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Coagulation Flashcards

Learn coagulation pathophysiology and disorders (77 cards)

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1
Q

What is hemostasis?

What is the goal?

A

Arrest of bleeding

Prevention of blood loss following vessel injury

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2
Q

Hemostasis involves what BLOOD STRUCTURES/COMPONENTS

A

Vessel wall, platelets, plasma coagulation proteins

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3
Q

How many stages of hemostasis are there?

A

3 Stages

Primary
Secondary
Clot Retraction

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4
Q

Primary hemostasis involves what?

A

1st stage of hemostasis

Vascular spasms
Interactions b/w platelets and vessel
Formation of platelet plug

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5
Q

Secondary Hemostasis is?

A

2nd stage of hemostasis

Formation of fibrin clot (coagulation)

involves clotting factors

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6
Q

Clot retraction is?

A

3rd stage of hemostasis

compression of fibrin to form firm clot

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7
Q

What are thrombocytes

A

They are platelets

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8
Q

What types of cells are platelets made from?

A

from megakaryocytes

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9
Q

Where do megakaryocytes come from?

A

Megakaryoblasts

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10
Q

How are platelets formed?

A

Goes through many rounds of mitosis but not cytokinesis

end up with 33-66 nucleus, the megakaryocyte then flakes apart

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11
Q

Function of platelets is to?

A

Adhere to collagen exposed by trauma

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12
Q

What happens when platelets activate?

A

They Degranulate!

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13
Q

What are platlet alpha granules

A

Platlet thrombospondin, fibrinogen, von willebrand factor, coag factor V & VIII

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14
Q

What are platlet dense granules

A

ADP, ATP, seratonin

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15
Q

What happens once platlets are activated and ADP released?

A

Released ADP reacts with collagen- causes formation of thromboxane A2 (TxA2)

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16
Q

How does asprin function as a blood anti coagulant

A

Asprin works by blocking ADP from reacting with collagen, thereby NOT allowing formation of thromboxane

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17
Q

What is the function of TxA2?

A

It stimulates glycoprotien IIb/IIIa receptor expression

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18
Q

What is the purpose of IIb/IIIa receptor expression?

What causes the receptors to be expressed

A

These receptors promote platelet adhesion

TxA2 causes the receptors to be expressed

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19
Q

Once platelets are formed they help with secondary hemostasis, how do they do this?

A

Catalyze interactions b/w activated coagulation factors

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20
Q

Do platlets play a role in clot retraction?

A

Yesss

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21
Q

Blood coagulation factors are all what kind of proteins?

A

Are all plasma proteins..EXCEPT FACTOR III

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22
Q

Where are blood coagulation factors synthesized?

A

synth in the liver

EXCEPT for factor VIII

some are also synth by megakaryocytes and endothelial cells

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23
Q

Factor II, VII, IX, protein C, and protein S are dependent on?

A

They are dependent on vitamin K for synthesis and activity

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24
Q

What blood coag factors depend of vitamin k? (5)

A

factor II, Factor, VIII, factor IX, protein C, protein S

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25
How does warfrin work?
warfrin is a vitamin K agonist pulls out vitamin K--causing disruption of coagulation leading to bleeding out
26
Are coagulation factors always for clot making?
nope! protein C and protein S dont make clots
27
Protein C function
INACTIVATES factor V and VIII prevents clot formation
28
Protein S function
Stimulates release of TPA (tissue plasminogen activator)
29
Fibrin clot formation
2 pathways intinsic and extrinsic both pathways work together
30
what is function of factor X in both the intrinsic and extrinsic pathway?
act as common final pathway at end of both
31
Intrinsic pathway
blood contacts altered vascular endothelium EX: high lvls of glucose, increased conc of lipids, htn, smoking include factor XII, HMWK, prekallikrien, XI ---formation of factor Xa = initiation of common pathway
32
Extrinsic pathway
trauma of vascular wall-crushing of vessel, shearing/trauma, cutting finger factor III activates VII---VIIa activates X
33
Intrinsic pathway factors are
Factor XII, HMWK, prekallikrien, factor XI
34
Extrinsic pathway factors are
factor III, factor VII
35
Fibrin clot at end of BOTH pathways is initiated by what factor?
by factor Xa in presence of factor V, calcium, phospholipids
36
Factor V does what in the common final pathway?
interacts with prothrombin to change prothrombin which is soluable to insoluable form: thrombin
37
Once thrombin is activated what happens?
Cleaves fibrinogen to fribrin and activates factor XIII | forms insoluable clot to aid in clot retraction
38
What is fibrinolysis
Clot dissolution, tearing clot apart initiated along with clot formation...clot is being both destroyed and built
39
Factors XII, HMWK, kallikrein, thrombin
release plasminogen activators (TPA) cleave plasminogen to plasmin
40
What is the function of plasmin
plasmin digests fibrinogen and fibrin (insol version) inactivates factor V and factor VIII
41
What is the purpose of fibrinolysis
maintain balance b.w clot formation and clot dissolution form sticky net, immed tear it apart, once torn, rebuild it prevents clot from getting too big helps to make sure clot eventually leaves and doesnt travel anywhere else
42
Evaluation -clinical assessment requires...
fam hx, location, severity duration, med hx most signs are skin/mucous membranes pale or jaundiced bruise easily
43
Petechiae
Flat, pinpoint, non-blanching red or purple spots push them = no color change indicate CAPILLARY bleeds vascular/platelet disorder
44
Purpura
petechia in groups/patches often pruritic
45
ecchymosis
blood escapes to tissues aka bruise
46
hematoma
raised ecchymosis
47
hemarthrosis
bleeding into joint
48
telanflectasia
lesion from capillary + small artery dialaiton---blanch and bleed-spider lesions
49
Hematochezia-melena hematuria-bloody urine hematemisis-bloody vomit hemoptysis =?
hemoptysis=gastric drainage that is bloody menorrhagia=excessive menstrual bleeding
50
Vascular disorders primary cause is
bleeding problem with vascular component of primary hemostasis can be acquried or inherited
51
Vascular Pupura What is it? What causes it? What are the 2 special forms?
When purpura is present on skin abnormality of vessles or tissues that support them allergic form= anaphylactoid purpura, hemochschonlein purpura) caused from autoimmune inflam of vessels drug induced pupura- many drugs dunno why tho
52
Structural abormalities of blood vessels are mechanism for some types of vascular purpura, can be inherited or acquired
good to know lol
53
Ehlers-Danlos syndrome, osteogenesis imperfecta
vascular purpura caused by decreased and poor quality of collagen and elastin
54
Scurvy
vasculat purpura caused by defective collagen
55
Loss of sub Q fat causes purpura because
skin mobility begins to shear vessels | old people/those with rapid weight loss
56
How do steroids cause vascular purpura
destroy support tissues
57
Vascular purpura ``` lesion behavior: allergic drug induced inherited forms scurvy ```
lesions appear/fade, do not blanch proximal extremities--allergic drug induced- gen lesions inherited- ecchymoses and hematomas scurvy- lesion around hair follciles on thighs,butt
58
Hereditary hemorrhagic telangiectasia aka? type of genetic disease happens where? describe lesions what is most common clinical problem what worsens this condition
aka---osler-weber-rendu dz it is autosomal DOMINANT d/t abnormality in vascular development happens on any mucousal surface most severe on lung, liver, brain lesions are bright red/ purple-nose, lips, palate, ect epistaxis is most common clinical problem worse after puberty
59
Platlet disorders are? examples of them are? (3)
abnormality in quantity or qualirt of thrombocytes thrombocytopenia thrombocytosis qualitative platlet disorders
60
Thrombocytopenia common cause of what? causes of it?
common cause of gen bleeding many causes
61
Thrombocytopenia idiopathic thrombocytopenia purpura is what? acute ITP chronic ITP
immune mediated acute itp - follows acute viral infection chronic itp- insiduous/women
62
four mechanism for thrombocytopenia
decreased platelet production, descreased platelet survival, splenic sequestration, platelet dilution
63
Thrombocytosis is what? follows? secondary response to?
is an excessive platelet numbers transitory following stress or excercise secondary responce to hemorrhage, inflam disease, malignancy, infection, hemolysis, splenectomy
64
3 forms of thrombocytosis
primary- abnormal megakaryocyte proliferation hemorrhaging and thrombotic complications secondary - actual production increase transitory - release of preformed
65
Qualitative platelet disorders
acquired disorders common drugs with uremia co existing hemotalogic dz one aspect of platelet function is abnormal
66
Coagulation disorders give examples
aka-coagulopathies occur d/t defect in normal clotting ``` bleeding d/t problems with clot formation stabilization lysis of clot, inappropriate activation of coagulation cascade ```
67
Hemophilia is what? dx when?
most common, severe inherited coag disorder neonatal dx - too much bleeding - following circumsicison - following vit k injection
68
Hemophilia A
classic form VIII deficit x linked recessive
69
Hemophilia B
factor IX deficit | classified by extent coag factor is deficit
70
Hemo A vs Hemo B
``` hemo A x linked recessive VIII deficit hemo b factor iX deficit ```
71
Von willebrand dz what is it? problem? s/s?
autosomal dom disorder of VIII carrier protein also includes platelet dyfunction several subtypes for both sexes von willebrand factor and factor VIII normally circulate as a complex VWW stabilizes VIII- normal platelet adherence in dz = descreased of absent = depression ov VIII s/s are epistaxis, mucosal bleeding, ecchymoses, gi bleed, menorrhagia
72
Vitamin K deficiency
aka bleeding in infancy newborns 48-72 hrs to 6months more common in BREAST FED infants rare- vit k admin to newborns deficit of vit k dependent factors---include factor II, VII, IX, X
73
factor II, VII, IX, X
all depend of vit k
74
Acquired vitamin K deficiency caused by changes to what important digestive secretion??
BILE vit K is fat soluable- absorbed in sm intenstice stored in liver dfcny d/t: malnutrition, malabsorbtion, chronic hepatic dz, antibioti therapy, oral anticoag therapy livers secretes bile- needed for fat absorbtion bile problems - no fat = no fat soluable vitamins possibly d/t liver immaturity
75
Disseminated intravascular coagulation what is it?
simultaneous clotting and bleeding widespread clotting in small vessels leads to cinsumption of clotting factors and platelets leads to bleeding elsewhwre can be acute or chronic Chronic form- malignant cancer pts liver and bone marrow have time to replenish more thromboses acute form-s econdary to other disorders thrombosis and hemorrhage
76
DIC paradox disorder!
intravascular clotting- contact of blood w/ damaged endothelium-coag factors rapidly consumed fibrinolysis begins- remove clot coagulation, anticoag, fibrinilysis lead to hemorrhage acrocyanosis- cold mottled fingers and toes
77
Hepatic disease
common complication---b/c factors produced in liver hepatic dz alters function and production of factors also alters bile production and transport!

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