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exam 3 and 4 Flashcards

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1
Q

bleeding types

A

acquired or congenital
localized or general

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2
Q

severe bleeding that requires physical intervention

A

hemorrhage

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3
Q

localized bleeding - bleeding from

A

single location

ex. injury, infection, tumor

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4
Q

generalized bleeding

A

from multiple sites
-spontaneous, recurring

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5
Q

example of primary hemostasis disease

A

blood vessel defects, platelet defects

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6
Q

secondary hemostasis disease

A

single or multiple coag factor deficiencies

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7
Q

bleeding can be

A

mucocutaneous (systemic) or soft tissue (anatomic)

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8
Q

mucocutaneous

A

petechiae
purpura
ecchymoses

primary hemo symp:
bleeding gums
nose bleeds
hematemesis
menorrhagia

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9
Q

mucocutaneous hemorrhage is usually associated with

A

TCP
qualitative plt disorders
VWD
vascular disorders

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10
Q

anatomic bleeding seen in

A

acquired or congenital defects in secondary hemostasis or plasma coag factor deficiencies

-bleeding will happen right after and recurrently

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11
Q

anatomic bleeding usually is

A

internal
bleeds into joints
body cavities
muscles
CNS

getting patient history and physical exam is vital to diagnosis

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12
Q

thrombosis disorder

A

abnormalities in blood flow such as stasis
abnormalities in coag system
inappropriate formation of platelet or fibrin clots that obstruct blood vessels

-plt function
-leukocyte activation molecules
-blood vessel wall

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13
Q

predisposition to thrombosis secondary to a congenital or acquired disorder

A

thrombophilia

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14
Q

causes of thrombophilia

A

-physical, chemical or biologic events
-inappropriate and uncontrolled platelet activation
-uncontrolled blood coag system activation
-uncontrolled fibrinolysis suppression

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15
Q

screening test for hemostatic diseases

A

PFA
PT and aPTT
PLT count and CBC
mixing studies
thrombin time

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16
Q

clinical signs to look for in vascular disorders: hereditary

A

-tendency to bruise easily
-spontaneous bleeding especially from mucosal surfaces

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17
Q

hereditary hemorrhagic telangiectasia

A

-defect in blood vessels
-telangiectasias form on lips, tongue, face, and hands
-epistaxis

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18
Q

hereditary hemorrhagic telangiectasia mode of inheritance

A

autosomal dominant

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19
Q

hereditary hemorrhagic telangiectasia diagnosis

A

-lesions
-history of repeated hemorrhage
-family history

no specific therapy

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20
Q

allergic purpura (henoch-scholein purpura)

A

non-thrombocytopenic purpura characterized by allergic manifestations including skin rash and edema

seen following upper respiratory tract infection or certain food

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21
Q

henoch-scholein purpura is used when accompanied by

A

transient arthralgia
nephritis
abdominal pain
purpura lesions

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22
Q

henoch-scholein purpura seen most in what age

A

male children 3-7

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23
Q

delayed skin rash which develop into a lesion commonly found

A

feet
elbow
knees
butt
chest

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24
Q

test for henoch-scholein purpura

A

normal plt count
normal coag

last 4 weeks
-recover without treatment

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25
senile purpura
elderly male -due to lack of collagen support for small blood vessels and loss of subcu. fat and elastic fibers -dark flat blotches, resolve slowly and often leave brown stain
26
senile purpura test
normal lab test no other symptoms no treatment
27
scurvy-- vitamin C deficiency
vitamin C necessary for collagen synthesis -collagen will degrade without it and capillaries become fragile
28
most thrombocytopenias can be linked to specific
chromosomal abnormalities or specific genetic defects
29
most common cause of clinically significant bleeding
TCP- thrombocytopenia -due to plt abnormalities and bleeding into mucous membrane
30
2 categories for decreased production of plts
1- MK hypoplasia in bone marrow 2- ineffective thrombopoiesis
31
symptoms of thrombocytopenia
small vessel bleeding petechiae purpura ecchymoses
32
congenital/ inherited hypoplasia (may hegglin)
giant plt with decreased count and dohle bodies inheritance: autosomal dominant -asymptomatic -TCP 1/3
33
congenital/ inherited hypoplasia (may hegglin) bleeding time
may be prolonged
34
acquired hypoplasia
radiation, chemo, etc. interlukin-11 used to treat chemo-induced TCP can occur with aplastic anemia
35
megaloblastic anemia deficient in
b12 and folate treatment: vitamin supplements
36
hypersplenism is treated with
splenctomy -dilution by RBC transfusion or IV fluids
37
2 categories for increased plt destruction
immunologic response mechanical damage or consumption or boht
38
increased destruction: immune response immune thrombocytopenic purpura
decreased PLT count with no cause -mucosal bleeding, bruising, and petechiae
39
acute ITP
seen in children and sometimes adults after infection ages:2-5 produces antibodies against viral agents and causes PLT destruction treatment: steroids no test, use symptoms
40
chronic ITP
women 20-50 symptoms: mucocutaneous bleeding, recurrent nose bleeds, menorrhagia plt: 30-80K develop IgG against something in PLT surface
41
autoantibodies form to receptors ____ and _____
GP IIb/IIIa GP Ia/IIa
42
chronic ITP blood smear treatment
giant plts treatment: prednisone
43
drug induced plt destruction
may trigger AB that also bind PLT ex. tylenol, sulfa drugs, penicillin -occur 1-2 weeks after exposure to drug PLT: 1-10 K stop drug treatment
44
drug induced HIT- heparin induced thromb.
immune mechanism PLT count decreased symptoms are thrombotic, not bleeding because plts are activated so thrombi form stop heparin
45
neonatal alloimmune TCP
mom has AB to baby's plt -mother lacks specific plt antigen that baby received from dad and developed AB -PLT normal at first than petechiae <30K treatment: infused mom with IVIG
46
secondary autoimmune TCP
5-10% CLL pts develop from receiving interferons presents like ITP
47
increased plt destruction: non immune
due to exposure of plts to non-endothelial surfaces from activation of coag processes or from plt consumption by endovascular injury w/o measurable depletion of coag factors
48
non immune TTP
aka moschcowitz decreased levels ADAMTS-13 -cleaves ultra large vwf into smaller microthrombi of just PLTs and VWF form
49
primary source of vwf
ECs -they secrete VWF and stored in wiebal bodies
50
ultra large VWF more effective than normal plasma at binding
PLTs
51
the more common form of TTP
does not recur -deficiency occurs because of autoantibodies
52
non immune TTP blood still tries to flow and forms
schistocytes
53
triad symptoms for non immune TTP
anemia TCP neurologic dysfunction
54
what is diagnostic for non immune TTP
schistocytes blood smear
55
treatment for non immune TTP
plasma exchange using fresh frozen plasma or cryo
56
APTT, PT, fibrinogen, FDP, and D-dimer help differentiate TTP from
DIC
57
non immune HUS
children 6 mon-4 yrs seen after shigella dysenteriae or E.coli OH -toxins enter blood stream and attach to renal EC which become damaged and release ultra VWF-- leads to thrombi
58
HUS leads to
renal failure TCP microangiopathic hemolytic anemia
59
lab results for HUS
elevated BUN and creatinine elevated protein casts RBCs in urine elevated retics and schistocytes <10 HGB
60
lack of neurological symptoms and presence of severe renal dysfunction differentiates HUS from
TTP
61
HELLP associated with
preeclampsia HELLP symptoms hemolysis elevated liver enzymes low plt
62
reactive (secondary) thrombocytosis causes
in response to acute blood loss, major surgery, childbirth, inflammation, exercise, IDA secondary to chronic blood loss PLT: 800K
63
platelet count for myeloproliferative disorders
>1 million
64
thrombocythemia -- essential/primary characteristics
most common cause of primary Thrombocytosis is persistent elevation of PLTS
65
plt count and characteristics thrombocytosis
uncontrolled proliferation of MK no correct plt function abnormal morphology high affinity for fibrinogen >1 mil
66
thrombocytosis seen in
older pts symptoms: hemorrhage plt dysfunction thrombosis - throbbing
67
benard soulier
intrisic defect of PLT defective receptor= GPIb/ 9 5 manifests in infancy Plt cout= 40k to almost normal
68
symptoms of bernard soulier
moderate bleeding of mucous mem
69
test results bernard soulier
prolonged bleeding time abnormal PFA enlarged PLTs decreased Plt count
70
inheritance of bernard soulier
autosomal recessive heterozygous pt asymptomatic treatment: apheresed plts is best
71
bernard soulier can mimic
VWF disease
72
VWF disease most severve and most common
severe -- type 3 common- type 1
73
most prevalent congenital bleeding disorder
VWF disease
74
why does VWF occur
VWF binding to plt receptors is impaired by deficiency in VWF or defect of VWF factor 8 is also decreased
75
symptoms of VWF disease
mucocutaneous hemorrhage
76
type 3 VWF disease
resembles hemophilia A -autosomal recessive VWF is absent; 8 decreased cause severe mucocutaneous and anatomic hemorrhage
77
type 1 VWF disease
autosomal dominant - quantitative disorder -- VWF deficiency VWF and 8 decreased mild-mod bleeding usually after surgery or dental extraction
78
VWF disease testing
PT = normal APTT= may or may not be normal CBC is needed to rule out TCP
79
diagnostic of VWF diease
family history of bleeding and the lab demonstration of decreased VWF activity
80
VWD test panel 3 assays:
quantitative VWF test vWF activity (Rco assay) factor VIII activity assay
81
acquired adhesion defect- cardiopulmonary bypass
-induces TCP and severe platelet function
82
Glanzmann's Thrombasthenia
disorder of platelet aggregation affecting GP llb/llla function -lack above receptor or abnormal -this is fibrinogen receptor so Plts can't aggregate
83
inheritance Glanzmann's Thrombasthenia
autosomal recessive -heterozygotes- normal homozygotes- serious bleeding problems
84
lab results Glanzmann's Thrombasthenia
normal Plt count and morphology -lack of aggregation with ADP, collagen, thrombin in ag studies -CBC normal
85
uremia
gives rise to circulating guanidine succinic acid or hydroxy phenolic acid -interfere with PLT function -removed by dialysis
86
clinical features of secretion defects
hemorrhage, hematuria, epistaxis, easy bruising
87
dense granule deficiency
overall affect of decreasing PLT ADP inheritance: autosomal dom patients have a long bleeding time, abnormal PFA
88
alpha granule def
rare -mild bleeding -platelets look gray on PBS
89
aspirin effect
acetylation permanently inactivates COX which blocks TXA2 production and causes impairment of platelet function -due to hereditary absence
90
main hemophilia factor deficiency
factor 8
91
hemophilia A
X linked recessive genes male hemizygotes whose sole X chromosome contains a factor 8 gene mutation experience anatomic bleeding
92
female carrier - unaffected man
25% norm daughter 25% carrier daughter 25% normal son 25% hemophilic son
93
male hemophilia A - non carrier woman
all sons normal because X from mother is normal all daughters obligate carriers of disease
94
symptoms of hem A
severe and prolonged bleeding after trauma hemarthrosis- bleeding into the joints
95
hem A lab testing
APTT- normal to prolonged PT and TCT- normal PLT count - normal diagnosis requires a factor 8 assay
96
in hem A patients can develop alloantibody inhibitors to
factor 8 -b/c body isn't used to amount of factor 8 given
97
factor 8 assay
-check for alloantibody inhibitor if not responding to therapy >30% factor 8 activity= no inhibitor <30% factor 8 activity= do mixing study
98
treatment for hem A
activated PCC -prothrombin complex concentrate factor 2,5,9,10
99
hem B
reduces thrombin production and causes soft tissue bleeding PT- normal APTT- prolonged factor 9 def 9-vit K dependent
100
hem C factor 11 deficiency
seen in Ashkenazi Jews autosomal dom !!! APTT- prolonged PT- normal give plasma
101
Afibrinogenemia
no fibrinogen present symptoms -easy bruising -mucocutaneous bleeding
102
Afibrinogenemia test results
PT APTT TCT all prolonged diagnosis fibrinogen assay
103
hypofibrinogenemia
low levels of fibrinogenemia moderate systemic bleeding
104
dysfibrinogenemia
poor function generalized soft tissue bleeding
105
dysfibrinogenemia test results
prolonged thrombin time very prolonged reptilase clotting time
106
prothrombin 2
def in factor 2 mild systemic bleeding test: PT and APTT prolonged (common pathway)
107
factor V
def factor 5 deficiency when <30% factor 5 def prolonged bleeding time but normal aggregation PT and aPTT prolonged TCT normal
108
factor 7
only disorder with normal aPTT and prolonged PT normal TCT treatment: novoseven
109
factor ten
PT and aPTT both prolonged normal TCT russell viper venom test prolonged vit k dependent
110
factor 12
thrombotic disorder 12 is a catalysts for conversion of plasminogen to plasmin prolonged aPTT
111
factor 13
normal PT, APTT, TCT

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