Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

HemOnc > Hemostasis and Coag > Flashcards

Hemostasis and Coag Flashcards

1
Q

a general term describing the process the body uses to arrest or limit the loss of blood after vascular injury

A

hemostasis

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

components of hemostasis (4)

A
  1. vascular constriction
  2. platelet activation (Fibrin is end product) –> coag cascade
  3. contraction of the platelet plug
  4. Clot dissolution (fibrinolysis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

extremely large bone marrow cells w/ lobulated nucleus give rise to platelets

A

megakaryocytes–no in circulation

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

pluripotential hemopoietic stem cells > megakaryoblast>

A

promegakaryocyte > megakaryocyte > platelets

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

produced by liver essential for production and right quantitiy of platelets

A

thrombopoietin (150-400K normal platelet count)

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

platelets count >600K aka and risk (2)

A

thrombocythemia,

stroke, DVT

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

platelet count <150K aka risk

A

thrombocytopenia,

hemorrhage

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

platelets express (2)

A
  1. MHC class I

2. ABO blood group antigens

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

(4) maintain normal circulating platelet activity

A
  1. prostacyclin (prostaglandin I2)
  2. nitric oxide
  3. endogenous heparins
  4. healthy endothelium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

___________ _____________ molecules activate platelets

A

subendothelial molecules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

important subendothelial molecules

A
  1. collagen
  2. von Willebrand factor vWF
  3. tissue factor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Other important factors leading to platelet activation (3)

A
  1. thromboxane A2 (TXA2)
  2. ADP (released by activated platelets)
  3. thrombin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

act as bridge btwn collagen and specific platetlet surface complexes

A

vWF won Willebrand factor

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

platelet count cut-off for surgery

A

<50K

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

platelet activation steps (5)

A
  1. Exocytosis of cytoplasmic granules (ADP, serotonin, PAF, vWF, etc)
  2. activation of platelet membrane enzyme phospholipase A2 –> thromboxane A2
  3. Change in platelet shape – more amorphis
  4. platelet plug forms (vWF, finger-like projections, fibrinogen)
  5. Coagulation Cascade promoted at surface
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

fibrinogen promotes

A

activated platelets to adhere to one another

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

components of hemostasis (3)

A
  1. vasoconstriction
  2. platelet activation
  3. platelet aggregation and involvement of the clotting cascade which binds everything together w/ fibrin threads to form a “clot”
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

activation of either extrinsic or intrisic coag pathways leads to

A

Final Common Pathway –> fibrin formation

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

extrisic pathway aka

intrinsic pathway aka

A
  • tissue factor pathway (usually more important)
  • contact activation pathway
  • –both involve numerous dif pts commonly called “clotting factors”
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

systemic inflammatory response syndrome SIRS, sepsis, and inflammation may activate the ______ ________ leading to ______

A

intrinsic pathway,

thrombosis

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

the extrinsic pathway is initiated at SITE of INJURY by

A

tissue factor III

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

intrinsic pathway activation occurs when (3) are exposed to a negatively charged surface

A
  1. prekallikerein
  2. kininogen
  3. factor XII
    CONTACT ACTIVATION
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

intrinsic pathway activation way also occur inappropriately when contact w/ (4) correlated w/ ^ CV risk of MI due to clot formation

A
  1. bacteria
  2. urate crystals
  3. amyloid B
  4. homocysteine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

means of controlling thrombus formation

A

thrombin regulation through control of prothrombin activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

thrombin inhibitors

A
  1. antithrombin III (natural inhibitor of prothrombin activation)
  2. Heparin
  3. Warfarin (Coumadin)
  4. Enoxaparin (Lovenox)
  5. Rivaroxaban (Xarelto)
  6. Apixaban (Eliquis)
  7. Dabigatran (pradaxa)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Heparin acts by

A

increasing effectiveness of antithrombin III – works for common pathway–IND DOSE DEPENDENT MANNER

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Warfarin aka works by

A

coumadin–inhibits production of clotting factors II, VII, IX, and X IN DOSE DEPENDENT MANNER

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Enoxaparin aka works by

A

Lovenox–inhibits factor Xa–FLAT DOSE RESPONSE CURVE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Rivaroxaban aka works by

A

Xarelto–oral–inhibits Xa–FLAT DOSE RESPONSE CURVE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

aPIXaban aka works by

A

Eliquis–oral–inhibits Xa–FLAT DONSE RESPONSE CURVE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Dabigatran aka works by

A

Pradaxa–DIRECT THROMBIN INHIBITOR– FLAT DOSE RESPONSE CURVE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

naturally occurring Vit K dependent anticoagulation factors

A

Proteins C, S, Z

ZinCS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

when activated, protein C will prevent (3)

A
  1. thrombus formation
  2. inflammation
  3. blood vessel cell wall permeability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Activated (by thrombin*) protein C inactivates factors (2)

A
  1. Va
  2. VIIIa
    localizes thrombosis to sites of vascular injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Proteins S and Z work

A

in similar fashion to protein C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

*Genetic defect in which factor Va is not inactivated by APC activated protein C

A

Factor V Leiden mutation–will lead to ^ coagulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

(2) ways to prevent thrombus formation

A
  1. Inhibit platelet function (antiplatelet) (ASA, Clopidogrel)
  2. Inhibit the clotting cascade (anticoag) (Hep, Warf, Vit K antagonist)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

How to monitor anticoagulation over time (2)

A
  • aPTT–Heparin–intrinsic pathway

- PT–Warfarin–extrinsic pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Antiplatelet Meds (6)

A
  1. Glycoprotein IIb/ IIIa inhibitors (receptor inhibitor)
  2. ADP receptor hinhibitor
  3. Prostaglandin analogue (PGI2)
  4. COX inhibitors
  5. Thromboxane inhibitors
  6. Phosphodiesterase inhibitors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

dissolution of Fibrin Clots aka

A

Fibrinolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

degradation of fibrin is a fx of ________, circulates inactive as _______

A

-plasmin-

plasminogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

______ ______ _____ (___) activates plasminogen

A

tissue plasminogen activator (tPA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Useful measure for DVT or DIC–fibrin breakdown products

A

“fibrin degradation products” FDP’s and the D-dimer test–fibrin breakdown products in serum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Anticoagulation drugs (4)

A
  1. Vit K antagonists
  2. Factor Xq inhibitors
  3. Direct thrombin (II) inhibitors
  4. Heparin/ low mol wgt heparin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Most common uses of coagulation tests (3)

A
  1. degree of anticoag w/ drug therapy (blood thinners)
  2. pre-surgery (clotting problems)
  3. Dx inherited or acquired coag abnormality (hyper/hypo)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Blood coagulation Tests–no single lab test provides global assessment of hemostasis (7)

A
  1. platelet count
  2. Bleeding time
  3. Prothrombin time (PT)
  4. International Normalized Ratio (INR)
  5. Activated Partial Thromboplastin TIme (aPTT or PTT)
  6. Thrombin Time (TT)
  7. specific clotting factor assays
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

don’t confuse “clot buster” with

A

anticoagulant – is clot already formed?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

T/F We have a good measure of the functional ability of platelets

A

F–only test for number of platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

small standardized cut is made on underside of forearm and time btwn cut and complete cessation of bleeding is measured

A

Bleeding Time (9.5 min)–only one for vWF Dz

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

*Measurement of time it takes blood in test tube to form a clot–Assesses factors? – Ca++ added

A 
Prothrombin Time (PT),
factors I, II, V, VII, X (INACTIVATED)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

PT tests which coag pathways

A

extrinsic and common pathways – clot time pt/ clot time control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

INCREASED platelets disorders (4)

A
  1. acute infx
  2. post surg
  3. malignancy
  4. myeloproliferative Dz
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

INR used to asses coag in pt.’s on

A

warfarin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

know insideout *test to assess the intrinsic (contact) and common pathways

A

aPTT Activated Partial Thromboplastin Time

55
Q

PTT assess factors (6)

A
  1. XI
  2. IX
  3. VIII
  4. X
  5. V
  6. II
56
Q

PTT used to assess coag in pt’s on ______

A

heparin

57
Q

For PT (3) is added to blood tube and time to clot is measured

A
  1. tissue factor
  2. thromboplastin
  3. Ca++
58
Q

Test that assesses the last step in the coag cascade

A

TT Thrombin Time

59
Q

TT screens for (3)

A
  1. hypofibrinogenemia
  2. hyperfibrinogenemia
  3. dysfibrinogenemia (poorly functioning fibrin)
60
Q

Other coag tests might look at (4)

A
  1. mixing studies
  2. antiphospholipid antibodies
  3. fibrinogen levels
  4. anti-factor Xa
61
Q

disorders of hemostasis may be ______ or ________

A

inherited or acquired

62
Q

most common inherited bleeding disorder

A

von Willebrand Dz (vWF)

63
Q

tests for coag to know inside-out

A
  1. platelet count
  2. bleeding time
  3. PT
  4. aPTT
64
Q

function of vWF

A

major adhesion molecule that tethers platelets to exposed subendothelium–Dz may present as along spectrum

65
Q

vWF Dz types (2)

A
  1. decreased quantity of vWF

2. decreased function of vWF

66
Q

vWF may present in LATER CHILDHOOD as (4)

A
  1. prolonged bleeding after surg (may be first clue)
  2. mucosal bleeding
  3. prolonged epistaxis
  4. menorrhagia etc
67
Q

Tx for vWF Dz

A

DDAVP–Desmopressing–synthetic vasopressin –>release of vWF from endothelium

68
Q

Hemophilia types (2) plus factor deficiency

A
  1. Hemophilia A - Factor VIII deficiency (80%)

2. Hemophilia B - Factor IX deficiency

69
Q

Hemophilia etiology

A

X-linked recessive hemorrhagic Dz–Males clinically affected, female carriers asymp

70
Q

platelet count, BT, aPTT results for hemophila

A
  1. platelet count and BT normal

2. aPTT is prolonged

71
Q

Tx of hemophilia (2)

A
  1. cryoprecipitate

2. Specific Factor VIII or IX

72
Q

Ashkenazic and Iraqi Jewish populations think

A

Factor XI deficiency (hemophilia C)

73
Q

DIC

A

disseminated intravascular coagulation–less of Dz than syndrome

74
Q

most common etiologies of DIC (3) “clot-lyse-clot-lyse-clot-lyse” –> using up all the clotting factors

A
  1. bacterial spesis (most common cx)
  2. malignant disorder
  3. obstetric complications
75
Q

the exposure of blood to (4) results in uncontrolled generation of thrombin

A
  1. phospholipids from tissue damage
  2. hemolysis
  3. endothelial damage
  4. tissue factor
76
Q

Clinical presentation of DIC (4)

A
  1. oozing from venipuncture site
  2. petechiae
  3. ecchymosis
    to more extreme 4. ^ GI, pulm, CNS bleeding
77
Q

most sensitive indicators of DIC

A

fibrin degradation products and D-dimer tests

78
Q

Tx of DIC (4)

A
  1. Tx underlying cause
  2. replace clotting factors and platelets
  3. control coagulation state–heparin
  4. support pt–vent, dialysis, transfusion
79
Q

Vit K necessary for production of factors (4) and Proteins (3)

A

factors II, VII, IX, X and proteins C,S,Z

80
Q

Causes of Vit K deficiency (6)

A
  1. inherited deficiency
  2. dietary deficiency (alcoholic, starvation, food tube w/out K)
  3. Surgical–removal or alteration to GI tract
  4. Chronic ABX–colonic flora disruption
  5. Chronic liver Dz–primary biliary cirrhosis v Vit K
  6. Iatrogenic– Warfarin
81
Q

Vit K characteristics

A

fat soluble vitamin absorbed in terminal ilium

82
Q

testing for Vit K dependent clotting factors

A

evaluated by PT

83
Q

disregulation of clotting and fibrinolysis

A

DIC

84
Q

Tx of Vit K deficiency

A
  1. parenteral Vit K (need liver to turn into coag factors)

2. (acute) fresh frozen plasma or cryoprecipitate will replenish Vit K dependent factors

85
Q

_______ often show low levels of Vit K–causes (3)

A

Newborns,

low transplacental transfer, low breast milk levels, sterile colon at birth

86
Q

liver failure may result in ________, due to liver’s…

A

bleeding,

coag factors and many natural anticaog proteins

87
Q

____________ common in pt’s w/ cirrhosis due to _________ _________

A

thrombocytopenia )

88
Q

Many Endothelial:
vasodilators are-
vasoconstrictors are-

A
  • platelet inhibitors

- platelet activators

89
Q

Thrombocytopenia <150K/ul may result in

A

widespread petechial rash

90
Q

thrombocytopenia cx (3)

A
  1. decreased production (marrow failure, infiltration, tumor)
  2. sequestration (spleen)
  3. increased destruction (over active clotting, autoimmune)
91
Q

purple top tube:
Green top:
blue top:

A

EDTA–an aminopolycarboxylic
heparin
sodium citrate

92
Q

using a “purple top” may cause

A

pseudothrombocytopenia–due to platelet agglutination–>falsely low platelet count

93
Q

______ ___ as a metabolic by product of the colonic flora

A

Vitamin K–so strict dietary deficiencies are very uncommon

94
Q

most common cause of non-iatrogenic thrombocytopenia

A

infection induced thrombocytopenia

95
Q

Types/ causes of thrombocytopenia (6)

A
  1. Pseudo–purple-top
  2. Infection induced
  3. Drug induced
  4. Heparin induced
  5. Immune thrombocytopenic PURPURA (ITP)
  6. Thrombotic thrombocytopenic PURPURA (TTP)
96
Q

Likely infection induced thrombocytopenia etiologies (3) (general category)

A
  1. Gram neg bac
  2. HIV
  3. mononucleosis EB
97
Q

infection induced thrombocytopenia may result in () – generally self-limiting

A
  1. direct suppression of platelet production
  2. decreased survival time of platelets
    - -IgG binds to platelets–>destroyed in spleen
98
Q

Warfarin may induce

A

skin necrosis

99
Q

Drug induced thrombocytopenia particularly cx by (4)

general category

A
  1. sulfonamides
  2. quinine
  3. herbal supplements
  4. vancomycin
100
Q

mechanisms of drug induced thrombocytopenia (3)

A
  1. direct marrow suppression (i.e. chemotherapy)
  2. production of DRUG DEPENDENT antibodies against specific platelet surface antigens (Type II Hypersen. Rxn) upon re/exposure to drug resolves 7-10d post d/c
  3. cross rxn of existing antibodies w/ drug bound platlets–IMMEDIATE thrombocytopenic development
101
Q

HIT (specific disease)

A

heparin (anticoagulant) induced thrombocytopenia

102
Q

wide spread patechial rash (pinhead size red spots that don’t blanch) punctate bleeding under skin

A

thrombocytopenia–starts where venous pressure highest

103
Q

Features of HIT (3)

A
  1. low platelet count btwn 5-14 days of starting heparin
  2. thrombocytopenia typically mild-moderate
    3.
104
Q

chloramphenicol

A

ABX–grey baby–destroys bone marrow–low platelets

105
Q

petechiae vs purpura

A

smaller vs. larger–both won’t blanch

106
Q

key finding in immune thrombocytopenic purpura ITP

A

isolated thrombocytopenia

107
Q

Immune Thrombocytopenic purpura ITP in children

A

Fairly common in children 2-4yo–follows infectious process and generally SELF-LIMITED, resolves w/in 1-2m

108
Q

presentation of immune thrombocytopenic purpura ITP pt’s (5)

A
  1. mucocutaneous bleeding
  2. ecchymosis (subcutaneous purpura >1 cm)
  3. petechiae
  4. epistaxis
  5. menorrhagia
109
Q

heparin induced thrombocytopenia HIT etiology

A

heparin attaches to platelet–looks like foreign invader–> destroyed

110
Q

in immune thrombocytopenic purpura–what might point to severe derangement which may become life threatening (2)

A
  1. wet purpura (blood blisters in mouth)

2. retinal hemorrhages

111
Q

Tx for immune thrombocytopenic Purpura ITP

A
  1. mild: watch and wait

2. severe thrombocytopenia s who relapse/bleed

112
Q

*Characteristics (5) of TTP aka

A

Thrombotic Thrombocytopenic Purpura,

  1. Microangiopathic hemolytic anemia
  2. Thrombocytopenia
  3. Renal Failure
  4. Neurologic defects
  5. Fever
113
Q

a hemolytic anemia occurring in the microvasculature evidenced by fragmented RBC’s schistocytes, helmet cells, etc. on peripheral blood smear

A

Microangiopathic hemolytic anemia

114
Q

microangiopathic hemolytic anemia will result in

A
  1. anemia
  2. increased LDH (RBC enzyme)
  3. increased indirect bilirubin
  4. decreased indirect bilirubin
  5. decreased haptoglobin (carries free Hgb in serum)
  6. increased reticulocyte count
115
Q

thrombosis etiology:
arterial-
venous-

A
  • atherosclerosis

- stasis

116
Q

role of haptoglobin

A

carries free Hgb in serum

117
Q

Tx for TTP

A

early recognition and prompt tx w/ plasma exchange (plasmapheresis) decreases mortality to 10-30%

118
Q

plasma exchange

A

plasmapheresis

119
Q

CNS sx of TTP

A
  1. headache
  2. AMS
  3. seizure
  4. stroke
120
Q

Thrombosis/ thrombophilia types (3)

A
  1. arterial thrombosis
  2. venous thrombosis
  3. venous and arterial thrombosis
121
Q

DX of TTP

A

ADAMST13 assay may be helpful + blood smear

122
Q

TTP blood smear findings

A
  1. helmet cells

2. schistocytes

123
Q

A disease primarly seen in children w/ 1. microangiopathic hemolytic anemia 2. acute renal failure 3. thrombocytopenia

A

Hemolytic uremic syndrome HUS (specific disease) very similar to TTP

124
Q

differentiation for HUS and TTP

A

HUS: children, bloody diarrheal Dz
TTP: adults, vWF, ADAMTS13, CNS SYMPTOMS!

125
Q

Thrombocytosis platelet count

A

> 400K

126
Q

(3) cx of thrombocytosis

A
  1. Fe deficiency
  2. Inflammation, cancer or infxn
  3. Myeloproliferative process (thrombocythema or polycythemia vera)
127
Q

genetic etiology of Thrombosis/ thrombophilia (3)

A
  1. ex. Factor V Leiden mutation

2. inherited deficiency of Protein C or S

128
Q

Venous thrombosis–> Virchow triad (3)

A
  1. HYPERcoagulability
  2. Stasis or turbulent blood flow
  3. Endothelial injury/dysfunction
129
Q

Differentiate ITP from TTP/HUC

A

peripheral blood smear– will not see Schistocytes/ helmet cells w/ ITP–also patient (most likely child) will be healthy and energitic w/ ITP

130
Q

Venous Thrombosis RF’s

A
  1. Virchow triad
  2. Meds (estrogen, OCP, prothrombotics, HRT)
  3. obesity
  4. Increased age
  5. pregancy
131
Q

Venous AND Arterial thrombosis cx’s (5)

A
  1. polycythemia versa (a bone marrow disease that leads to an abnormal increase in the number of blood cells (primarily red blood cells)) Hgb 17 viscous blood
  2. malignancy
  3. dysfibrinogenemia
  4. essential thrombocythemia
  5. TTP, DIC, and HIT
132
Q

strongest predictor of recurrent venous thrombosis

A

idopathic thrombosis (thrombosis w/out apparent cx)

133
Q

major cx of arterial thrombosis

A

atherosclerosis

HemOnc (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions