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general medicine > Hematology > Flashcards

Hematology Flashcards

1
Q

the tetramer, iron containing oxygen transport protein in rbc

A

hemoglobin Hb

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2
Q

Hb S stands for

A

sickle cell variant

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3
Q

hemoglobinopathies

A

blood diseases characterized by presence of abnormal hemoglobin

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4
Q

reasons for abnormal hemoglobin

A

structural mutations (Hb S, Hb C

  1. Decreased globin production (thalassemia)
  2. both
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5
Q

group of inherited disorders characterized by presence of hemoglobin S

A

sickle cell disease

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6
Q

how do you get sickle cell disease

A

autosomal recessive

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7
Q

what are the hallmarks of sickle cell disease

A

vaso-occulsive pain, hemolysis

Rbc live 10-20 days instead of 90-120

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8
Q

percentage of sickle cell people with “classic” sickle cell

A

Hb SS 65%

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9
Q

people with Hb SC percent

A

25

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10
Q

people with HbSB+ thalassemia

A

8

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11
Q

people with Hb SB 0 thalasemia

A

2

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12
Q

sickle cell trait is what

A

Hb AS (heterozygous), not a disease bc more A than S.

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13
Q

Sickle cell trait affects

A

8-10 percent of African america
2.5-3 million people in US
300 milllion in world

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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

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15
Q

where is Hb S most common

A

African, mediterranean, indian and middle eastern decent

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16
Q

what parasite causes malaria

A

plasmodium

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17
Q

what transmits malaria

A

anopheles mosquitos

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18
Q

how does sickle cell affect parasite

A

rbc are hemolyzed quickly but it also affects parasites ability to digest the hemoglobin

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19
Q

how many infants are identified with sickle cell disease each year

A

2000, 1 in 500 african american births

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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

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21
Q

what drug do you give infants with sickle cell

A

PCN (penicillin) prophylaxis

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22
Q

why do you give the sickle cell infants PCN prophylaxis

A

prevents pneumoccocal sepsis in chidren accrodin gto PROPS

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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

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24
Q

what dosage should 2 mo to 3 years old get of PCN prophylaxis

A

125 mg PO BID

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25
Q

what dosage should over 3 years olds with sickle cell get

A

250 mg

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26
Q

what is the life expectancy of SCD

A

45-50 yrs

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27
Q

what immunizations do SCD need

A

flu, Pneumovax23 and MEnactra- and routine ones

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28
Q

what is the 1 cause of ED visits and hospitalizations in pts. with SCD

A

pain

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29
Q

what types of pain do SCD wxperience

A

vaso-occlusive pain in back, chest, extremities, neuropathic pain(infarction or iron overload), dactylics (swelling of hands and feet)

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30
Q

Pain management of SCD

A
  1. hydration
  2. heat.
  3. NSAIDS
  4. Opiods (give stool softeners with)
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31
Q

physiologic response to opiods resulting in decreased duration of medication action

A

tolerance

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32
Q

tolerance resulting in physical symptoms of withdrawal with discontinuation of medcine

A

phsyiological dependence

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33
Q

psychologic dependence with continued use despite adverse consequences

A

addiction

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34
Q

characteristics of addiction secondary to inadequate treatment

A

pseduoaddiction

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35
Q

what is an EMERGENCY with SCD pts.

A

fever of 101.3 /38.5

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36
Q

labs to order if sickle cell has fever

A

CBC with retic

  1. Urine analysis
  2. BLood and urine
  3. CXR,
  4. Lumbar puncture if toxic
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37
Q

fever treatment for sickle cell with fever

A
  1. empiric antibiotics (ceftrizxone, zxithromycin, vanomycin)
  2. antipytetics (reduce fever)
  3. fluids
  4. admit to hospital
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38
Q

what is the most common cause of death in sickle cell people? and the 2nd most common cause of hospitilization

A

Acute chest syndrome

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39
Q

chest xray pt if any one of these four

A
  1. have lower respiratory symptoms
  2. fever
  3. chronic pain
  4. hypoxemia (low O2 concentration in blood)
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40
Q

acute chest syndrome may come after

A

infection, infarction or emoblization

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41
Q

children have a ___ incidence but — mortality from acute chest syndrome and more than __ percent of SCD have had one in life

A

higher, lower, 50

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42
Q

when a large number of red blood cells become trapped in the spleen

A

splenic sequestration

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43
Q

what its he most common cause of acute, severe anemia

A

splenic sequestration

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44
Q

signs of splenic sequestration

A

2g/dL drop from baseline Hb

  1. decrease platelet
  2. increase reticulatocyte
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45
Q

when is the peak incidence for splenic sequestration and how often will it occur

A

6 mo to 3 yrs. in 50 %

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46
Q

what are outward signs of splenic sequestration

A

fatigue, pallor, lethargy, acute, tender spleen

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47
Q

how do you correct spelenic sequestration

A

IVF to correct hypovolemia (low number of Rbc)

  1. PRCB tranfusion (packed red blood cells)
  2. splenectomy sometimes
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48
Q

what happens after prbc transfusion in splenic sequestration

A

splenic release phenomenon

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49
Q

stroke and CNS disease are caused by what

A

decreased O2 supply to brain

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50
Q

in case of stroke what is protocol

A

imaging- CT or MRI but do NOT delay treatment for imaging.

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51
Q

stroke/CNS disease Tx

A
  1. hydration
  2. PRBC transfusion (exchange preferred)
  3. supportive care (maintain BP and glycemia)
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52
Q

what is primary prevention for stroke/cns disease

A

transcranial doppler- ages 2-16 years.

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53
Q

how does trasncranial dopler work-

A

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

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54
Q

what is secondary prevention in stroke and CNS

A

chronic transfusion (3-4 weeks.

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55
Q

what is the major complication of chronic transfusions of SCD pts?

A

iron overload

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56
Q

how is iron overload fixed

A

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

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57
Q

Aplastic crisis is caused by what

A

Parvovirus B 19. it also causes fith disease. toxic to erythroid precursors

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58
Q

s/s of aplastic crisic

A

fatigue, fever, URI, hemolytic anemia, rash is absent1!!!

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59
Q

what is the lab you would run and the results for aplastic crisis

A

reticulaoctyes low below 10, 000

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60
Q

what other medical complications occur with sickle cell

A
  1. funcitonal asplenia
  2. pulmonary HTN
    .3 reinopathy
  3. AVN
  4. leg ulcer
  5. Priapism
  6. growth delay
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61
Q

what its th treatment options for SCD

A
  1. Hydroxyurea
  2. chronic transfusions
  3. bone marrow trasnplant
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62
Q

what are the indications for using Hydroxyurea on sickle cell pts

A
  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
  5. ledvated LDH>2X ULN
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63
Q

what is the only way to cure sickle cell

A

bone marrow transplant

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64
Q

what are the potential complications of bone marrow trasnplant

A 
Infection
Graft-versus-host disease (GVHD)
Graft failure
Veno-occlusive disease (VOD)
Malnutrition
Infertility
Social & emotional concerns
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65
Q

what percent surival when matched with related donor in bone marrow translplant

A

85

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66
Q

group of inherited hemolytic anemias resulting in abnormal hemoglobin syntesis

A

thalassemia

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67
Q

thalassemias are gotten how

A

autosomal recessive

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68
Q

where thalasemia is alpha or beta depends on

A

which gene is affecting and resulting hemoglobin

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69
Q

what is microytosis

A

when red blood cells are unusually small

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70
Q

“microcytosis out of proportion to degree of anemia”

A

thalassemias

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71
Q

why are rbc so small in thalassemsia

A

there isn’t enough Hb A to fill them up

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72
Q

where is alpha thalasemmia found

A

sub-saharan arica, southesast asia, and middle east

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73
Q

where is beta thalasemai found

A

mediteranean (greece turkey italy)

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74
Q

what are thalassemia symptoms

A
  1. varying degrees of anemia
  2. growth delay
  3. bone marrow expansion (abnormal facies)- chipmunk faces
  4. splenomegaly
  5. signs of hemolysis (jaundice, icterus
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75
Q

treatment for thalaseemias

A
  1. varies depending on presentaiton

2. chronic transfusion and chelation therapy in sever thalaseemia

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76
Q

all forms of beta thal carry risk of what

A

iron overload even without trasnfussions

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77
Q

alpha thal

A

has Hb Barts

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78
Q

failure of organ/tissue (bone marrow) to function normally

A

aplastic anemia

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79
Q

bone marrow fails to produce cells in

A

aplastic anemia

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80
Q

panyctopenia

A

all cell lilnes down (RBC< WBC< platlets

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81
Q

characteristics or aplastic anemia

A
  1. aplasia
  2. pancytopienia
  3. hypo cellular bone marrow
    normally acquired
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82
Q

leukopenia

A

low wbc

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83
Q

thromobocytopenia

A

something wrong with platelets

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84
Q

epidemiology of aplastic anemia

A

2 in a milion in US each years. everyone can get it

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85
Q

causes of aplastic anemia

A
  1. idiopathic (50%)
  2. infection
  3. autoimmune
  4. drugs/toxins/radiation
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86
Q

s/s of aplastic anemia

A
  1. anemia (fatigue, pallor, tachycardia)
  2. leuokopenia: infection
  3. thrombocytopenia: petechiae, bruising, hemorrhage
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87
Q

What labs would you run for aplastic anemia

A

most important : CBC with retic (retic will be same)

  1. bone marrow biopsy
  2. AB testing
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88
Q

what is the aplastic anemia treatment

A
  1. immunosuppression
  2. blood transfusion
  3. stem cell transplate
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89
Q

what is the survival rate for aplastic anemia

A

5 year is 70 percent with treatments

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90
Q

a group of acquired hematologic disorders characterized by cytogenetic (chromosomes) and morphologic changes in the myeloid, erythrooid and/or megakaryocytic lines

A

myelodysplastic syndromes

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91
Q

myelodysplastic syndromes leads to __ and often terminated in

A
  1. progressive bone marrow failure

2. acute myeloid leukemia

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92
Q

who normally has myelodysplastic syndromes

A

middle aged and elderly (median age at diagnoses is 70 years

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93
Q

what causes myelodysplastic syndromes

A 
de novo (random)
2. radiation or chemotherapy
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94
Q

what are the most common morphological findings for myelodysplastic syndrome

A
  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
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95
Q

the more prognostically favorable categories of Myellodysplastic syndrome have what

A

anemia is the only cytopenia

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96
Q

more aggressive forms of Myelodysplastic sydrome

A

they may have pancytopenia (all cell lines) or bicytopoenia (two cell lines)

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97
Q

explain the role of apoptosis in Myelodysplastic syndrome1

A

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

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98
Q

Myelodystplastic syndrome blood cell measurements

A
  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
  8. elevated RDW (variation in size of Rbc)
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99
Q

who classifications of MDS

A
  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)
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100
Q

having 20 percent blasts in bone marrow means

A

you have leukemia

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101
Q

types of refractory cytopenias with unilineage dysplasia in Myelodysplastic syndrome

A
  1. refractory anemia
  2. refractory neurtopenia
  3. trefractory thrombocytopenia
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102
Q

median survial and progression to acute myeloid leukemia for MDS with refractory anemia

A

66 months- 6%

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103
Q

median survival and progression to acute myeloid leukemia for MDS with Refractory anemia with ringed sideroblasts (RARS)

A

72 mo 1-2%

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104
Q

median survival and progression to acute myeloid leukemia for MDS RCMD (refractory cytopenia with multilineage dysplasia)

A

33 mo; 11%

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105
Q

median survival and progression to acute myeloid leukemia for MDS RAEB-1 (refractory anemia with excess blasts-1)

A

18 mo; 25%

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106
Q

median survival and progression to acute myeloid leukemia for MDS RAEB-2 (refractory anemia with excess blasts-2)

A

10 mo; 33%

107
Q

median survival and progression to acute myeloid leukemia for MDS 5q-sydnrome

A

long survival

108
Q

Prognostics Indicators for MDS

A
  1. cytopenias

2. % blast in bone marrow

109
Q

as an indicate for mds what is bad as far as cytopenias

A

hgb <100, 000/micronleter

110
Q

what percentage of blasts in bone marrow gives you a good, intermediate, and bad survival chabe,

A

good is less that 5%
intermediate 5-9%
bad is more than 10%

111
Q

what karyotypes are good prognostic indicators for MDS

A

normal, missing either y, 5q, or 20q

112
Q

what karyotypes are poor prognostic indicators for MDS

A

complex (three or more abnormalities or chromosome 7 abnormalities

113
Q

what is the most common leukemia

A

myeloproliferative diseases (counted bc blood abnormalities that can’t be treated and normally kill you)

114
Q

the problem with diagnosing leukemia is

A

there is no specific symptom- give everyone in ER a cbc

115
Q

systemic symptoms of leukemia

A

weight loss, fever, frequent infections

116
Q

lung problems in leukemia

A

easy shortness of breath

117
Q

muscular problems in leukemia

A

weakness

118
Q

bone and joint symptoms of leukemia

A

pain or tenderness

119
Q

Psychological symptoms of leukemia

A

loss of appetite, fatuigue

120
Q

what happens to lymph nodes and spleen and live in leukemai

A

sewlling- spleen and liver enlarge

121
Q

what skin symptoms are there in leukemia

A

night sweats

  1. easy bruising and bleeding
  2. purplish patches/ peticheai
122
Q

with chronic leukemia how can we tell what is effected

A

morphologically we can see what line it came from

123
Q

treatment for hematologic malignancies are successful for cells of

A

either myeloid or lymphoid origin

124
Q

myeloid include cells of

A

granulocytic, erythrocytic, megakaryoocytic, or monocytic origin

125
Q

in acute disorders, the clonal defect occurs at a ____

A

very early stage of development before the distinct morphologic features

126
Q

blasts can’t be classified by morphology alone, what else is used

A
  1. cytochemical stains
  2. immunophenotyping (flow cytometry)
  3. cytogenetics (including FISH)
  4. molecular testing (PCR)
127
Q

What is a definitive sign of leukemia

A

ANY blasts on a peripheral blood smear

128
Q

diagnoses iof leukemia is made worse when,

A

there are more than 20% blasts in the bone marrow

129
Q

what is a morphological indication that a blast is of myeloid origin

A

Auer rod

130
Q

if you had a recurring cytogenetic abnormality in Acute myeloid leukemia

A

your did better and were less likely to relapse

131
Q

40-90 percent of patients with acute promyelocytic leukemia (FAB M3) have

A

reciprocal translocation of 15 and 17. this translocation has only been seen in that.

132
Q

what are the breaking point region on gene 17 and 15. for acute promyelocytic anemia

A

q22 on 15

q12 on RARa gene on 17

133
Q

in acute promylocytic leukemia, the gene goes to gene 17 producing the

A

PML-RARa fusion gene

134
Q

what is the treatment for promyelocytic leukemia

A

all trans retinoid acid (ATRA) first then start chemotherapy. it is curable with this

135
Q

how does all-trans retinoid acid work

A

causes cells to mature.

136
Q

the treatment for acute prokyleocytic leukemia is the same as what

A

M1 and M2

137
Q

you must treat DIC with

A

anticoagulant therapy (heparin) prior to chemo

138
Q

what disease causes the gums and soft tissue to swell (gingiva, sinuses, rectal tissue)

A

Monocytic leukemias- gingival hyptertrophy

139
Q

Acute lymphoblastic leukemia three types:

A

ALL L-1, ALL-L2, ALL-L#

140
Q

what type of acute lymphoblastic leukemia is most common in Children b-cells

A

ALL-L1

141
Q

what type of acute lymphoblastic leukemia is most common in adult b-cells

A

ALL0L2

142
Q

ALL-L3 is what

A

burkitts leukemia/lymphoma b-cell

143
Q

what is CALLA a marker for

A

Acute lymphoblastic leukemia (ALL-1)

144
Q

what are markers for t-cell leukemisas

A

CD4 or *

145
Q

most childhood ALL is ___ positive, i.e. early pre-b cell or pre-b cell

A

CALLA (CD10)

146
Q

most adult ALL is

A

mature b cell

147
Q

presence of a ___ is a poor prognostic indicator for ALL immunophenotypeing

A

Philadelphia chromosome

148
Q

what type of leukemia is most common in adolescent males and prevents with a mediastinal mass

A

T-cell leukemia

149
Q

DVT stands for

A

deep vein thrombosis

150
Q

DVT may lead to

A

pulmonary embolism

151
Q

defined as the tendency to form clots to easily, resulting in abnormal funciotn

A

thrombophilia

152
Q

most often manifests clinically in form of venous thrombosis (DVT) or pulmonary embolism

A

thrombophilia

153
Q

dissolves clots/ inhibits thrombosis

A

t-pa

154
Q

Virchow’s triad

A

Endothelial damage, hyper coagulability, stasis

155
Q

what is the clinical presentation of acute thromboembolic disease

A

nonspecific- leg pain, shortness of breath, trouble walking, loss of concecousness.

156
Q

what is something that can be the primary reason for hypercoagulability

A

medications like birth control

157
Q

___ is important in hypercoagulability

A

inherited condiotnio do genogram

158
Q

tachypnea and tachycardia suggest

A

Pulmonay embolism

159
Q

asymmetrical swelling of limbs, especially legs suggests

A

dvt

160
Q

what test best shos if a clot is forming

A

d-dimer shows if its breaking down to go to lungs or something dangerous

161
Q

what is hamptons hump

A

if a clot is forming, it is were diaphragm is elevated on chest x ray bc lung is collapsing

162
Q

what imaging should you use for dvt

A 
Duplex Venous Ultrasound 
Chest X-Ray (CXR)
Spiral Chest CT
Radionucleotide
Angiography
163
Q

know the graph about positive and negative predictive valuues

A

k

164
Q

if they don’t have a elevated d-dimer then __ percent of the time they don’t have PE

A

92

165
Q

main microcytic anemias

A

iron deficiency, anemia of chronic disease, thalassemia, and lead poisoning

166
Q

a disorder in which at the bone marrow no longer produces red blood cells, abc, or platelets

A

aplastic anemica

167
Q

criteria for establishing diagnoses of acuter DVT

A

lack of vein compressibility (principle)
vein does not “wink” when gently compressed in cross section
failure to appose the walls of vein

168
Q

what is a nomrla response to doppler flow dynamics in ultrasonography of the deep leg viens

A

caf compression augments doppler flow signal and confirms vein patcncy proximal and distal to doppler

169
Q

abnormal doppler flow dynamics of ultrasonogrpahy of deep leg viens

A

glow blunted (less sharp) rather than augmented (greater) with calf compression

170
Q

what is the principle imaging test for diagnosing PC

A

computed tomography (CT) of chest iwht intravenous contrast

171
Q

CT are best suited for detecting

A

clots in main pulmonary artery

172
Q

what is the sensitivity and specificity of CT scan looking for PE or DVT

A

93; 97

173
Q

what is a second line test for diagnosing PE

A

Radionuclide lung scan

174
Q

how does radio nuclide lung scans work

A

small particle of albumin labeled with gamma radionuclide are inject IV and trapped in pulmonary capillary bed

175
Q

what does radionuclide lung scan detect

A

absence or decreased blood flow possibly due to pe

176
Q

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)

A

90%

177
Q

What is the gold standard for detecting pulmonary emboli

A

Pulmonary angiography

178
Q

what is pulmonary angiography

A

used for pts. with bad chest Ct bc invasive catheter

179
Q

what is a definitive diagnoses of PE using pulmonary angiography

A

intraluminal filling defect in more than one projection

180
Q

another name for disseminated intravascular coaggulation

A

consumptive coagulopathy

181
Q

what happens in disseminated intravascular coagulation

A

large and microscopic thrombi cause vascular occlusion, infarction and tissue enecrosis—platelets and clotting factors gets used up and bleeding happens

182
Q

what normally causes disseminated intravascular coagulation

A

shock or sepsis

183
Q

how do you treat disseminated intravascular coagulation

A

figure out cause! IV fluids, plasma platelets sometimes dopamine or norepinephrine

184
Q

Primary hypercoagulability diseases:

A

1 decreased antithrombotic proteins

2. increased prothrombotic proteins

185
Q

increased prothrombotic proteins diseases

A

Activated Protein C Resistance (Factor V Leiden)

Prothrombin Gene G20210A Mutation

186
Q

decreased anti-thrombotic proteins

A

Antithrombin III Deficiency
Protein C Deficiency
Protein S Deficiency

187
Q

Antithrombin III deficiency

A

antithrombin decreases clotting so this disease leads to fibrin accumulations.

188
Q

antithrombin 3 deficiency is genetics?

A

autsomal dominant

189
Q

how often does antithrobin 3 occur

A

1 in every 2 to 5 thousan

190
Q

antithrombin 3 deficiency usually causes what

A

VTE by age 45

191
Q

Protein C deficient works how

A

protein c has cofactor protein s. it prevents 5 and 8 from becoming activated

192
Q

where is protein c made and what is it dependent on?

A

in liver, vitamin k also has to have protein S

193
Q

what is protein c function

A

inactivate facter 5a and 8a

194
Q

what does protein c deficiency lead to

A

excess intrinsic pathway

195
Q

protein c deficiency is

A

autosomal dominant

196
Q

how many mutations cause protein c deficiency

A

more than 160

197
Q

how many people have disease

A

1 in every 2 to 5 thousand

198
Q

what causes a worsening of protein c dificency

A

warfarin unless heparins also used

199
Q

where is protein s made

A

liver and megakaryocytes

200
Q

what of the protein s is active

A

35 to 40 percent- that part is free circulation

201
Q

what is protein s function

A

turn protein c into activated protein c

202
Q

deficiency in protein s leads to what

A

inability to regulat factors 5a and 8a

203
Q

inheritance of protein s

A

autsomal dominant

204
Q

what percentage of cases of VTE are caused by protein S

A

3 to 5

205
Q

point mutation in gene for factor 5

A

FACTOR 5 LEIDEN

206
Q

WHAT happens in factor 5 leiden

A

renders factor 5a incapable of being activated by APC

207
Q

heterozygous factor 5 leiden increases risk for VTE how much? what about homozygous?~

A
  1. 5 to 10 times

2. 100 times

208
Q

what population is more likely to have factor 5 leiden

A

whites

209
Q

what percentage of cases of VTE does Factor 5 leiden make up

A

10-63

210
Q

what happens in prothrombin G20210A mutation

A

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
Q

who has prothrombin G20210A mutation

A

1-6 percent of white populatio

212
Q

what percentage of VTE are cause by Prothrombin G201210A Mutation

A

3-18%

213
Q

what are the secondary hyper coagulability diseases

A
  1. antiphospholipid syndrome

2. hyperhomocyteinemia

214
Q

what is an autoimmune disorder with circulating procoagulant antibodies

A

antiphospholipid syndrome

215
Q

what is one variety of antiphospholipid syndrome

A

lupus anticoagulant (they didn’t know it caused coagulation with discovered)

216
Q

how does antiphospholipid syndrome work

A

1 .dirct platelet and complement activation

2. inflammatory effects on the endothelium

217
Q

antiphospholipid syndrom is common in what kinds of conditions

A

rheumatological conditions

218
Q

antiphosopholpid syndrome is found in ____ diagnosed iwht VTE

A

60 percent of SLE (lupus)

219
Q

what disorder has elevated levels of homocystein that are markers for VTE risk

A

hyperhomocysteinemia

220
Q

what is the mechanism of hyperhomocysteinemia

A

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
Q

how do you get hyperhomocyteinemia

A

can be inherited or aquired

222
Q

how do you cure hyperhomocysteinemia

A

vitamin and nutritional therapy can normalize homocystein levels, but hasn’t been shown to normalize risk of VTE

223
Q

what hyper coagulable states are at high risk for perioperatie thrombosis

A
  1. antithrombin deficiency
  2. proein C deficiency
  3. Protein S deficiency
  4. antiphospholipid antibody syndrome
224
Q

moderated risk for preoperative thrombosis

A 
Factor V Leiden genetic polymorphism
Prothrombin G20210A genetic polymorphism
Hyperhomocysteinemia
Postoperative prothrombotic state
Malignancy
Immobilization
225
Q

Patients diagnosed with any form of thrombophilia are most often managed with___

A

lifelong anticoagulation (Warfarin)

226
Q

risk of a PE is highest when during pregnancy

A

3rd trimester and postpardum

227
Q

___ women are at a high risk so are anti coagulated throughout pregnancy

A

Antithrombin 3

228
Q

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.

A

Prophylaxis

229
Q

what patients are at a higher risk for VTE

A

surgery, trama, malignancy (cancer and radiation), acute medical illness (ex. stroke, neuromuscular weakness)

230
Q

what are the methods of thromboprophylaxis

A

mechanical and pharmacological

231
Q

what are the mechanical methods of thromboprophylaxis

A

external leg compression

232
Q

what are the pharmacolgic methods of thromboprophylaxis

A

Low dose unfractionated heparin
Low molecular weight heparin
Adjusted dose warfarin
Fondaparinaux

233
Q

how does graded compression stockings work to prevent thrombosis VTE

A

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
Q

what is the least effective prophylactic method for VTE

A

gradend compression stockings (thromboembolic deterrent (TED stockings)

235
Q

what are intermittent pneumatic compresssion

A

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
Q

who do you use intermittent pneumatic compression on

A

patients with a higher risk of bleeding

237
Q

heparin is a

A

indirect acting ddrug

238
Q

how does heparin work

A

binds to cofactor Antithrombin 3 to inactivate 2a (thrombin), 9a, 10a, 10ia, and 12a

239
Q

inactivation of which factor is sensitive Rn occur at heparin doses much lower than the others need

A

IIa (so small heparin doses inhibit thrombus formation without producing full anticoaulgaiton)

240
Q

what is the doing regimen for low dose unfractionated heparin

A

5000 unites BID or TID

241
Q

what is more potent and more uniform anticoagulant activity than UFH

A

low molecular weight heparin

242
Q

what is the advantage of low molecular weight heparin

A

less frequent dosing, lower risk of bleeding and Hit, and no need for routine monitoring

243
Q

what is the disadvantage of low molecular weight heparin as opposed to low dose unfractionated heparin

A

10 times more costly

244
Q

dpse for moderate risk conditions for low molecular weight heparin

A

enoxaprin 40 mg QD

245
Q

dose for high risk conditions for low molecular weight heparin

A

30 mg BID

246
Q

what other kinds of low molecular with heparin are there

A

dalteparin OD dose 2500 moderate and 5000 high risk. excreted b kidney

247
Q

how does adjusted dose warfarin work

A

vitamin k antagonist prevents activation of coaulation factors 2, 7, 9 and 10

248
Q

what are the advantages of adjusted dose warfarin

A

Preop dose not increase bleeding tendency during surgery due to delayed onset
Can be continued after discharge if prolonged prophylaxis

249
Q

what are the disadvantages of adjusted dose warfarin

A

Multiple drug interactions
Monitoring lab test
Difficulty adjusting doses due to delayed onset

250
Q

what is the dosage of adjusted dose warfarin

A

initially 5-10 mg PO daily then increase or decrease based on labs by 2-3

251
Q

what is a synthetic anticoagulant, an anti-factor Xa agent- with a predictable anticoagulant effect that doesn’t require monitoring in lab

A

fondaparinux

252
Q

fondaparinus is contraindicated

A

Severe renal impairment creatinine clearance < 30ml/hr.

Wt. < 50 kg – marked increase in bleeding

253
Q

what is reserved for life threatening cases with hemodynamic instability- drug for stoping to much clotting

A

throbolytic therapy t-PA

254
Q

alteplase

A

type of t-PA .6 mg/kg over 15 minutes

255
Q

reteplase

A

type of t-PA give 10 units of IV bolus and repeat in 30 min

256
Q

when is t-Pa contracindicated

A

intracranial disease, recent surgery, trauama

257
Q

what is the bleeding rate wihen using t-PA

A

10 percent, and 1-3 risk of intracranial hemorrhage

258
Q

what is a mesh like filter device used to prevent VTE that can be placed in IVC

A

inferior vena caval filters

259
Q

how do inferior vena cabal filters work

A

they trap thrombi that break loose from leg vein and prevent them from traveling to lungs

260
Q

when should you use inferior vena cabal filters

A

(1) active bleeding that precludes anticoagulation

(2) recurrent venous thrombosis despite intensive anticoagulation.

261
Q

most clinically important andf fatal embolism occur from )) rather than__ dvt in leg

A

proximal; distal

262
Q

PE occurs in __ percent of pts. with proximal DVt, while asypmomatic thrombosis of leg vein is observed in __ percent pf [ts/ wotj {E

A

50,,,70

263
Q

inadequate treatment may result in what percent risk of recurrent VTE

A

20 to 30

general medicine (1 decks)

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