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Medical Physiology > Coagulation > Flashcards

Coagulation Flashcards

Learn coagulation pathophysiology and disorders

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USMLE® Step 1 flashcards
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
Q

How does warfrin work?

A

warfrin is a vitamin K agonist

pulls out vitamin K–causing disruption of coagulation leading to bleeding out

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26
Q

Are coagulation factors always for clot making?

A

nope!

protein C and protein S dont make clots

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27
Q

Protein C function

A

INACTIVATES factor V and VIII

prevents clot formation

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28
Q

Protein S function

A

Stimulates release of TPA (tissue plasminogen activator)

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29
Q

Fibrin clot formation

A

2 pathways
intinsic and extrinsic

both pathways work together

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30
Q

what is function of factor X in both the intrinsic and extrinsic pathway?

A

act as common final pathway at end of both

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31
Q

Intrinsic pathway

A

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
Q

Extrinsic pathway

A

trauma of vascular wall-crushing of vessel, shearing/trauma, cutting finger

factor III activates VII—VIIa activates X

33
Q

Intrinsic pathway factors are

A

Factor XII, HMWK, prekallikrien, factor XI

34
Q

Extrinsic pathway factors are

A

factor III, factor VII

35
Q

Fibrin clot at end of BOTH pathways is initiated by what factor?

A

by factor Xa in presence of

factor V, calcium, phospholipids

36
Q

Factor V does what in the common final pathway?

A

interacts with prothrombin to change prothrombin which is soluable to insoluable form: thrombin

37
Q

Once thrombin is activated what happens?

A

Cleaves fibrinogen to fribrin and activates factor XIII

forms insoluable clot to aid in clot retraction

38
Q

What is fibrinolysis

A

Clot dissolution, tearing clot apart

initiated along with clot formation…clot is being both destroyed and built

39
Q

Factors XII, HMWK, kallikrein, thrombin

A

release plasminogen activators (TPA)

cleave plasminogen to plasmin

40
Q

What is the function of plasmin

A

plasmin digests fibrinogen and fibrin (insol version)

inactivates factor V and factor VIII

41
Q

What is the purpose of fibrinolysis

A

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
Q

Evaluation -clinical assessment requires…

A

fam hx, location, severity
duration, med hx

most signs are skin/mucous membranes

pale or jaundiced

bruise easily

43
Q

Petechiae

A

Flat, pinpoint, non-blanching red or purple spots
push them = no color change
indicate CAPILLARY bleeds
vascular/platelet disorder

44
Q

Purpura

A

petechia in groups/patches

often pruritic

45
Q

ecchymosis

A

blood escapes to tissues

aka bruise

46
Q

hematoma

A

raised ecchymosis

47
Q

hemarthrosis

A

bleeding into joint

48
Q

telanflectasia

A

lesion from capillary + small artery dialaiton—blanch and bleed-spider lesions

49
Q

Hematochezia-melena
hematuria-bloody urine
hematemisis-bloody vomit
hemoptysis =?

A

hemoptysis=gastric drainage that is bloody

menorrhagia=excessive menstrual bleeding

50
Q

Vascular disorders primary cause is

A

bleeding problem with vascular component of primary hemostasis

can be acquried or inherited

51
Q

Vascular Pupura

What is it?

What causes it?

What are the 2 special forms?

A

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
Q

Structural abormalities of blood vessels are mechanism for some types of vascular purpura, can be inherited or acquired

A

good to know lol

53
Q

Ehlers-Danlos syndrome, osteogenesis imperfecta

A

vascular purpura

caused by decreased and poor quality of collagen and elastin

54
Q

Scurvy

A

vasculat purpura caused by defective collagen

55
Q

Loss of sub Q fat causes purpura because

A

skin mobility begins to shear vessels

old people/those with rapid weight loss

56
Q

How do steroids cause vascular purpura

A

destroy support tissues

57
Q

Vascular purpura

lesion behavior: 
   allergic 
   drug induced 
   inherited forms 
  scurvy
A

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
Q

Hereditary hemorrhagic telangiectasia

aka?
type of genetic disease
happens where?
describe lesions

what is most common clinical problem

what worsens this condition

A

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
Q

Platlet disorders are?

examples of them are? (3)

A

abnormality in quantity or qualirt of thrombocytes

thrombocytopenia
thrombocytosis
qualitative platlet disorders

60
Q

Thrombocytopenia

common cause of what?
causes of it?

A

common cause of gen bleeding

many causes

61
Q

Thrombocytopenia

idiopathic thrombocytopenia purpura is what?

acute ITP
chronic ITP

A

immune mediated

acute itp - follows acute viral infection

chronic itp- insiduous/women

62
Q

four mechanism for thrombocytopenia

A

decreased platelet production, descreased platelet survival, splenic sequestration, platelet dilution

63
Q

Thrombocytosis

is what?

follows?

secondary response to?

A

is an excessive platelet numbers

transitory following stress or excercise

secondary responce to hemorrhage, inflam disease, malignancy, infection, hemolysis, splenectomy

64
Q

3 forms of thrombocytosis

A

primary- abnormal megakaryocyte proliferation
hemorrhaging and thrombotic complications

secondary - actual production increase

transitory - release of preformed

65
Q

Qualitative platelet disorders

A

acquired disorders common
drugs
with uremia
co existing hemotalogic dz

one aspect of platelet function is abnormal

66
Q

Coagulation disorders

give examples

A

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
Q

Hemophilia
is what?
dx when?

A

most common, severe inherited coag disorder

neonatal dx - too much bleeding

- following circumsicison 
- following vit k injection
68
Q

Hemophilia A

A

classic form
VIII deficit
x linked recessive

69
Q

Hemophilia B

A

factor IX deficit

classified by extent coag factor is deficit

70
Q

Hemo A vs Hemo B

A 
hemo A 
    x linked recessive 
    VIII deficit 
hemo b
    factor iX deficit
71
Q

Von willebrand dz

what is it?
problem?

s/s?

A

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
Q

Vitamin K deficiency

A

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
Q

factor II, VII, IX, X

A

all depend of vit k

74
Q

Acquired vitamin K deficiency

caused by changes to what important digestive secretion??

A

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
Q

Disseminated intravascular coagulation

what is it?

A

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
Q

DIC

paradox disorder!

A

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
Q

Hepatic disease

A

common complication—b/c factors produced in liver

hepatic dz alters function and production of factors

also alters bile production and transport!

Medical Physiology (4 decks)

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