module 4 disorders of hemostasis Flashcards

1
Q

Coagulopathy s/s (5)

A
prolonged pt/ptt
joint bleeding
tissue hematoma
large, spontaneous, centrally located ecchymosis
bleeding delayed
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2
Q

Thrombocytopenia

A

mucosal bleeding
bleed immediately
petechiae maybe

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3
Q

adequate plt count
rarely develop purpura even w trauma
asymptomatic, risk for excessive bleed w trauma
spontaneous bleeds, maybe petechiae

A

> 50,000
30,000-50,000
10,000-30,000
<10,000

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4
Q

causes of thrombocytopenia (5)

A
hemodilution (esp Post-op)
splenomegaly (ca/cirrhosis)
HIV, BM failure
Hemolysis
Medications
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5
Q

Medications causing thrombocytopenia

A
Heparin
sulfa, vanc, piperacillin, PCN, rifampin
quinine
linezolid
valproic acid, carbamazapine, phenytoin
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6
Q

Idiopathic Thrombocytic Purpura

mostly in ______
Primary
Secondary

A

mostly in women
Primary: acquired d/t destruction of plts
secondary: d/t SLE, CML, antiphospholipid, meds

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7
Q

Acute vs chronic Idiopathic thombocytic pupura

A

acute w kids 1-2 months d/t viral infections, sle, drug allergies

chronic- idiopathic (primary) and progessive

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8
Q

Platelet destruction in Idiopathic thrombocytic pupura starts w
___ by ___ who ___ to ____=____
___ binds to ____=destroyed plt

A

phagocytosis by macrophages who present digested plt peptides to CD4 cells-> = immune response
IgG bind to glycoproteins ->plt destroyed

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9
Q

Neonatal thrombocytopenia is when
can be 2 reasons
Risk of

A

Moms IgG’s cross over to fetus’ plts=destroyed
Can be bc mom has Idiopathic thrombocytic pupura or just an alloimmune response
intracranial hemorrhage risk when plt <20,000

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10
Q

Idiopathic thrombocytic pupura symptoms

A

petechiae, purpura, bruising
GI/GU, nose bleeds
intracranial hemorrhage
older adults more severe bleeds bc of comorbidities (htn)

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11
Q

How can Thrombotic Thrombocytopenic purpura cause platelet consumption and organ ischemia

A

thrombocytic microangiopathy caused when platelets aggregate and occlude the microcirculation
=plt consumption/organ ischemia in brain, heart, kidneys

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12
Q

Acquired vs Familial Thrombotic Thrombocytopenic purpura

A

familial- affects children, appears chronic, recurring episodes q3wks, responsive to treatment
acquired- acute/severe, females 30+

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13
Q

Thrombotic Thrombocytopenic purpura causes

A

autoimmune, family, HIV, CA, post-op, meds (antiplt, quinine, mitomcyin, cisplatin, bleomycin)

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14
Q

Patho of Thrombotic thrombocytopenic purpura
gene mutation causing _______=________ ->_____ = _____ in _____ = organ death

^_______

A

vADAMS13 (d/t mutation in gene making adams13)=^Von willebrand factor
=hypercoaguable =microthrombi in organs

^plasminogen activator inhibitor

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15
Q

Thrombocytic Thrombocytopenic purpura

s/s

A

may have neuro symptoms (seziure, hemiplegia, ams)
fatigue w anemia (microangiopathic d/t rbc lysis)
petechiae, pallor, jaundice
fever
dark urine from hemoglobinurua
n/v/d abd pain, GI symptoms common
CP, HF, shock ,death
thrombocytopenia, NORMAL pt/ptt, fibrinogen
^cr, BUN, LDH, bili
blood smear=shistocytes

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16
Q

Hemophilia sites of bleeding

A

knees, elbows, ankles
GI
Spontaneous=severe disease

17
Q

Hemophilia diagnostic testing

A

normal platelets
normal pt
prolonged ptt

18
Q

Hemophilia children diagnosed when _

will see__

A

diag in children when they start crawling/standing

Bruising, swelling, joint redness, mouth bleeding

19
Q

Disseminated intravascular coagulation

activation of ____ and ___ d/t ___

A

activation of coagulation cascade and fibrinolytic cascade d/t underlying disease

20
Q

Disseminated intravascular coagulation triggered by

A

CA, sepsis, obstetrical complications, trauma/surguries

ards, rabdo, bites, acidemeia, transfusion rxcn

21
Q

Patho of Disseminated intravacular coagulation
____= exposed ____= ______
______ broken down->______ prevents adhesion =_____
may cause ____ d/t ______

A

endothelial damage=exposed TF=coagulation cascade
widespread fibrin deposition broken down-> products adhere to plts, prevent adhesion=bleeding
may cause organ failure d/t micro thrombi

22
Q

Disseminated intravascular coagulation

s/s

A

bleeding from wounds, venipuncture
stroke, PE, necrotic skin lesions
hemorrhaging into closed compartments
multisystem failure= neuro, oligura, hematuria, hypotension, cyanosis of toes/fingers

23
Q
Disseminated intravasular coagulation 
pt/ptt
fibrinogen
d diner
plt
A

prolonged pt/ptt
low fibrinogen
^d-dimer
plt <100,000

24
Q

arterial vs venous thrombus

main complication w either

A

arterial: high blood flow, fibrin/plts (stroke)
venous: low blood flow, rbcs/fibrin few plts (PE)

25
Q

virchows triad (dvt) 3:

A

injury to blood vessel (atherosclerosis, htn, smoking)
abnormalities in blood flow (turbulent w sickle cell, ^viscocity)
hypercoagulable states (chf, MI, bed rest)

26
Q

Unusual sites for thombus (4)

A

mesenteric vein, renal vein, hepatic, cerebral

27
Q

arterial thrombosis associated w 3 deficiencies and ___

A

protein c
protein s
antithrombin

lupus anticoagulants

28
Q

Factor 5 Leidan Mutation (hereditary hypercoagulable)
common cause of ___
causes factor ____ to be resistant to _______= _______ by APC= ^_________

A

common cause of thrombophilia in caucasians

factor Va resistant to activated protein c (APC)
= factor Va not broken down=^thrombin

=thrombophilic state

29
Q

Protein S deficiency (hereditary hypercoagulable)

activates ____ which inactivates ___ and ____

why does inflammation=risk for clots

A

activates protein C which inactivates Va and VIIIa

some attaches to complement
during inflammation=vProtein S=^coagulable

30
Q

Protein C deficiency (hereditary hypercoagulable)

what kind of mutation causes this

A

activated by protein S to form activated protein c
APC inactivates Va and VIIIa

autosomal dominant mutation in PROC gene