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SBM Haeme > 2013-10-28 Intro to Coagulation > Flashcards

2013-10-28 Intro to Coagulation Flashcards

0
Q

fibrinogen
—where made?
—fxn?
—stored?

A

made in liver
circulates in plasma
fxn is to aggregate platelets to one another by cross-linking GpIIb/IIIa

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1
Q

vWF

  • made where?
  • synth?
  • fxn?
A
  • MADE: most from endothelium (multimers stored in Weibel-Palade bodies) megakaryoccytes (multimers stored in alpha granules);
  • SYNTH: multimers —-ADAMSTS13—-> monomers
  • FXNS: [1] tether platelets to basement membrane, [2] chaperone Factor VIII
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2
Q

normal endothelial coags

A

PGI2 (prostacyclin), NO, Heparins

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3
Q

Bernard-Soulier Dz

A

lack Gp1b
platelets can’t find to basement membrane
-big platelets (B.ig S.uckers) but thrombocytopenia

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4
Q

Glanzmann’s Dz

A

GpIIb/IIIa deficieny —> no platelet aggregation

—similar to action of abciximab

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5
Q

Steps of 1° Hemostasis

A
  1. vasoconstriction (neurogenic + endothilin)
  2. platelet adhesion (BM–vWF–Gp1b–Plt)
  3. platelet activation/degranulation
    —ADP-causes expression on GpIIb/IIIa
    —TXA2-calls other platelets
    —Other agonists: 5-HT, thrombin, epi, collagen
  4. platelet adhesion
    —PLT—GpIIb/IIIa-< fibrinogen>-GpIIb/IIIa—PLT
  5. Support of coag with PF3 (platelet factor 3): phosphatidyl serine (PS) & phosphatidyl ethanolamine (PE)
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6
Q

Scott’s Dz

A

missing PF3 (platelet factor 3) = phosphatidyl serine + p. ethanolamine

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7
Q

Secondary Hemostasis

  • -main point
  • -where does it occur?
  • -where are factors made?
A

POINT: ∆ cross-linking fibrinogen into FIBRIN using enzyme THROMBIN which comes from prothrombin
OCCURS: within the membrane of the platelet
–all the factors are made in the liver, except VIII (platelets)

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8
Q

Extrinsic pathway….GO!!!!

A

HERE WE GO
1. TF is released by damaged tissue
2. VII—-TF—->VIIa
3. FT-VIIa forms “extrinsic tenase” by activating:
—X to Xa directly
—IX to IXa which forms extrinsic tenase (IXa-VIIa-TF)
4. X—-IXa-VIIa-TF-Ca++—->Xa
5. prothrombin (II)—-Xa-Ca++—->thrombin (IIa) s…l…o…w…l…y

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9
Q

Intrinsic pathway….GO!

A
  1. The small amts of thrombin made thru extrinsic path activating XII* and XI
    —*XII (Haegman factor) not necess. in vivo, but it:
    ——activates HMW kininogen —> binds PK + XI
    ——activates PK—>kallikrein
    ——activates XI—>XIa
  2. XIa causes THROMBIN BURST
  3. This makes lots of IX—>IXa
  4. X—->INTRINSIC TENASE: IXa + VIIIa (from platelets)—->Xa
  5. II—->Xa + Va—->IIa
  6. I—->IIa—->Ia (fibrin!!)
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10
Q

Which steps need Ca2+?

A 
intrinsic tenase (VIIa-TF + IXa)
extrinsic tenase (VIIIa + IXa)
prothrombinase (Xa + Va)
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11
Q

Which factors require Vitamin K?

A

II, VII, IX, X

-proteins C&S

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12
Q

Besides activating fibrinogen—>fibrin, what else does thrombin do?

A

—amps up its own prod via V, VIII, IX
—activates VIII which stabilizes thrombin
—agonist of plts
—stimulates PAI-1 to inhibit fibrinolysis
—also INHIBITS coag: binds thrombomodulin to activate Prot C & S

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13
Q

How is clotting controlled?

A
  1. blood flow removes factors
  2. reticuloendothelial system (esp liver) removes activated factors
  3. thrombin’s anth-thrombotic effects
  4. anti-thromb proteins of endothel: Prots C&S, antithrombin, TFPI
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14
Q

antithrombin

A
  • made by liver and endothlium
  • inhibits: thrombin, Xa and XIa
  • potentiated by HEPARIN 1-4k fold!
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15
Q

activated proteins C&S

A
  • circulate in inactive form

- need vitamin K

16
Q

TFPI (tissue factor pathway inhibitor)

A

binds and inactivates Xa

17
Q

How does fibrinolysis go down?

A

Plasminogen—->tPA/uPA*—->plasmin**
*inhib by PAI1 (plasminogen activator inhibitor) **alpha2-antiplasmin
fibrin—->plasmin—->D-dimers, etc.

18
Q

quantitative platelet tests

qualitative platelet tests

A

QUANT: CBC, smear
QUAL: PFA-100, bleeding time, plt aggr studies, also smear

19
Q

Lab tests for 2° hemostasis/fibrin formation

A
  • PT/INR
  • aPTT (activated partial thromboplastin time)
  • mixing studies
  • individual factor assays
  • thrombin time
  • fibrinogen
  • D-dimers
20
Q

What does thromboplastin (as in aPTT) mean?

A

*thromboplastin = TF + phospholipid

21
Q

aPTT

A 
activated partial thromboplastin time
—INTRINSIC path (T-T couple still together mnemonic)
—measure in vitro things: XII, PK, HK
—VIII, IX, XI
—common path, too: X, V, II*, I**
*II = prothrombin
*I = fibrinogen
22
Q

PT/INR

A

Prothrombin Time
—EXTRINSIC (T-T couple broke up/”ex” mnemonic)
—measures VII + common path (X, V, II, I)
—nl INR = 1
—tests warfarin but not heparin b/c it is degraded

23
Q

What top tube should you use when drawing blood for coag panel?

A

light blue top!
—contains citrate which binds Ca2+
—Ca2+ added back in the lab

24
Q

Top to use with CBC + additive

A

purple

—has EDTA as anti-coag which preserves cell morphology

25
Q

serum vs. plasma

A 
serum = fluid left after clot is formed (i.e. does not have coag factors)
plasma = fluid part of blood pre-clot
26
Q

Pseudo-thrombocytopenia

A

some folks’ platelets clump when exposed to EDTA

—verify thrombocytopenia reading w/ smear to look for clumps

27
Q

ITP

  • cateogry
  • presentation
  • labs
  • tx
A

QUANT THROMBOYTOPENIA: Immune thrombocytic purpura
—most common cause of thrombocytopenia in kids & adults
—ACUTE: kids, ~wks s/p viral infx or vaccin; self-limited w/in wks
—CHRONIC: adults, usu women of child-bearing age; 1° or 2° (e.g. due to SLE. [may cause short-lived thrombocytopenia in infants b/c IgG cross the placenta]
—Common in HIV
—anti-platelet abs made in spleen—>plts eaten in spleen
—labs: plts roids; adults: IVIG, splenectomy

28
Q

TTP

  • category
  • cause
  • s/sx
  • labs
A

QUANT THROMBOYTOPENIA: Thrombotic Thrombocytopenic Purpura
—decr ADAMSTS13: vWF multimers pile up —> abnl plt adhesion
—s/sx: pentad:1)MAHA, 2)thrombocytopenia, 3) fever, 4) neuro ∆s, 5) renal failure [neuro > renal vs HUS]
—labs: thrombocytopenia, incr bleeding time, anemia w/ schistocytes shorn off by that platelet plug), incr megakaryocytes **nl PT/aPTT

29
Q

TCT
—what?
-how
—explanation for prolonged TCT?

A 
Thrombin clotting time
—detect fibrinogen deficiency or abnl
—add bovine thrombin to pt plasma, measure clotting time in sec
—hypofibrinogenemia
—dysfibrogenemia
—heparin, thrombin inhibs
30
Q

presentation of quantitative platelet d/o

—general causes

A

not clinically serious until <20k
—bruising, petichiae, mucosal bleeding (nose, gums, GI)
—menorrhagia
—destruction, consumption, sequestration, decr prod

31
Q

destructive thrombocytopenia b/c of meds

A

QUANT THROMBOYTOPENIA: med-induced
quinine: low plts and bleeding
abx
heparin **rarely causes a hypercoaguable state in some pts

33
Q

HELLP

  • category?
  • stands for
A

QUANT THROMBOYTOPENIA: HELLP Syndrome

  • Hemolysis, Elevated Liver enzymes, Low Platelets
  • similar to TTP
34
Q

thrombocytopenia 2° to splenomegaly

  • category
  • common causes of splenomegaly
A

SEQUESTRATION
-nl holds 30% of circ plts at any given time
-enlarged can hold >90%!
Causes: portal HTN (cirrhosis, portal or hepatic vein thrombosis), myeloproliferative d/o

SBM Haeme (14 decks)

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