BM? not Fe def

no FE in BM? confirms Fe def

99
Q

treatment for Fe def

A

oral supplementation FeSO4 or Fe gluconate

if it doesn’t work sublingual supplementation

100
Q

side effects of Fe supplementation

A

diarrhea, constipation, bloating, gas,

101
Q

issues with Fe absorption indicated by?

A

dark stools

Clinical Medicine (1 decks)

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