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Clinical Medicine > Coagulopathies > Flashcards

Coagulopathies Flashcards

1
Q

hemostasis

A

aka coagulation
-the first step in all wound
healing
-limits blood loss by precisely regulated
interactions between components of the blood vessel
wall, platelets, and plasma proteins

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2
Q

regulation of hemostasis

A 
Ongoing process of formation and
dissolving
-plasmin system
-individual plasma proteins
 >> C
 >> S
 >> Z
*keeps you from coagulating too
much
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3
Q

Unregulated activation of hemostasis

A

can cause

thrombosis and embolism

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4
Q

embolism

A

formation of clot in one location which
flows downwards and travels
elsewhere causing thrombosis

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5
Q

major steps of hemostasis

A

1) vasoconstriction
2) temporary blockage of a break in the wall of a blood vessel by a platelet plug via platelet adhesion
3) formation of a fibrin clot

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6
Q

vasoconstriction in hemostasis

A 
1st step in hemostasis in which the blood vessel contracts and
spasms
-neuromuscular reflex arch that
nervous system signals
musculayer of blood vessel to
contract
-clamps down, closes off and
slows bleeding
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7
Q

platelet adhesion

A 
2nd step of hemostasis
-Platelets get together, become
sticky, aggregate, form a gooey
and sticky plug
-not an efficient clot to maintain
plug in hole
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8
Q

formation of a fibrin clot

A 
3rd step of hemostasis
-Plasma protein as a result in
activation (final pathway) in
clotting cascade
-accomplished by a # of clotting
factors
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9
Q

fibrin

A 
plasma protein/fibers in piece of glaze
that form loose mesh, forming in
all directions
At first loose, mesh tightens and
holes close down- forming solid
plug
-gradually weave and become
tighter as clot forms
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10
Q

thrombomodulin

A

heparin-like molecule
-Protein made by endothelial
cells of intact blood vessels
-Inhibits thrombin (clotting factor IIa)
*converts II (prothrombin) into IIa (anticoagulant)
-helps protein S activate protein C
*keeps final clot of clotting cascade from forming

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11
Q

von Willebrand factor

A

secreted by endothelial cells during injury

  • pro-thrombin factor that initiates platelet adhesion
  • important for platelet plug formation
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12
Q

clotting disorders

A

Disorder of platelets/protein or
clotting problem which is qualitative or quantitative
-based on potential to limit platelet numbers and/or function (primary hemostasis) OR
based on their potential to affect the quantity and/or quality of
clotting factors (secondary hemostasis).

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13
Q

primary hemostasis

A

platelet plug/early responder
-after vasoconstriction and seconds after injury of blood vessel, platelets adhere to the blood vessel wall
and aggregate

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14
Q

secondary hemostasis

A

plasma coagulation system that
results in fibrin mesh formation—starts within 20 sec of injury
-longer than primary hemostasis

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15
Q

thrombocytosis

A 
Aka thrombocythemia 
too many platelets → thrombosis or bleeding
Too many platelets = qualitative
function as well as quantitative
lab: platelet count > 500k
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16
Q

Thrombocytopenia

A

too few platelets → bleeding : lab < 100k platelets
Caused by:
– decreased bone marrow production
– increased splenic sequestration
– accelerated destruction of platelets (ITP, TTP)

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17
Q

Von Willebrand’s disease

A

platelet disorder involving lack of platelets due to lack of von willebrand factor

  • defective adhesion; not really the platelets’ fault
  • quantitative and qualitative platelet disorder
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18
Q

Physical /Lab findings of Platelet Defects

A

Petechiae, some purpura
• Lab tests: bleeding time and platelet count
• Local measures generally suffice to control bleeding (either high or low)

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19
Q

Petechiae

A

Small capillary hemorrhages

forming red dots on skin

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20
Q

purpura

A

blending of petechiae to form small purple spots
–formation of purpura together ->
ecchymosis

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21
Q

causes of thrombocytosis

A
  1. an acute reactive process (an APR: recent surgery,
    bacterial infection, iron deficiency, or trauma) OR
  2. bone marrow disorder (a
    malignancy/cancer in the platelets) -> pt have 0.5% risl/year of progressing to leukemia (Acute myeloid leukemia
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22
Q

symptoms of thrombocytosis

A

vasomotor symptoms, thrombosis or bleeding

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23
Q

treatments for thrombocytosis

A

– Treat underlying cause if possible
– Antiplatelet medications, unless there is bleeding
– Platelet-pheresis might be needed
– hydroxyurea or anagrelide to lower platelet count in high-risk patients

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24
Q

Aspirin 81mg

A

anti-platelet that irreversibly blocks the aggregation of platelets
by interfering with the production of thromboxane

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25
Q

splenic sequestration

A

Gobbling up platelets, storing
them and not allowing them to go
into circulation
-leads to thrombocytopenia

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26
Q

Idiopathic thrombocytic purpura

A

generally autoimmune which leads to accelerated destruction of platelets, eventually leads to thrombocytopenia

  • mostly seen in children w/ sudden onset of severe thrombocytopenia following recovery from a viral illness (> 90% recover in 3 – 6 mos)
  • detected anti-platelet antibodies
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27
Q

risk for spontaneous ICH

A 
once platelet count falls below 20,000/microliter
> Endothelial cells always trying-
some clotting necessary in body
> If you cannot generate baseline
clots needed to make
-body may not be able to plug in
brain for normal regeneration of
endothelium
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28
Q

Pseudo-thrombocytopenia -

A

occurs when platelets
clump causing the counter to falsely report the platelet
count as low

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29
Q

treatment for ITP

A

only when platelets < 20k

  1. high dose steroids
  2. IVIG
    - pooled IGMg from donors’ mixed plasma Of immunoglobulins Ex) pool of 5 donors mixed together to have plasma-> hope of at least one of these plasmas that there is an antibody to take out ITP
  3. Splenectomy is indicated for refractory cases
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30
Q

Thrombotic Thrombocytopenic Purpura

A 
Sudden cascade of clotting after vessel wall injury -
Thrombocytopenia
Hemolysis
Renal failure
CNS problems (mild to severe;
fluctuant in consciousness, cannot
do long division, seizures, coma)
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31
Q

exaggerated clotting cascade

A 
initiated in TTP
Fibrin clot - fibrin mesh formation
-as it gets tighter and weave gets
pulled together
-red cells try to pass through and
then get lysed
-fibrin mesh closes so tightly that
nothing can pass -> hemolysis
-bleeding is not usually severe
-triggered by plavix, chemo HIV, pregnancy, Lupus
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32
Q

tetrad of thrombocytopenia in TTP

A
  • thrombocytopenia
  • hemolysis
  • renal failure
  • CNS signs
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33
Q

renal failure in TTP

A 
Clots in kidney- function
disrupted
-hemolyzing enough- extra HgB in
liver- > cannot handle -> urine
turns pink
Hgb gets stuck in filters of kidney
leading to damage
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34
Q

triggers leading to TTP

A

triggered by plavix, chemo HIV, pregnancy, Lupus

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35
Q

TTP without brain manifestation

A

Related to Hemolytic-Uremic Syndrome (HUS), a similar disease seen
in children, which is caused by infection with E. coli O157:H7, Shigella,
or Campylobacter. In this disease, the CNS less commonly affected

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36
Q

treatments for TTP

A

supportive tx -> d/c plavix

  1. plasmapheresis
  2. exchange transfusion
  3. dialysis PRN
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37
Q

Von Willebrand Factor

A

only major clotting factor not made by the liver -> made by vascular endothelial cells and in the bone marrow, by
megakaryocyte

38
Q

functions of vW factor

A

Binds to and protects inactive factor VIII from spontaneous degradation in the plasma
-thrombogenic (binds to vascular collagen); when expose to damaged vascular endothelial cells -> it uncouples from factor VIII which has the
added advantage of allowing free factor VIII to participate in the clotting cascade

39
Q

deficiency of vWF

A

Factor VIII degrades rapidly in the plasma

- leads to a reduction in factor VIII

40
Q

thrombin

A

responsible for the uncoupling of factor VIII from vWF

-self perpetual cycle

41
Q

mechanism of free vWF

A

binds to platelets and makes them “sticky”
> mechanism is
most efficient under high shearing stress
ex) rapid blood flow in narrow blood
vessels as occurs in arterial blood flow

42
Q

Von Willebrand disease

A

most common hereditary coagulation abnormality
> Can be inherited as either an autosomal dominant or recessive trait
2 types of the disease (type 1 & type 2)
quantitative vs. qualitative

43
Q

type 1 Von Willebrand disease

A

low levels of normal vW factor and possibly factor VIII (75% of cases)
-quantitative platelet disorder

44
Q

type 2 Von Willebrand disease

A

normal levels of abnormal vW factor (15-20% of cases) in which platelets are either sticky or not sticky enough

45
Q

type 3 Von Willebrand’s Disease

A

essentially no vW factor and extremely low factor VIII (very rare;
compare with type 1)

46
Q

acquired vW disease

A

pt can develop any form of vW disease as result of other pathologies
-Heyde’s syndrome: occurs in patients with aortic valve stenosis, leading
to gastrointestinal bleeding
– Hypothyroidism
– SLE
– Malignancies: Wilm’s tumor, lung cancer, lymphomas, P. vera, myeloma
– Drugs: ciprofloxacin, griseofulvin, and valproic acid

47
Q

treatment of vW disease

A

– vWF/factor VIII concentrate - transfusion
– recombinant von Willebrand factor (r-vWF) man made & not from donors
– desmopressin, which raises vWF (synthetic form of vasopressin/ADH) -> Given for
surgery, major trauma, or other active bleeding
• OCPs for women with menorrhagia

48
Q

desmopressin

A

synthetic vasopressin which stimulates endothelial cells and megakaryocytes to churn out more vW factor
-given for surgery pre-op and major bleeding such as major trauma

49
Q

coagulation disorders

A

problem with secondary clotting cascade = fibrin plug

nothing to do with platelets

50
Q

liver

A 
primary site of synthesis of most of the clotting factors as well as the proteins involved in
the fibrinolytic system
-liver makes all anti coagulant factors 
AND
-coagulation factors
51
Q

fibrinolytic system

A

body’s natural system of anticoagulation that serves as a constant servo-mechanism offsetting the coagulation cascade

  • AKA natural anti-clotting system
  • Both of these systems are constantly in motion
    ex) when healing, blood clot is dissolved by fibrinolytic system
52
Q

vitamin K-dependent PRO-coagulant factors

A 
factors 
II (prothrombin)
VII
IX
X
2, 7, 9, 10
*vit K needed to mature activated form*
53
Q

vitamin K-dependent ANTI-coagulant factors

A

proteins C, S, Z
made in liver which interfere with clotting cascade
* if liver does not have enough vit K, it cannot synthesize proteins C, S, Z

54
Q

non-vitamin K-dependent, pro-coagulant factors

A

factors I (fibrinogen), V, XIII

55
Q

non-vitamin K-dependent anti-coagulant factors

A

antithrombin-III and plasminogen

56
Q

exceptions that are neither synthesized by liver nor vitamin K dependent

A

all made by vascular endothelial cells

  • vWF (pro-coagulant)
  • thrombomodulin (effectively an anticoagulant )
  • tPA (tissue plasminogen activator which is an anti-coagulant)
57
Q

factor IV

A

calcium

  • needed to move clotting cascade forwards
  • not made by liver
58
Q

vitamin K

A

important to the activation of factors II,

VII, IX, X, protein S, protein C, and protein Z (the “ vitamin K dependent factors”)

59
Q

presentation of coagulation factor disorders

A

Typically manifest as large palpable ecchymoses and
large, spreading, deep soft tissue hematomas
-severe clotting disorder/trauma -> Hemorrhage into synovial joints (hemarthrosis)
ex) pt with coagulation factor disorder will not bleed until post-op due to lack of secondary hemostasis
-cannot make fibrinous clot after platelet plug dissolves
-delayed problem

60
Q

intrinsic pathway

A

coagulation pathway that is always working in response to damaged endothelium

  • depends on activated factors XI & XII (11, 12) and unbound VIII (from vWF) & IX (8, 9)
  • AKA aPTT (activated partial thromboplastin)
61
Q

aPTT

A

measures intrinsic pathway abnormality in activated factors XI & XII (11, 12) and unbound VIII (from vWF) & IX (8, 9)

  • think of (P)laying (T)able (T)ennis, which is played indoors
  • also tests final common pathway
62
Q

extrinsic pathway

A

tissue factor pathway that responds to tissue trauma (ex MVC)

  1. tissue factor III activates factor VII in presence of phospholipids
    - measured by PT
63
Q

PT (protime)

A

measures abnormality in extrinsic pathway

  • the larger the # , the longer the pathway
  • think of (P)laying (T)ennis, which is played outdoors
64
Q

PTT

A

partial thromboplastin phospholipids in presence of factors X & V
* think of (P)laying (T)able (T)ennis, which is played indoors

65
Q

thrombin time

A

ests for quantitative (fibrinogen deficiency) or qualitative
(dysfunctional fibrinogen) defect
> Thrombin is added to the patient’s plasma
in the lab - time till clot formation begins is noted

66
Q

labs used to evaluate bleeding patient

A 
CBC
platelet count
bleeding time
prothromin time 
aPTT
thrombin time
67
Q

Hemophilia A

A

Factor VIII Deficiency
most common inherited plasma coagulopathy
-secondary hemostasis coagulopathy that is most common
• X-linked disorder, frequency 1:10,000 males

68
Q

severe cases of hemophilia A

A

discovered early on in pts due to either:

  • hemorrhage after circumcision
  • pericranial hematomas from birth trauma
69
Q

mild cases of hemophilia A

A

sx do not manifest until adolescence

  • when pt frequently falls/bumps into things upon learning how to crawl/walk
  • Treatment is factor VIII concentrate infusion
70
Q

common sx in Hemophilia A

A

hemarthrosis

hematuria

71
Q

Hemophilia B

A

deficiency in factor IX
-termed Christmas Disease due to pt in 1952 named Stephen Christmas
-Second most common inherited plasma coagulopathy
• X-linked, occurs in 1:100,000 male births
-clinical presentation indistinguishable from Hemophilia A -> diagnosed by assay

72
Q

treatment for Hemophilia B

A

fresh frozen plasma or factor IX concentrate

-sometimes gene therapy

73
Q

Factor XI Deficiency

A

Less severe form of hemophilia that is autosomal recessive (most common in Ashkenazi Jews from
Eastern European)
-discovered in pts that are post-op, have post-traumatic bleeding, or menorrhagia

74
Q

treatment for factor XI deficiency

A

daily infusion of fresh frozen plasma
when bleeding is active or is anticipated
ex) surgery or childbirth

75
Q

plasmin system

A

body’s natural system of anti-
coagulation that keeps coagulation in check
-nature’s anticoagulants

76
Q

plasmin

A

aka fibrinolysin

  • proteolytic enzyme that lyses fibrin clots
  • activated from inactive forrm
77
Q

plasminogen

A

inactive form of plasmin that is activated by:
-Kallikrein
-Factors XIa & XIIa (intrinsic)
tPA

78
Q

Kallikrein

A

a serine protease [enzyme] capable of cleaving
peptide bonds in proteins
-activates plasmin
-think of enzyme biting off -ogen from plasminogen

79
Q

tissue plasminogen activator

A

the same substance used
in the emergency room to reduce the size of brain infarcts
after an acute, occlusive (thrombotic) stroke

80
Q

fibrin degradation products

A

FDPs aka fibrin split products which results from fibrinolysis

81
Q

D-Dimer

A

lab test used to measure clotting

  • D-Dimer is the most easily detected FSP/FDP
    ex) elevated FDPs = increased clotting
82
Q

protein S

A

activates protein C with the help of
thrombomodulin
-part of nature’s anticoagulants

83
Q

protein C

A

inactivates factors Va and VIIIa

-part of nature’s anticoagulants

84
Q

antithrombin

A 
inactivates thrombin (IIa) and Xa 
-part of nature's anticoagulants
85
Q

tissue factor pathway inhibitor (TFPI)

A

inactivates VIIa

- VIIa is the first step of the extrinsic pathway

86
Q

factor V Leiden mutation

A

when the liver transcribes abnormal gene that codes for factor Va
-still able to participate in common pathway but is insensitive/impervious to protein C

87
Q

anti-platelet drugs

A

Aspirin
Plavix
Brilinta

88
Q

Warfarin (Coumadin)

A

-blocks the activity of Vitamin K
-Prothrombin time (PT
or “protime”) is used to monitor the anticoagulant effects of warfarin
-drug is unpredictable

89
Q

Heparin

A

naturally occurring mixture of varied chain lengths of
glycosaminoglycans (GAGs) derived from porcine intestine
-also
produced by basophils and mast cells
-Activates antithrombin which inactivates IIa & X
*considered an equal opportunity inhibitor

90
Q

low molecular weight heparin

A

LMWH which is more selective to Factor Xa

  • more predictable than Warfarin because it exerts AC effects more on F Xa inhibition
    ex) Lovenox (enoxaparin)

Clinical Medicine (5 decks)

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