Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pharm 2 final > Bleeding Disorders and Assessment > Flashcards

Bleeding Disorders and Assessment Flashcards

1
Q

what mediates primary hemostasis?

A

platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

coagulation is what type of process?

A

chemical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

vasoconstriction is what type of process?

A

mechanical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

hemostasis tripod

A
  1. primary hemostasis
  2. coagulation
  3. vasoconstriction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

hemostasis tripod is balanced by what?

A

anticoagulant activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

anticoagulant activity prevents what?

A

prevents excessive coagulation and keeps blood flowing appropriately

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

in primary hemostasis, how does platelets adhere to disrupted vessel wall?

A
  1. platelet surface membrane glycoprotein receptor Ib

2. von Willebrand factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

other than vessel wall, platelets also adhere to one another in primary hemostasis via what?

A
  1. surface receptor glycoprotein IIb/IIIa

2. fibrinogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

platelets also produce which arachidonic acid vasoconstrictors?

A
  1. thromboxane A2

2. prostaglandins (PGs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

which proteins are released from platelet storage granules?

A
  1. platelet agonists ADP and serotonin
  2. coagulation factors von Willebrand factor and coagulation factor V
  3. heparin-binding proteins platelet factor 4 and beta-thromboglobulin
  4. growth factor/chemokines PDGF, platelet TGF-β, TPO
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

platelet surface provides a site for what?

A
  1. generation of thrombin

2. subsequent fibrin formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

coagulation: tissue factor-factor VII pathway “extrinsic system”

A
  1. tissue factor exposed to blood
  2. complex forms between tissue factor and factor VII
  3. factor VII is activated: factor VIIa
  4. tissue factor-factor VIIa complex binds and activates factor X
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

after tissue factor-factor VIIa complex binds and activates factor X, factor Xa converts what?

A

prothrombin (factor II) to thrombin (factor IIa)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is required for factor Xa to convert prothrombin (factor II) to thrombin (factor IIa)?

A

factor V as a cofactor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

when is factor Xa more efficient at converting prothrombin (factor II) to thrombin (factor IIa)?

A

in the presence of a phospholipid surface (i.e. activated platelet)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

alternate “secondary” pathway to coagulation

A
  1. activation of factor IX by tissue factor-factor VIIa complex
  2. factor IXa and cofactor VIII activate factor X
  3. thrombin formation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

third coagulation pathway

A
  1. thrombin itself activates factor XI
  2. factor XIa activates factor IX
  3. pathway proceeds to additional thrombin formation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

thrombin is essential for what?

A

conversaion of fibrinogen into fibrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what does thrombin activate?

A

coagulation factors and cofactors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

thrombin is a strong activator of what?

A

platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

thrombin mediates what in the coagulation pathway?

A

mediates fibrinogen cleavage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what happens after fibrinogen is cleaved in coagulation pathway?

A
  1. forms fibrin monomers and subsquent polymers

2. crosslinking of fibrin takes place by thrombin-activated factor XIII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is the ultimate step in the coagulation cascade?

A

crosslinking of fibrin by thrombin-activated factor XIII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are some natural anticoagulation mechanisms?

A
  1. tissue factor pathway inhibitor (TFPI)
  2. protein C
  3. antithrombin III
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
circulating protein C is activated by what?
endothelial cell-bound enzyme thrombomodulin in association with thrombin
26
activated protein C degrades what important cofactors?
V and VIII
27
what is required in order to activate protein C?
protein S
28
antithrombin III inactivates what?
thrombin and factor Xa
29
what strongly enhances antithrombin III?
presence of heparin
30
where are tPA and uPA (plasminogen activators) found?
in endothelial cells
31
how are tPA and uPA (plasminogen activators) released during fibrinolysis?
by several stimuli, including hypoxia, acidosis
32
at which levels are fibrinolysis inhibited?
1. activator inhibitors (PAIs) | 2. circulating protease inhibitors (e.g. alpha2-antiplasmin)
33
what is the most common congenital coagulation disease?
von Willebrand disease
34
what are the 3 major subtypes of von Willebrand disease?
1. type 1 2. type 2 3. type 3
35
type 1 von Willebrand disease
reduced concentration of vWF (10-45% normal levels)
36
type 2 von Willebrand disease
dysfunctional vWF
37
type IIa von Willebrand disease
variable qualitative defect in GP-1 binding and multimer formation
38
type IIb von Willebrand disease
"gain in fxn" defect, excessive binding to platelet GP-1
39
type IIm von Willebrand disease
monomers have decreased GP-1 binding, multimers normal
40
type IIn von Willebrand disease
defect in binding to factor VIII
41
type IIn von Willebrand disease may be diagnosed as what?
hemophilia A
42
type III von Willebrand disease
absent von Willebrand factor (homozygous for gene defect)
43
what is the treatment for type I and IIa von Willebrand disease?
demopressin (DDAVP)
44
demopressin (DDAVP) is analogue to what?
vasopressin
45
what does demopressin (DDAVP) promote?
release of vWF stored in endothelial cell-associated Weibel-Palade bodies
46
demopression (DDAVP) increases circulating vWF by how much?
2-3 fold
47
demopressin (DDAVP) is contraindicated in whaT?
type IIb vWD
48
treatment for more severe forms of von Willebrand disease?
replacement of transfused factors
49
people with severe von Willebrand disease who have had replaced their transfused factors, what does that result in?
late re-bleeding after fibrinolysis
50
what is the most commonly inherited coagulation disorder?
hemophilia A (classic hemophilia)
51
T/F: hemophilia A (classic hemophilia) is autosomal dominant
false, sex-linked recessive
52
hemophiliac patients with factor VIII levels greater than 5% rarely bleed spontaneously but what will have what after surgery or trauma?
will have bleeding problems
53
what develops in 10-15% of severely affected hemophiliacs?
anti-factor VIII antibodies (factor VIII inhibitors)
54
why are factor VIII levels also decreased in patients with von Willebrand disease?
because vWF acts as a carrier molecule for factor VIII
55
treatment of mild to moderate hemophilia A
demopressin (DDAVP)
56
demopressin (DDAVP) causes release of endogenous factor VIII from what in patients with mild to moderate hemophilia A?
liver sinusoids and endothelial cells
57
treatment for severe hemophilia A patients
factor VIII transfusion
58
hemophilia B (Christmas disease)
similar to hemophilia A but affecting factor IX
59
how is hemophilia B (Christmas disease) treated if severe?
with factor transfusion
60
hypercoagulable coagulation diseases
1. protein C deficiency, protein S deficiency | 2. factor V leiden
61
protein C and S are synthesized where?
liver
62
protein C and S are what type of proteins?
vitamin-K dependent proteins
63
mild forms of protein C or S deficiency predispose patients to what?
thrombosis
64
severe forms of protein C or S deficiency are not compatible with what?
life
65
factor V leiden
polymorphic factor V which resists inactivation by activated protein C
66
factor V leiden is present in about 5% of which population?
north american caucasians
67
factor V leiden is rare in what population?
Asians
68
factor V leiden predispose patients to what?
deep venous thrombosis
69
which organ is the source of coagulation factors?
liver
70
the liver is also a source for what?
1. protein C 2. protein S 3. fibrinogen
71
what causes thrombocytopenia in patients with coagulation problems?
portal HTN and associated with splenomegaly
72
thrombocyte fxn is impaired in what type of patients?
cirrhotic
73
formula for end-stage liver disease (MELD) score is based on what?
1. serum bilirubin 2. serum creatinine 3. INR
74
end-stage liver disease (MELD) score predicts what?
3-month mortality
75
end-stage liver disease (MELD) score may be a more useful predictor of what?
bleeding complications than INR alone
76
how do you manage patients with coagulation problems and liver disease?
may include transfusion with missing factors and/or platelets
77
patients with renal failure often present with what?
coagulation abnormalities
78
patients with renal failure are at risk for enhanced bleeding. why?
it's attributed to impaired platelet adhesion, aggregation and release
79
a low hematocrit in patients with renal failure may contribute to what?
impaired fxn of primary hemostasis
80
how can the extent of impaired fxn of primary hemostasis in patients with renal failure be tested?
platelet fxn assay or comparable assay
81
what has been shown to correct prolonged bleeding time in patients with uremia?
DDAVP (demopressin)
82
aspirin is an irreversible inhibitor of what?
platelet membrane-associated cyclooxygenase
83
what does aspirin block?
formation of thromboxane A2
84
thromboxane A2
potent platelet agonist and vasoconstrictor
85
aspirin inhibits less of what?
other PGs, such as platelet antagonist and vasodilator prostacyclin (PGI2)
86
aspirin may be associated with what?
significant impairment of primary hemostasis and mild enhancement of bleeding
87
life span of platelets
10 days
88
how many days are usually required for termination of aspirin use to restore adequate platelet fxn and effective hemostasis?
5-7 days
89
what are the most important adverse effects of aspirin?
1. bleeding 2. hemorrhagic gastritis 3. gastric ulceration
90
T/F: for most dental procedures, patients should discontinue aspirin us
false, it's NOT indicated for it may pose greater risks than benefits

Pharm 2 final (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions