Hematology Flashcards
1
Q
the tetramer, iron containing oxygen transport protein in rbc
A
hemoglobin Hb
2
Q
Hb S stands for
A
sickle cell variant
3
Q
hemoglobinopathies
A
blood diseases characterized by presence of abnormal hemoglobin
4
Q
reasons for abnormal hemoglobin
A
structural mutations (Hb S, Hb C
- Decreased globin production (thalassemia)
- both
5
Q
group of inherited disorders characterized by presence of hemoglobin S
A
sickle cell disease
6
Q
how do you get sickle cell disease
A
autosomal recessive
7
Q
what are the hallmarks of sickle cell disease
A
vaso-occulsive pain, hemolysis
Rbc live 10-20 days instead of 90-120
8
Q
percentage of sickle cell people with “classic” sickle cell
A
Hb SS 65%
9
Q
people with Hb SC percent
A
25
10
Q
people with HbSB+ thalassemia
A
8
11
Q
people with Hb SB 0 thalasemia
A
2
12
Q
sickle cell trait is what
A
Hb AS (heterozygous), not a disease bc more A than S.
13
Q
Sickle cell trait affects
A
8-10 percent of African america
2.5-3 million people in US
300 milllion in world
14
Q
sickle cell trait traits
A
normal life expectancy , normal labs, may have higher UTIs and dehydrate and heat illness with intense physical exertion
15
Q
where is Hb S most common
A
African, mediterranean, indian and middle eastern decent
16
Q
what parasite causes malaria
A
plasmodium
17
Q
what transmits malaria
A
anopheles mosquitos
18
Q
how does sickle cell affect parasite
A
rbc are hemolyzed quickly but it also affects parasites ability to digest the hemoglobin
19
Q
how many infants are identified with sickle cell disease each year
A
2000, 1 in 500 african american births
20
Q
why neonatal screenings
A
symptoms are rear before 2 months of age due to high Hb F. and you want to prevent sepsis
21
Q
what drug do you give infants with sickle cell
A
PCN (penicillin) prophylaxis
22
Q
why do you give the sickle cell infants PCN prophylaxis
A
prevents pneumoccocal sepsis in chidren accrodin gto PROPS
23
Q
stop giving PCN prophylaxis to sickle cell ids if
A
after 5 years of age no splenectormy, non history of pneumoccocal sepsis and are up to date on immunizations. otherwise continue forever
24
Q
what dosage should 2 mo to 3 years old get of PCN prophylaxis
A
125 mg PO BID
25
what dosage should over 3 years olds with sickle cell get
250 mg
26
what is the life expectancy of SCD
45-50 yrs
27
what immunizations do SCD need
flu, Pneumovax23 and MEnactra- and routine ones
28
what is the 1 cause of ED visits and hospitalizations in pts. with SCD
pain
29
what types of pain do SCD wxperience
vaso-occlusive pain in back, chest, extremities, neuropathic pain(infarction or iron overload), dactylics (swelling of hands and feet)
30
Pain management of SCD
1. hydration
2. heat.
3. NSAIDS
4. Opiods (give stool softeners with)
31
physiologic response to opiods resulting in decreased duration of medication action
tolerance
32
tolerance resulting in physical symptoms of withdrawal with discontinuation of medcine
phsyiological dependence
33
psychologic dependence with continued use despite adverse consequences
addiction
34
characteristics of addiction secondary to inadequate treatment
pseduoaddiction
35
what is an EMERGENCY with SCD pts.
fever of 101.3 /38.5
36
labs to order if sickle cell has fever
CBC with retic
2. Urine analysis
3. BLood and urine
4. CXR,
5. Lumbar puncture if toxic
37
fever treatment for sickle cell with fever
1. empiric antibiotics (ceftrizxone, zxithromycin, vanomycin)
2. antipytetics (reduce fever)
3. fluids
4. admit to hospital
38
what is the most common cause of death in sickle cell people? and the 2nd most common cause of hospitilization
Acute chest syndrome
39
chest xray pt if any one of these four
1. have lower respiratory symptoms
2. fever
3. chronic pain
4. hypoxemia (low O2 concentration in blood)
40
acute chest syndrome may come after
infection, infarction or emoblization
41
children have a ___ incidence but --- mortality from acute chest syndrome and more than __ percent of SCD have had one in life
higher, lower, 50
42
when a large number of red blood cells become trapped in the spleen
splenic sequestration
43
what its he most common cause of acute, severe anemia
splenic sequestration
44
signs of splenic sequestration
2g/dL drop from baseline Hb
2. decrease platelet
3. increase reticulatocyte
45
when is the peak incidence for splenic sequestration and how often will it occur
6 mo to 3 yrs. in 50 %
46
what are outward signs of splenic sequestration
fatigue, pallor, lethargy, acute, tender spleen
47
how do you correct spelenic sequestration
IVF to correct hypovolemia (low number of Rbc)
2. PRCB tranfusion (packed red blood cells)
3. splenectomy sometimes
48
what happens after prbc transfusion in splenic sequestration
splenic release phenomenon
49
stroke and CNS disease are caused by what
decreased O2 supply to brain
50
in case of stroke what is protocol
imaging- CT or MRI but do NOT delay treatment for imaging.
51
stroke/CNS disease Tx
1. hydration
2. PRBC transfusion (exchange preferred)
3. supportive care (maintain BP and glycemia)
52
what is primary prevention for stroke/cns disease
transcranial doppler- ages 2-16 years.
53
how does trasncranial dopler work-
low frequency doppler ultrasound using 2MHz probe. measures velocity of cerebral blood flow in circle of willis. high velocity blood flow puts you at high risk. this test is cheap and painless
54
what is secondary prevention in stroke and CNS
chronic transfusion (3-4 weeks.
55
what is the major complication of chronic transfusions of SCD pts?
iron overload
56
how is iron overload fixed
chelation therapy but its expensive and hard to deal with. you could do anaitplatlent agents or coumadin but you have to run them in IV for 12 hous
57
Aplastic crisis is caused by what
Parvovirus B 19. it also causes fith disease. toxic to erythroid precursors
58
s/s of aplastic crisic
fatigue, fever, URI, hemolytic anemia, rash is absent1!!!
59
what is the lab you would run and the results for aplastic crisis
reticulaoctyes low below 10, 000
60
what other medical complications occur with sickle cell
1. funcitonal asplenia
2. pulmonary HTN
.3 reinopathy
4. AVN
5. leg ulcer
6. Priapism
7. growth delay
61
what its th treatment options for SCD
1. Hydroxyurea
2. chronic transfusions
3. bone marrow trasnplant
62
what are the indications for using Hydroxyurea on sickle cell pts
1. recurrent vaso onculsive pain
2. Acute chest syndrome (esp. if complicated or recurrent)
3. chronic hypoxemia (low O2)
4. really low HB 20, 000
9. ledvated LDH>2X ULN
63
what is the only way to cure sickle cell
bone marrow transplant
64
what are the potential complications of bone marrow trasnplant
```
Infection
Graft-versus-host disease (GVHD)
Graft failure
Veno-occlusive disease (VOD)
Malnutrition
Infertility
Social & emotional concerns
```
65
what percent surival when matched with related donor in bone marrow translplant
85
66
group of inherited hemolytic anemias resulting in abnormal hemoglobin syntesis
thalassemia
67
thalassemias are gotten how
autosomal recessive
68
where thalasemia is alpha or beta depends on
which gene is affecting and resulting hemoglobin
69
what is microytosis
when red blood cells are unusually small
70
"microcytosis out of proportion to degree of anemia"
thalassemias
71
why are rbc so small in thalassemsia
there isn't enough Hb A to fill them up
72
where is alpha thalasemmia found
sub-saharan arica, southesast asia, and middle east
73
where is beta thalasemai found
mediteranean (greece turkey italy)
74
what are thalassemia symptoms
1. varying degrees of anemia
2. growth delay
3. bone marrow expansion (abnormal facies)- chipmunk faces
4. splenomegaly
5. signs of hemolysis (jaundice, icterus
75
treatment for thalaseemias
1. varies depending on presentaiton
| 2. chronic transfusion and chelation therapy in sever thalaseemia
76
all forms of beta thal carry risk of what
iron overload even without trasnfussions
77
alpha thal
has Hb Barts
78
failure of organ/tissue (bone marrow) to function normally
aplastic anemia
79
bone marrow fails to produce cells in
aplastic anemia
80
panyctopenia
all cell lilnes down (RBC< WBC< platlets
81
characteristics or aplastic anemia
1. aplasia
2. pancytopienia
3. hypo cellular bone marrow
normally acquired
82
leukopenia
low wbc
83
thromobocytopenia
something wrong with platelets
84
epidemiology of aplastic anemia
2 in a milion in US each years. everyone can get it
85
causes of aplastic anemia
1. idiopathic (50%)
2. infection
3. autoimmune
4. drugs/toxins/radiation
86
s/s of aplastic anemia
1. anemia (fatigue, pallor, tachycardia)
2. leuokopenia: infection
3. thrombocytopenia: petechiae, bruising, hemorrhage
87
What labs would you run for aplastic anemia
most important : CBC with retic (retic will be same)
2. bone marrow biopsy
3. AB testing
88
what is the aplastic anemia treatment
1. immunosuppression
2. blood transfusion
3. stem cell transplate
89
what is the survival rate for aplastic anemia
5 year is 70 percent with treatments
90
a group of acquired hematologic disorders characterized by cytogenetic (chromosomes) and morphologic changes in the myeloid, erythrooid and/or megakaryocytic lines
myelodysplastic syndromes
91
myelodysplastic syndromes leads to __ and often terminated in
1. progressive bone marrow failure
| 2. acute myeloid leukemia
92
who normally has myelodysplastic syndromes
middle aged and elderly (median age at diagnoses is 70 years
93
what causes myelodysplastic syndromes
```
de novo (random)
2. radiation or chemotherapy
```
94
what are the most common morphological findings for myelodysplastic syndrome
1. presence of progressive cytopenias despite cellular bone marrows (cells get taken out before make it to blood bc they are messed up)
2. dyspoiesis : more than one line messed up
95
the more prognostically favorable categories of Myellodysplastic syndrome have what
anemia is the only cytopenia
96
more aggressive forms of Myelodysplastic sydrome
they may have pancytopenia (all cell lines) or bicytopoenia (two cell lines)
97
explain the role of apoptosis in Myelodysplastic syndrome1
in the beginning stages, apoptosis is increased killing many cytopenias. IN later stages, it is decreased allowing increased neoplastic cell survival and expansion of abnormal clone
98
Myelodystplastic syndrome blood cell measurements
1. one or more cytopenias
2. normocytic or macarocytic anemia
3. low or normal retic count
4. normal to low WBC
5. normal to low platelet
6. monocytosis (more monocytes in blood, leukemia symptom)
7. elevated MCV
7. elevated RDW (variation in size of Rbc)
99
who classifications of MDS
1. refractory cytopenias with unilineage dysplasia
2. refractory anemia with ringed dieroblasts
3. refractory cyoptenia with multilineage dysplasia
4. refractory anemia with excess blasts -1
5. refractory anemia with excess blasts-2
6. myelodysplastic syndrome - unclassified
7. MDS associated with isolated del (5q)
100
having 20 percent blasts in bone marrow means
you have leukemia
101
types of refractory cytopenias with unilineage dysplasia in Myelodysplastic syndrome
1. refractory anemia
2. refractory neurtopenia
3. trefractory thrombocytopenia
102
median survial and progression to acute myeloid leukemia for MDS with refractory anemia
66 months- 6%
103
median survival and progression to acute myeloid leukemia for MDS with Refractory anemia with ringed sideroblasts (RARS)
72 mo 1-2%
104
median survival and progression to acute myeloid leukemia for MDS RCMD (refractory cytopenia with multilineage dysplasia)
33 mo; 11%
105
median survival and progression to acute myeloid leukemia for MDS RAEB-1 (refractory anemia with excess blasts-1)
18 mo; 25%
106
median survival and progression to acute myeloid leukemia for MDS RAEB-2 (refractory anemia with excess blasts-2)
10 mo; 33%
107
median survival and progression to acute myeloid leukemia for MDS 5q-sydnrome
long survival
108
Prognostics Indicators for MDS
1. cytopenias
| 2. % blast in bone marrow
109
as an indicate for mds what is bad as far as cytopenias
hgb <100, 000/micronleter
110
what percentage of blasts in bone marrow gives you a good, intermediate, and bad survival chabe,
good is less that 5%
intermediate 5-9%
bad is more than 10%
111
what karyotypes are good prognostic indicators for MDS
normal, missing either y, 5q, or 20q
112
what karyotypes are poor prognostic indicators for MDS
complex (three or more abnormalities or chromosome 7 abnormalities
113
what is the most common leukemia
myeloproliferative diseases (counted bc blood abnormalities that can't be treated and normally kill you)
114
the problem with diagnosing leukemia is
there is no specific symptom- give everyone in ER a cbc
115
systemic symptoms of leukemia
weight loss, fever, frequent infections
116
lung problems in leukemia
easy shortness of breath
117
muscular problems in leukemia
weakness
118
bone and joint symptoms of leukemia
pain or tenderness
119
Psychological symptoms of leukemia
loss of appetite, fatuigue
120
what happens to lymph nodes and spleen and live in leukemai
sewlling- spleen and liver enlarge
121
what skin symptoms are there in leukemia
night sweats
2. easy bruising and bleeding
3. purplish patches/ peticheai
122
with chronic leukemia how can we tell what is effected
morphologically we can see what line it came from
123
treatment for hematologic malignancies are successful for cells of
either myeloid or lymphoid origin
124
myeloid include cells of
granulocytic, erythrocytic, megakaryoocytic, or monocytic origin
125
in acute disorders, the clonal defect occurs at a ____
very early stage of development before the distinct morphologic features
126
blasts can't be classified by morphology alone, what else is used
1. cytochemical stains
2. immunophenotyping (flow cytometry)
3. cytogenetics (including FISH)
4. molecular testing (PCR)
127
What is a definitive sign of leukemia
ANY blasts on a peripheral blood smear
128
diagnoses iof leukemia is made worse when,
there are more than 20% blasts in the bone marrow
129
what is a morphological indication that a blast is of myeloid origin
Auer rod
130
if you had a recurring cytogenetic abnormality in Acute myeloid leukemia
your did better and were less likely to relapse
131
40-90 percent of patients with acute promyelocytic leukemia (FAB M3) have
reciprocal translocation of 15 and 17. this translocation has only been seen in that.
132
what are the breaking point region on gene 17 and 15. for acute promyelocytic anemia
q22 on 15
| q12 on RARa gene on 17
133
in acute promylocytic leukemia, the gene goes to gene 17 producing the
PML-RARa fusion gene
134
what is the treatment for promyelocytic leukemia
all trans retinoid acid (ATRA) first then start chemotherapy. it is curable with this
135
how does all-trans retinoid acid work
causes cells to mature.
136
the treatment for acute prokyleocytic leukemia is the same as what
M1 and M2
137
you must treat DIC with
anticoagulant therapy (heparin) prior to chemo
138
what disease causes the gums and soft tissue to swell (gingiva, sinuses, rectal tissue)
Monocytic leukemias- gingival hyptertrophy
139
Acute lymphoblastic leukemia three types:
ALL L-1, ALL-L2, ALL-L#
140
what type of acute lymphoblastic leukemia is most common in Children b-cells
ALL-L1
141
what type of acute lymphoblastic leukemia is most common in adult b-cells
ALL0L2
142
ALL-L3 is what
burkitts leukemia/lymphoma b-cell
143
what is CALLA a marker for
Acute lymphoblastic leukemia (ALL-1)
144
what are markers for t-cell leukemisas
CD4 or *
145
most childhood ALL is ___ positive, i.e. early pre-b cell or pre-b cell
CALLA (CD10)
146
most adult ALL is
mature b cell
147
presence of a ___ is a poor prognostic indicator for ALL immunophenotypeing
Philadelphia chromosome
148
what type of leukemia is most common in adolescent males and prevents with a mediastinal mass
T-cell leukemia
149
DVT stands for
deep vein thrombosis
150
DVT may lead to
pulmonary embolism
151
defined as the tendency to form clots to easily, resulting in abnormal funciotn
thrombophilia
152
most often manifests clinically in form of venous thrombosis (DVT) or pulmonary embolism
thrombophilia
153
dissolves clots/ inhibits thrombosis
t-pa
154
Virchow's triad
Endothelial damage, hyper coagulability, stasis
155
what is the clinical presentation of acute thromboembolic disease
nonspecific- leg pain, shortness of breath, trouble walking, loss of concecousness.
156
what is something that can be the primary reason for hypercoagulability
medications like birth control
157
___ is important in hypercoagulability
inherited condiotnio do genogram
158
tachypnea and tachycardia suggest
Pulmonay embolism
159
asymmetrical swelling of limbs, especially legs suggests
dvt
160
what test best shos if a clot is forming
d-dimer shows if its breaking down to go to lungs or something dangerous
161
what is hamptons hump
if a clot is forming, it is were diaphragm is elevated on chest x ray bc lung is collapsing
162
what imaging should you use for dvt
```
Duplex Venous Ultrasound
Chest X-Ray (CXR)
Spiral Chest CT
Radionucleotide
Angiography
```
163
know the graph about positive and negative predictive valuues
k
164
if they don't have a elevated d-dimer then __ percent of the time they don't have PE
92
165
main microcytic anemias
iron deficiency, anemia of chronic disease, thalassemia, and lead poisoning
166
a disorder in which at the bone marrow no longer produces red blood cells, abc, or platelets
aplastic anemica
167
criteria for establishing diagnoses of acuter DVT
lack of vein compressibility (principle)
vein does not "wink" when gently compressed in cross section
failure to appose the walls of vein
168
what is a nomrla response to doppler flow dynamics in ultrasonography of the deep leg viens
caf compression augments doppler flow signal and confirms vein patcncy proximal and distal to doppler
169
abnormal doppler flow dynamics of ultrasonogrpahy of deep leg viens
glow blunted (less sharp) rather than augmented (greater) with calf compression
170
what is the principle imaging test for diagnosing PC
computed tomography (CT) of chest iwht intravenous contrast
171
CT are best suited for detecting
clots in main pulmonary artery
172
what is the sensitivity and specificity of CT scan looking for PE or DVT
93; 97
173
what is a second line test for diagnosing PE
Radionuclide lung scan
174
how does radio nuclide lung scans work
small particle of albumin labeled with gamma radionuclide are inject IV and trapped in pulmonary capillary bed
175
what does radionuclide lung scan detect
absence or decreased blood flow possibly due to pe
176
diagnoses of PE is unlikely in pts. with normal radionuclide lung scans but is __ percent in ones with high probability scans (two or more perfusions)
90%
177
What is the gold standard for detecting pulmonary emboli
Pulmonary angiography
178
what is pulmonary angiography
used for pts. with bad chest Ct bc invasive catheter
179
what is a definitive diagnoses of PE using pulmonary angiography
intraluminal filling defect in more than one projection
180
another name for disseminated intravascular coaggulation
consumptive coagulopathy
181
what happens in disseminated intravascular coagulation
large and microscopic thrombi cause vascular occlusion, infarction and tissue enecrosis---platelets and clotting factors gets used up and bleeding happens
182
what normally causes disseminated intravascular coagulation
shock or sepsis
183
how do you treat disseminated intravascular coagulation
figure out cause! IV fluids, plasma platelets sometimes dopamine or norepinephrine
184
Primary hypercoagulability diseases:
1 decreased antithrombotic proteins
| 2. increased prothrombotic proteins
185
increased prothrombotic proteins diseases
Activated Protein C Resistance (Factor V Leiden)
| Prothrombin Gene G20210A Mutation
186
decreased anti-thrombotic proteins
Antithrombin III Deficiency
Protein C Deficiency
Protein S Deficiency
187
Antithrombin III deficiency
antithrombin decreases clotting so this disease leads to fibrin accumulations.
188
antithrombin 3 deficiency is genetics?
autsomal dominant
189
how often does antithrobin 3 occur
1 in every 2 to 5 thousan
190
antithrombin 3 deficiency usually causes what
VTE by age 45
191
Protein C deficient works how
protein c has cofactor protein s. it prevents 5 and 8 from becoming activated
192
where is protein c made and what is it dependent on?
in liver, vitamin k also has to have protein S
193
what is protein c function
inactivate facter 5a and 8a
194
what does protein c deficiency lead to
excess intrinsic pathway
195
protein c deficiency is
autosomal dominant
196
how many mutations cause protein c deficiency
more than 160
197
how many people have disease
1 in every 2 to 5 thousand
198
what causes a worsening of protein c dificency
warfarin unless heparins also used
199
where is protein s made
liver and megakaryocytes
200
what of the protein s is active
35 to 40 percent- that part is free circulation
201
what is protein s function
turn protein c into activated protein c
202
deficiency in protein s leads to what
inability to regulat factors 5a and 8a
203
inheritance of protein s
autsomal dominant
204
what percentage of cases of VTE are caused by protein S
3 to 5
205
point mutation in gene for factor 5
FACTOR 5 LEIDEN
206
WHAT happens in factor 5 leiden
renders factor 5a incapable of being activated by APC
207
heterozygous factor 5 leiden increases risk for VTE how much? what about homozygous?~
1. 5 to 10 times
| 2. 100 times
208
what population is more likely to have factor 5 leiden
whites
209
what percentage of cases of VTE does Factor 5 leiden make up
10-63
210
what happens in prothrombin G20210A mutation
substitutes G for a nucleotide 20210 of prothrombin gene. this causes person to make to much prothrombin. this leads to to many fibrin and clots
211
who has prothrombin G20210A mutation
1-6 percent of white populatio
212
what percentage of VTE are cause by Prothrombin G201210A Mutation
3-18%
213
what are the secondary hyper coagulability diseases
1. antiphospholipid syndrome
| 2. hyperhomocyteinemia
214
what is an autoimmune disorder with circulating procoagulant antibodies
antiphospholipid syndrome
215
what is one variety of antiphospholipid syndrome
lupus anticoagulant (they didn't know it caused coagulation with discovered)
216
how does antiphospholipid syndrome work
1 .dirct platelet and complement activation
| 2. inflammatory effects on the endothelium
217
antiphospholipid syndrom is common in what kinds of conditions
rheumatological conditions
218
antiphosopholpid syndrome is found in ____ diagnosed iwht VTE
60 percent of SLE (lupus)
219
what disorder has elevated levels of homocystein that are markers for VTE risk
hyperhomocysteinemia
220
what is the mechanism of hyperhomocysteinemia
it is a mechanism of hyper coagulability assumed to be related to inflammatory changes in the endothelium, leading to both increased atherogeneis and increased tendency to form clots
221
how do you get hyperhomocyteinemia
can be inherited or aquired
222
how do you cure hyperhomocysteinemia
vitamin and nutritional therapy can normalize homocystein levels, but hasn't been shown to normalize risk of VTE
223
what hyper coagulable states are at high risk for perioperatie thrombosis
1. antithrombin deficiency
2. proein C deficiency
3. Protein S deficiency
4. antiphospholipid antibody syndrome
224
moderated risk for preoperative thrombosis
```
Factor V Leiden genetic polymorphism
Prothrombin G20210A genetic polymorphism
Hyperhomocysteinemia
Postoperative prothrombotic state
Malignancy
Immobilization
```
225
Patients diagnosed with any form of thrombophilia are most often managed with___
lifelong anticoagulation (Warfarin)
226
risk of a PE is highest when during pregnancy
3rd trimester and postpardum
227
___ women are at a high risk so are anti coagulated throughout pregnancy
Antithrombin 3
228
agency for health care research and quality says that ____ for venous thromboemboism is the single most important measure for ensuring patients safety in hospitalized pts.
Prophylaxis
229
what patients are at a higher risk for VTE
surgery, trama, malignancy (cancer and radiation), acute medical illness (ex. stroke, neuromuscular weakness)
230
what are the methods of thromboprophylaxis
mechanical and pharmacological
231
what are the mechanical methods of thromboprophylaxis
external leg compression
232
what are the pharmacolgic methods of thromboprophylaxis
Low dose unfractionated heparin
Low molecular weight heparin
Adjusted dose warfarin
Fondaparinaux
233
how does graded compression stockings work to prevent thrombosis VTE
an 18 mm Hg pressure is created at ankles and an 8 mmHG at thighs this results in a 10 mm HG pressure gradient that drives venous flow from legs
234
what is the least effective prophylactic method for VTE
gradend compression stockings (thromboembolic deterrent (TED stockings)
235
what are intermittent pneumatic compresssion
inflatable bladders that trap around leg creatins a 35 mmHg at ankles and a 20 at thicghts. you inflate at deflate at regular intervals
236
who do you use intermittent pneumatic compression on
patients with a higher risk of bleeding
237
heparin is a
indirect acting ddrug
238
how does heparin work
binds to cofactor Antithrombin 3 to inactivate 2a (thrombin), 9a, 10a, 10ia, and 12a
239
inactivation of which factor is sensitive Rn occur at heparin doses much lower than the others need
IIa (so small heparin doses inhibit thrombus formation without producing full anticoaulgaiton)
240
what is the doing regimen for low dose unfractionated heparin
5000 unites BID or TID
241
what is more potent and more uniform anticoagulant activity than UFH
low molecular weight heparin
242
what is the advantage of low molecular weight heparin
less frequent dosing, lower risk of bleeding and Hit, and no need for routine monitoring
243
what is the disadvantage of low molecular weight heparin as opposed to low dose unfractionated heparin
10 times more costly
244
dpse for moderate risk conditions for low molecular weight heparin
enoxaprin 40 mg QD
245
dose for high risk conditions for low molecular weight heparin
30 mg BID
246
what other kinds of low molecular with heparin are there
dalteparin OD dose 2500 moderate and 5000 high risk. excreted b kidney
247
how does adjusted dose warfarin work
vitamin k antagonist prevents activation of coaulation factors 2, 7, 9 and 10
248
what are the advantages of adjusted dose warfarin
Preop dose not increase bleeding tendency during surgery due to delayed onset
Can be continued after discharge if prolonged prophylaxis
249
what are the disadvantages of adjusted dose warfarin
Multiple drug interactions
Monitoring lab test
Difficulty adjusting doses due to delayed onset
250
what is the dosage of adjusted dose warfarin
initially 5-10 mg PO daily then increase or decrease based on labs by 2-3
251
what is a synthetic anticoagulant, an anti-factor Xa agent- with a predictable anticoagulant effect that doesn't require monitoring in lab
fondaparinux
252
fondaparinus is contraindicated
Severe renal impairment creatinine clearance < 30ml/hr.
| Wt. < 50 kg – marked increase in bleeding
253
what is reserved for life threatening cases with hemodynamic instability- drug for stoping to much clotting
throbolytic therapy t-PA
254
alteplase
type of t-PA .6 mg/kg over 15 minutes
255
reteplase
type of t-PA give 10 units of IV bolus and repeat in 30 min
256
when is t-Pa contracindicated
intracranial disease, recent surgery, trauama
257
what is the bleeding rate wihen using t-PA
10 percent, and 1-3 risk of intracranial hemorrhage
258
what is a mesh like filter device used to prevent VTE that can be placed in IVC
inferior vena caval filters
259
how do inferior vena cabal filters work
they trap thrombi that break loose from leg vein and prevent them from traveling to lungs
260
when should you use inferior vena cabal filters
(1) active bleeding that precludes anticoagulation
| (2) recurrent venous thrombosis despite intensive anticoagulation.
261
most clinically important andf fatal embolism occur from )) rather than__ dvt in leg
proximal; distal
262
PE occurs in __ percent of pts. with proximal DVt, while asypmomatic thrombosis of leg vein is observed in __ percent pf [ts/ wotj {E
50,,,70
263
inadequate treatment may result in what percent risk of recurrent VTE
20 to 30
