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Pathology > Coagulation and platelet > Flashcards

Coagulation and platelet Flashcards

1
Q

normal hemostasis is a Precisely orchestrated process involving ___________________ that occur at the site of vascular injury and
culminates in the formation of blood clot, which
serves to prevent or limit the extent of bleeding.

A

platelets, clotting factors, and endothelium

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2
Q

STEPS IN HEMOSTASIS

A

ARTERIOLAR VASOCONSTRICTION

PRIMARY HEMOSTASIS

SECONDARY HEMOSTASIS

CLOT STABILIZATION AND RESORPTION

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3
Q

Occurs immediately and markedly reduces blood

flow to the injured area

A

ARTERIOLAR VASOCONSTRICTION

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4
Q

Reflex neurogenic mechanism

A

ARTERIOLAR VASOCONSTRICTION

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5
Q

Disruption of endothelium exposes _____ and _____,

which promote platelet adherence and activation, this is beginning of primary hemostasis

A

vWF and collagen

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6
Q

Activation of platelet results in

A

dramatic shape

change as well as release of secretory granules

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7
Q

Within a few minutes, the secreted products
recruit additional platelets that undergo
aggregation to form a primary hemostatic plug

A

primary hemostasis

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8
Q

 Vascular injury exposes tissue factors at the site
of injury
 Tissue factors binds and activates factor VII,
setting in motion a cascade of reactions that
culminates in thrombin generation.

A

SECONDARY HEMOSTASIS

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9
Q

cleaves fibrinogen into insoluble fibrin

and activates platelets (2ndary)

A

thrombin

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10
Q

consolidates the initial platelet plug

A

secondary hemostasis

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11
Q

 Polymerized fibrin and platelet aggregates
undergo contraction to form a solid, permanent
plug

A

CLOT STABILIZATION AND RESORPTION

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12
Q

At this stage, counter-regulatory mechanisms (tPA) are set into motion that limit clotting to the site
of injury and eventually lead to clot resorption and
tissue repair.

A

CLOT STABILIZATION AND RESORPTION

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13
Q

Excessive bleeding can result from:

A
  1. Increased fragility of vessels
  2. Platelet deficiency or dysfunction
  3. Derangement of coagulation, alone or in
    combination
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14
Q

The normal hemostatic response involves the

A

blood vessel wall, the platelets, and the

clotting cascade

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15
Q

Assesses the extrinsic and common coagulation
pathways (factors VII, X, V, II [prothrombin], and
fibrinogen)

A 
PROTHROMBIN TIME (PT)
7,10,5,2
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16
Q

Prolonged PT can result from deficiency or

dysfunction of

A

factor V, factor VII, factor X, prothrombin, or fibrinogen

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17
Q

Assesses the intrinsic and common clotting
pathways (factors XII, XI, IX, VIII, X, V, II, and
fibrinogen)

A

PARTIAL THROMBOPLASTIN TIME (PTT)

12, 11, 10, 9, 8, 5, 2

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18
Q

fibrinogen)
 Prolongation of the PTT can be due to deficiency
or dysfunction of factors

A

V, VIII, IX, X, XI, or XII,
prothrombin, or fibrinogen, or to interfering
antiphospholipid antibodies

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19
Q

platelet reference range

A

150x10^3 to 350x10^3

platelets/uL

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20
Q

platelet High counts may be indicative of a

A

myeloproliferative neoplasm, but are more likely

to reflect reactive processes that increases platelet production

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21
Q

T or F

No single test provides an adequate assessment
of the complex function of platelet

A

T

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22
Q

Test of platelet fx

A

Tests of platelet aggregation

Quantitative and qualitative test of von Willebrand factor

Bleeding time-

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23
Q

infections which Often induce petechial and purpuric hemorrhages

A

meningococcemia, other forms of septicemia infective endocarditis and several of the rickettsioses

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24
Q

Infection induced petechial and purpuric hemorrhage mechanism

A

Microbial

damage to the microvascular (vasculitis) and disseminated intravascular coagulation

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25
Q

vascular injury is mediated by the deposition of drug
induced immune complexes in vessel walls,
leading to

A

hypersensitivity (leukocytoclastic)

vasculitis

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26
Q

Associated with microvasculature bleeding due to

collagen defects that weaken vessel walls.

A

SCURVY AND THE EHLERS-DANLOS SYNDROME

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27
Q

HENOCH-SCHONLEIN PURPURA is Systemic immune disorder characterized by

A

purpura, colicky abdominal pain, polyarthralgia, and acute

glomerulonephritis

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28
Q

result from the deposition of circulating immune complexes within vessels
throughout the body and within the glomerular
mesangial regions

A

HENOCH-SCHONLEIN PURPURA

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29
Q

Autosomal dominant disorder that can be caused by mutations in at least five different genes, most of which modulate TGF-B Signaling

A

HEREDITARY HEMORRHAGIC

TELANGIECTASIA (WEBER OSLER-RENDU SYNDROME

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30
Q

Dilated , tortuous blood vessels with thin walls

that bleed readily

A

HEREDITARY HEMORRHAGIC

TELANGIECTASIA (WEBER OSLER-RENDU SYNDROME

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31
Q

in HEREDITARY HEMORRHAGIC
TELANGIECTASIA (WEBER OSLER-RENDU SYNDROME, Bleeding can occur anywhere , but it is most
common

A

under the mucous membranes of the
nose (epitaxis), tongue, mouth,and eyes and
through gastrointestinal tract

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32
Q

 Weaken blood vessel walls and cause bleeding
 This complication is most common with amyloid light chain (AL) amyloidosis and often manifests as mucocutaneous petechiae.

A

PERIVASCULAR AMYLOIDOSIS

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33
Q

Among these conditions, serious bleeding is most

often associated with

A

HEREDITARY HEMORRHAGIC

TELANGIECTASIA (WEBER OSLER-RENDU SYNDROME

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34
Q

Bleeding disorders due to vessel wall abnormalities

A 
Infections
Drug Rxns
Scurvy and the ehlers-danlos syndrome
Henoch-schonlein pupura
HEREDITARY HEMORRHAGIC 
TELANGIECTASIA (WEBER OSLER-RENDU SYNDROME
PERIVASCULAR AMYLOIDOSIS
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35
Q

Count less than________ is generally

considered to constitute thrombocytopenia.

A

150,000 platelets /ul

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36
Q

can aggrevate

posttraumatic bleeding.

A

20,000 to 50000 platelets/ul

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37
Q

When thrombocytopenia is isolated, the PT and

PTT are

A

normal

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38
Q

causes of thrombocytopenia

A

Decreased platelet production
Decreased platelet survival
Sequestration
Dilution

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39
Q

`causes decreased platelet production

A 
 Conditions that depress marrow output 
generally or affect megakaryocytes 
selectively.
 Certain drugs and alcohol
 HIV, which may infect megakaryocytes and 
inhibit platelet production.
 Myelodysplastic syndrome.
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40
Q

is caused by the

deposition of antibodies or immune complexes on platelets

A

Immune thrombocytopenia

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41
Q

non immunologic causes of thrombocytopenia

A

o Disseminated intravascular coagulation
(DIC) and the thrombotic microangiopathies.
o Mechanical injury such as individuals with
prosthetic heart valves

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42
Q

platelet _____ can rise to 80% to 90% when the spleen is
enlarged , producing moderate degress of
thrombocytopenia

A

Sequestration

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43
Q

 Massive transfusions can produce dilutional

thrombocytopenia.

A

Dilution

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44
Q

 Autoantibody mediated destruction of platelets
 It can occur in the setting of a variety of predisposing
conditions and exposures(secondary) or in the
absence of any known risk factors( primary or
idiopathic)

A

CHRONIC IMMUNE THROMBOCYTOPENIC PURPURA

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45
Q

CITP pathogenesis

A

 Auto-antibodies , against glycoproteins IIb-IIIa or Ib-IX , can be demonstrated in the plasma and
bound to the platelet surface in about 80% of the
patients

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46
Q

CITP spleen morphology

A

normal size.
congestion of the sinusoids
enlargement of the splenic follicles
often associated with prominent reactive germinal centers.

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47
Q

CITP marrow morphology

A

modestly increased
number of megakaryocytes. Some are apparently
immature with large, non-lobulated , single nuclei.

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48
Q

CITP peripheral blood morphology

A

abnormally

large platelets.

49
Q

CITP female to male ratio

A

3:1

50
Q

Pinpoint hemorrhages (petechiae) are especially
prominent in the dependent areas where the
capillary pressure is

A

higher

51
Q

 Typical laboratory findings (CITP)

A

o Low platelet count
o Normal or increased megakaryocytes in the
bone marrow and large platelets in the
peripheral blood
o PT and PTT are normal
o Tests for platelet autoantibodies suffer from
low sensitivity and specificity and are not
clinically useful.
o Therefore, the diagnosis is one of the
exclusion and can be made only after other
causes of thrombocytopenia have been ruled
out

52
Q

CITP treatment

A 
 Respond to glucocorticoids
Splenectomy (severe thrombocytopenia)
Immunomodulatory agents such as IV 
immunoglobulin or anti-CD20 antibody 
(rituximab) are often effective
53
Q

T or F

AITP is Mainly a disease of childhood occurring with
equal frequency in both sexes.

A

T

54
Q

AITP symptoms occur

A

Often 1 to 2 weeks after a self-limited

viral illness

55
Q

AITP is usually resolved within

A

6 months

56
Q

drugs most commonly implicated in DIT

A

quinine (anti-malarial), quinidine (antiarrhythmic), and vancomycin (antibiotic)

57
Q

Thrombocytopenia, which may be severe, can

occur in those who are taking

A

platelet inhibitory
drugs that bind glycoprotein IIb/IIIa (ex.
abciximab, tirofiban)

58
Q

Thrombocytopenia occurs in about 5% of persons

receiving heparin and is of two types:

A

o Type I HIT

o Type II HIT

59
Q 
 Occurs rapidly after the onset of 
therapy and is of little clinical 
importance, sometimes 
resolving despite the 
continuation of therapy.
A

o Type I HIT

60
Q

It most likely results from a direct platelet-aggregating effect of heparin.

A

o Type I HIT

61
Q

 Occurs 5 to 14 days after therapy begins (or sooner if the person has been sensitized to heparin)
and, paradoxically, often leads to venous and arterial thrombosis.

A

o Type II HIT

62
Q

Caused by antibodies that

recognize complexes of heparin and platelet factor 4, a normal component of platelet granules.

A

o Type II HIT

63
Q

receptor and co-receptor,
respectively, for HIV, are found on megakaryocytes, allowing these cells to be
infected

A

CD4 and CXCR4

64
Q

HIV-infected megakaryocytes are prone to

A

apoptosis

65
Q

HIV infection also causes B-cell

A

hyperplasia and

dysregulation

66
Q

THROMBOTIC MICROANGIOPATHIES

A

TTP & HUS

67
Q

Clinical syndromes that are caused by insults that
lead to excessive activation of platelets, which deposit
as thrombi in small blood vessels

A

THROMBOTIC MICROANGIOPATHIES

68
Q

Defined as the pentad of fever,
thrombocytopenia, microangiopathic
hemolytic anemia, transient neurologic
deficits, and renal failure.

A

THROMBOTIC THROMBOCYTOPENIC PURPURA

TTP

69
Q

Also is associated with microangiopathic
hemolytic anemia and thrombocytopenia but
is distinguished by the absence of
neurologic symptoms, the prominence of
acute renal failure, and its frequent
occurrence in children.

A

 HEMOLYTIC UREMIC SYNDROME (HUS)

70
Q

THROMBOTIC THROMBOCYTOPENIC PURPURA

 Caused by a deficiency in a plasma enzyme called

A

ADAMTS13, also designated “vWF metalloprotease.”

71
Q

ADAMTS13 degrades

A

very high-molecular-weight multimers of vWF

72
Q

T or F

In its absence (ADAMTS13), large multimers accumulate in plasma
and tend to promote spontaneous platelet activation
and aggregation.

A

T

73
Q
  • an autoantibody that inhibits the
    metalloprotease activity of ADAMTS13 is
    present.
A

Acquired

74
Q

the onset is often delayed until adolescence, and the symptoms are episodic.
 Thus, factors other than ADAMTS13 deficiency (e.g., a superimposed
vascular injury or prothrombotic
state) must be involved in triggering
full-blown TTP.

A

Hereditary

75
Q

removes
autoantibodies and provides functional ADAMTS13,
TTP (which once was uniformly fatal) can be treated successfully in more than 80% of patients

A

plasma exchange

76
Q

Strongly associated with infectious
gastroenteritis caused by Escherichia coli
strain O157:H7, which elaborates a Shigalike toxin.

A

 “Typical” HUS

77
Q

Defects in complement factor H, membrane
cofactor protein (CD46), or factor I, proteins
that act to prevent excessive activation of the
alternative complement pathway.

A

 “Atypical” HUS

78
Q

BLEEDING RELATED TO REDUCED PLATELET

NUMBER: THROMBOCYTOPENIA

A

CHRONIC IMMUNE THROMBOCYTOPENIC PURPURA

ACUTE IMMUNE THROMBOCYTOPENIC PURPURA

DRUG-INDUCED THROMBOCYTOPENIA

HEPARIN-INDUCED THROMBOCYTOPENIA

HIV-ASSOCIATED THROMBOCYTOPENIA

THROMBOTIC MICROANGIOPATHIES: TTP & HUS

THROMBOTIC THROMBOCYTOPENIC PURPURA

HEMOLYTIC UREMIC SYNDROME (HUS)

79
Q

BLEEDING DISORDERS RELATED TO DEFECTIVE

PLATELET FUNCTION

A

BERNARD-SOULIER SYNDROME

GLANZMANN THROMBASTHENIA

STORAGE POOL DISORDERS

INGESTION OF ASPIRIN AND OTHER NSAID

80
Q

 Inherited disorders of platelet function can be

classified into three pathogenically distinct groups:

A
  1. Defects of adhesion
  2. Defects of aggregation
  3. Defects of platelet secretion (release reaction)
81
Q

 Defective adhesion of platelets to subendothelial

matrix

A

BERNARD-SOULIER SYNDROME

82
Q

BERNARD-SOULIER SYNDROME
is an Inherited deficiency of the platelet membrane
glycoprotein complex

A

Ib-IX

83
Q

This glycoprotein is a receptor for vWF and is
essential for normal platelet adhesion to the
subendothelial extracellular matrix

A

glycoprotein complex Ib-IX

84
Q

bernard soulier syndrome clinical manifestations:

A

variable, often severe,

bleeding tendency.

85
Q

 Bleeding due to defective platelet aggregation

A

GLANZMANN THROMBASTHENIA

86
Q

GLANZMANN THROMBASTHENIA
- Platelets fail to aggregate in response to ADP,
collagen, epinephrine, or thrombin because of
deficiency or dysfunction of

A

glycoprotein IIb-IIIa

87
Q

Characterized by the defective release of certain
mediators of platelet activation, such as
thromboxanes and granule-bound ADP.

A

STORAGE POOL DISORDERS

88
Q

s a potent, irreversible inhibitor of
cyclooxygenase, an enzyme that is required for the
synthesis of thromboxane A2 and prostaglandins.

A

aspirin

89
Q

BLEEDING DISORDERS RELATED TO

ABNORMALITIES IN CLOTTING FACTORS

A 
HEREDITARY DEFICIENCIES
ACQUIRED DEFICIENCIES
FACTOR VIII-vWF COMPLEX
VON WILLEBRAND DISEASE
HEMOPHILIA A (FACTOR VIII DEFICIENCY)
HEMOPHILIA B (CHRISTMAS DISEASE, FACTOR IX 
DEFICIENCY)
DISSEMINATED INTRAVASCULAR COAGULATION (DIC)
90
Q

Bleeding due to coagulation factor deficiencies

commonly manifest as

A

large posttraumatic
ecchymoses or hematomas, or prolonged bleeding
from a laceration or after a surgical procedure

91
Q

The most common and important inherited

deficiencies of coagulation factors affect

A

factor 8

hemophilia A) and factor 9 (hemophilia B

92
Q

Vitamin K deficiency impairs the synthesis of

A

factors II, VII, IX, X and protein C

93
Q

 All coagulation factors are produced in the liver
except____ which is produced by endothelial
cells.

A

factor VIII (8)

94
Q

are caused by qualitative or quantitative defects

A

hemophilia A and von Willebrand disease

95
Q

aids F IX in activation of F X.

A

F VIII-VWF

96
Q

o Essential cofactor of factor IX, which converts F
X to FXa
o Binds to and is stabilized by vWF, an interaction
that increases the half-life of F VIII from about
2.4 hours to about 12 hours.

A

 Factor VIII

97
Q

o Secreted into the circulation by endothelial cells

o Function in stabilization of FVIII

A

vWF

98
Q

promote adhesion of platelets to the

subendothelial matrix

A

vWF

99
Q

vWF also may promote platelet aggregation by

binding to activated

A

GpIIb/IIIa integrins

100
Q

vWF function is assessed using the

A

Ristocetin

agglutination test

101
Q 
 The most common symptoms:
 Spontaneous bleeding from mucous 
membranes (e.g. epistaxis), excessive 
bleeding from wounds, menorrhagia
 It is usually transmitted as an autosomal 
dominant disorder
A

VON WILLEBRAND DISEASE

102
Q

AD (autosomal dominant) disorder characterized by a mild to moderate vWF
deficiency

A

 Type 1 and Type 3 von Willebrand disease

103
Q

– is associated with a spectrum of
mutations, including point substitutions
that interfere with maturation of the vWF
protein or that result in rapid clearance
from plasma; this disorder is mild; there
is still production of vWF

A

type 1 vWF disease

104
Q 
disease is an autosomal 
disorder usually caused by deletions or
frameshift mutations involving both 
alleles, resulting in little to no vWF 
synthesis; mutations here are bigger, 
more severe
A

type 3vWF disease

105
Q

the most common subtype in type 2 VWF disease

A

2a

106
Q

vWF is expressed in normal amounts, but missense mutations are present that
lead to defective multimer
assembly.

A

 Type 2 von Willebrand disease

107
Q

accounts for 25% of all cases and is associated

with mild to moderate bleeding.

A

Type 2 von Willebrand disease

108
Q

T or F

Type 2 vWF is Associated with a prolonged PTT

A

T (intrinsic)

109
Q

Type 1 or 2 vWF tx

A

can be treated with
desmopressin as a prophylactic
measure, or infusions of plasma concentrates containing factor VIll and
vWF, or with recombinant vWF.

110
Q 
must be treated 
prophylactically with plasma 
concentrates and factor VIll infusions to 
prevent severe "hemophilia-like" 
bleeding.
A

Type 3 disease

111
Q

Most common hereditary disease associated with

life-threatening bleeding

A

HEMOPHILIA A (FACTOR VIII DEFICIENCY)

112
Q

is inherited as an X-linked
recessive trait and thus affects mainly males and
homozygous females.

A

Hemophilia A

113
Q

Most severe deficiencies result from an

A

inversion involving the X chromosome that

completely abolishes the synthesis of factor VIll.

114
Q

T or F

In Factor VIII deficiency, Petechia are characteristically absent

A

T

115
Q

Hemophilia a TREATMENT

A

 Infusions of recombinant factor VIll.
 Recently, bispecific antibodies have been
developed that bind factor IXa to factor X;
these antibodies bypass the need for factor
VIll and are particularly effective in patients
with factor VIII antibody inhibitors

116
Q

A wide spectrum of mutations involving the gene that

encodes factor IX is found in

A

hemophilia B

117
Q

T or F

Hemophilia B is X-linked recessive trait like hemophilia A

A

T

118
Q

Hemophilia b Diagnosis is possible only by

A

assay of the factor
levels, that’s the only way to differentiate them, you
have to assay or do a mixing studies between factor
8 and 9 but clinically they are the same

119
Q

T or F

In hemophilia B, PTT is prolonged and PT is normal

A

T

Pathology (31 decks)

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