Exam 1 Flashcards
(101 cards)
1
Q
granulocytes: what precursor and which cells?
A
myeloid
basophils, eosinophils, neutrophils, mast cells
2
Q
problem with AIDS patients
A
low CD4 T cell numbers, can’t fight off infections
3
Q
senescence
A
cells die of old age
4
Q
immature neutrophils are sent out when and called?
A
when reserve runs out
bands
5
Q
what do bands indicate
A
acute infection
6
Q
where does blood cell development begin fetally?
A
embryonic yolk sac
7
Q
where do adults have BM?
A
axial skeleton, proximal femur and humerus
8
Q
Where are bone marrow Bx taken from?
A
iliac crest or sternum
9
Q
diseases that stress marrow capacity
A
marrow fibrosis, myeloproliferative diseases, severe hemolytic anemia (thalassemia major)
10
Q
what will BM do in response to infection?
A
increase neutrophil production
11
Q
what will BM do in response to hemorrhage or hypoxia?
A
increase production of erythrocytes
12
Q
what will happen if BM can’t keep up with the amount of RBCs needed?
A
release premature, reticulocytes
13
Q
what is a blast?
A
precursor cell to white blood cells in the myeloid and lymphoid cell line
14
Q
eosinophil characteristics
A
parasites and allergic rxns
have pink granules and C-shaped nucleus
15
Q
basophil characteristics
A
allergic rxns (contain histamine), contain anticoagulants, extremely large granules that obscure the nucleus
16
Q
neutrophil
A
3-5 lobe nucleus, 1st responder in infections
17
Q
monocytes
A
large nucleus, large area of cytoplasm
18
Q
underproduction of mature cells
A
aplastic anemia
19
Q
overproduction of mature cells
A
myeloproliferative disorders
20
Q
failed differentiation of mature cells with production of excessive numbers of immature forms
A
myelodysplasia, acute leukemia
21
Q
what happens in acute leukemia?
A
WBC increases but they are premature and nonfunctional
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”
23
Q
define aplastic anemia
A
failure of hematopoietic stem cells to produce mature RBCs
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
25
characteristics of AA
pancytopenia and hypocellular bone marrow
26
congenital causes of AA (mechanisms)
failure of DNA repair proteins or defect in maintenance of telomere lengths
27
Acquired AA; dose related
chemotx (wipes out good and bad) antibiotics such as chloramphenicol and trimethoprimsulfamethoxale
28
idiosyncratic drugs AA
not dose related; gold, chloramphenicol, NSAIDs, cimetidine, sulfonamides, anticonvulsants, antifungals, penicillamine,
29
toxins that cause AA
benzene, insecticides
30
viral infections AA
hepatitis, E-B virus, HIV
31
immune disease AA
host vs graft, hypogammagloburinemia
32
other causes of AA
radiation, pregnancy, paroxysmal nocturnal hemoglobinuria
33
causes of toxicity to BM in AA; how do they damage?
radiation, cancer drugs, chemicals, cytotoxic chemotherapy
| damage proliferating stem cells and differentiating SCs by producing DNA damdage
34
hypothesis of cause of AA
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
35
how does AA come on?
insidiously
36
symptoms of AA with erythocytopenia
weakness, fatigue, dyspnea, palpitations
37
symptoms of AA with leukocytopenia
recurrent infections
38
symptoms of AA with thromobocytopenia
gingival bleeding, nose bleeds (epistaxis), petechiae, purpura
39
what will bone marrow bx show in AA
```
confirm hypocellularity (only 5-15%)
decreased progenitor cells, increased fat
precursor cells morphologically normal but are nonfunctional
```
40
DDx of AA
```
myelodysplastic disease (see dysplastic hematopoietic cells), (acute leukemia
see increased blasts)
```
41
AA treatment if mild
monitor
42
AA if severe and not treated
poor survival rate of 2-6 months if untreated. die from overwhelming infections, need antifungals and antivirals which have bad side effects
43
AA severe (but not severe AA) treatment
RBC/platelet transfusions
44
Severe AA reticulocyte count
>1%
45
Severe AA; neutrophil, platelet counts, bone marrow cellularity
N < 500 n./microliter (<200 if very severe), P < 20,000 p./microliter, BM cell < 5%
46
treatment of severe AA
bone marrow transplant
47
what you need to get a BM transplant
HLA compatible donor
48
after BM transplant what do you need?
immunosuppressant drugs
antithymocyte globulin (ATC)
cyclosporin (t-cell inhibitor)
49
BM transplant success in ___% of patients with a ___ year survival rate of ___%
70-80%; 5 year; 90%
50
side effects of immunosuppression therapy
anaphylaxis, serum sickness (violently ill, can be fatal)
51
what diseases are AA pts at his for?
myelodysplasia, serum sickness, paroxysmal nocturnal hemoglobinuria
52
myeloproliferative disorders
leukocytosis, thrombocytosis, erythrocytosis, splenomegaly, bone marrow hypocellularity
53
pathogenesis of myeloproliferative disorders
occurs due to failure of stem cells to respond properly to feedback mechanism, system produces more and more RBCs
54
cause of polycythemia vera
increased blood cell mass (amount) due to defect in stem cell's ability to stop producing RBCs
55
what is first identified in P.V.?
elevated Hgb and then increased RBCs
56
normal reasons for increased RBC production?
hypoxemia, anemia, hemolysis, acute blood loss
57
signs P.V
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
adverse effects of PV?
increased risk of thromboembolic diseases
cerebral, coronary, mesenteric circulation
arterial and venous thrombosis
stokes, MI
59
symptoms of PV
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
what will peripheral smear PV look like?
microcytic
61
bone marrow PV?
hypercellular
62
treatment for PV and risk factor
intermittent phlebotomy
| thrombosis or splenomegaly
63
if phlebotomy doesn't work for PV what is next? and side effect of this??
cytoreductive therapy with allopurinol
| hyperuricemia
64
other treatment for PV
```
low dose chemo (chlorambucil, busulifan)
radioactive phosphorus
cytotoxic agents
IFN-alpha
aspirin
```
65
prognosis of PV
transformation to myelofibrosis or myeloid leukemia is 5-20% over 20 yrs
66
unique about RBC sturcture
malleable to fit thru small spaces
67
most CO2 stored as? secondarily?
carbonic acid, carried unbound by hgb
| bound to globular part of hgb molecule
68
bohr effect
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
examples of diseases with abnormal hgb
sickle cell
| thalassemia
70
what is hemolytic anemia
more cells go to spleen for destruction than the BM produces
71
2 reasons for anemia
decreased production
| increased hemolysis
72
MCV
size of the RBC
73
example of microcytic anemia
Fe deficiency
74
example of macrocytic
pernicious anemia
75
MCH
how much hgb is in each RBC; determined by color
76
MCHC
avg concentration of hgb in RBCs
| % of RBC that the hgb makes up
77
hematocrit
cellular portion of the blood
78
when bleeding rapidly what occurs in the cardiovasculature
HR will go up to increase CO but with decreased BP
79
cardiac index
cardiac output per body mass
80
signs of low CI
murmur, conjunctiva, mucosa, nails are pale
| fatigue, decreased exercise tolerance, dyspnea
81
reticulocyte count in instances where blood loss is occurring
increases
82
why does reticulocyte count increase
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
reticulocyte index
reticulocyte count x (pt HCT/normal HCT)
84
what do spherocytes indicate?
immune hemolysis
85
schistocytes indicate?
microangiopathic hemolysis
86
aniocytosis?
big range in size of RBC, large RDW
87
basophilic stippling
erythrocytes have small dots at periphery
88
signs of Fe deficiency anemia
hypo chromic and microcytic, target cells, elongated
89
what is iron incorporated into?
heme
90
what does alcohol abuse cause?
enzyme inhibition in heme synthesis
91
what does lead poisoning cause?
iron deficiency because lead binds to heme instead
92
what causes thalassemia?
failure of globin synthesis
93
how does iron absorption occur?
in the proximal small intestine; Fe binds to transferrin to be incorporated into RBC; rest is stored in other places with ferritin
94
other places Fe is stored
liver, spleen, bone marrow, muscle
95
TIBC in Fe def
total iron binding capacity
| high because more spots are available
96
transferrin saturation Fe def
percentage of transferrin molecules saturated with iron
| low in Fe deficiency
97
ferritin in Fe def, chronic disease and why
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
bone marrow stores of Fe to confirm dx
Fe in BM? not Fe def
| no FE in BM? confirms Fe def
99
treatment for Fe def
oral supplementation FeSO4 or Fe gluconate
| if it doesn't work sublingual supplementation
100
side effects of Fe supplementation
diarrhea, constipation, bloating, gas,
101
issues with Fe absorption indicated by?
dark stools
