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Pathology Term 3 > Week 6 - HAEMOSTASIS > Flashcards

Week 6 - HAEMOSTASIS Flashcards

Diagnosing Hemostatic Disorders, Bleeding Disorders, DIC, Hypercoagulability, Transfusion (76 cards)

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1
Q

What is placed in samples of blood and why?

A
  • blood sample in sky blue cap

- SODIUM CITRATE –> halts coagulation process and preserves coagulation factors (by blocking calcium)

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2
Q

What is normal bleeding time?

A

<10 mins

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3
Q

What does prothrombin time (PT) measure and when is it prolonged?

A
  • tests extrinsic and common pathway
  • prolonged in acquired disorders:
  • vit. K deficiency
  • liver disorders
  • warfarin Tx.
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4
Q

What is INR?

A

International Normalised Ratio

  • standardised PT value
  • correction for different thromboplastin reagents used (animal product)
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5
Q

What does an INR of 1 mean?

A

-pts. plasma has the same extrinsic pathway as that of a normal plasma corrected for various commercial reagents

** high INR = longer it takes for blood to clot

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6
Q

What is suspected if both PT + PTT are increased?

A

pathology is in the COMMON pathway

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7
Q

What does partial thromboplastin time (PTT) measure and when is it prolonged?

A
  • intrinsic + common pathways
  • prolonged in congenital bleeding disorders
  • hemophilias (A + B)
  • von Willebrand disease
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8
Q

When is thrombin time performed and what does it test?

A
  • when both PT + PTT are abnormal
  • tests fibrinogen levels (COMMON pathway)
  • *useful in DIC
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9
Q

When is FDP/D-Dimer increased?

A

DIC (clot breakdown occurring)

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10
Q

What are the test priniples for PT + PTT?

A

PT:
-animal tissue thromboplastin (with sodium citrate) –> FVIIa –> CLOT

PTT:
-kaolin + cephalin –> FXIIa –> FVIIIa/FIXa –> CLOT

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11
Q

What is suspected if a pts. plasma with increased PT/PTT is mixed with normal plasma and the PT/PTT corrects?

A

clotting factor deficiency

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12
Q

What is suspected if pts. plasma with increased mixed with normal plasma and the PT/PTT does not correct?

A
  • PT/PTT inhibited
  • therefore –> coagulation inhibitors

i.e. heparin; specific factor inhibitor (FVIII or FV); non-specific inhibitor (lupus anticoagulants)

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13
Q

What is a thromboelastogram (TEG)?

A
  • quick test before and during major surgery
  • measures clot formation, strength + lysis
  • global assessment of hemostatic function
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14
Q

What are the lab. findings (Plt count, BT, PT, PTT) for common hemostatic disorders:

  • ITP?
  • vWD?
  • Hemophilia?
  • DIC?
  • Aspirin?
  • Warfarin/Heparin?
A

ITP:

  • plt count –> low
  • BT –> high
  • PT –> normal
  • PTT –> normal

vWD:

  • plt count –> normal
  • BT –> high
  • PT –> normal
  • PTT –> high

Hemophilia:

  • plt count –> normal
  • BT –> normal
  • PT –> normal
  • PTT –> high

DIC:

  • plt count –> low
  • BT –> high
  • PT –> high
  • PTT –> high

Aspirin:

  • plt count –> normal
  • BT –> high
  • PT –> normal
  • PTT –> normal

Warfarin/Heparin:

  • plt count –> normal
  • BT –> normal
  • PT –> high
  • PTT –> high
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15
Q

Where is vWF located and what does this mean for its function?

A

Subendothelial region
-aidss plt. adhesion to endothelial defects

Plasma
-carries FVIII and prevents early degeneration

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16
Q

Clinically, what is the commonest bleeding disorder?

A

Thrombocytopenia

-commonest cause of bleeding

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17
Q

Outline plt production

A

thrombopoietin stimulates endomitotic synchronous nuclear replication of megakaryocytes –> cytoplasmic granulation –> cytoplasmic fragments separate out as platelets (loaded w coag. factors)

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18
Q

What is the lifespan of plts and what results afterwards?

A

8 - 9 days
-either involved in hemostasis
OR
-destroyed in spleen

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19
Q

Describe typical bleeding characteristics in thrombocytopenia

A

-superficial bleeding (capillary damage)

Clinically:

  • petechiae
  • purpura
  • ecchymosis
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20
Q

What hemostatic factors are contained in platelets?

A
  • ADP
  • calcium
  • vWF
  • PF4
  • fibrinogen
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21
Q

What are the causes of thrombocytopenia?

A
  • autoimmune, drugs, infections - viral
  • BM suppression
  • megaloblastic anemia
  • aplastic anemia
  • increased consumption (DIC, TTP + HUS)
  • Plt function disorders: - less common
  • vWD, Bernard Soulier syndrome, Glauzman thrombasthenia
  • plts are present but NOT functional
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22
Q

What is normal plt. count and what counts result in excess + spontaneous bleeding?

A

normal: 150 - 250 x 10^9/L
excess bleeding: <50 x 10^9/L (i.e. after trauma/surgery)
spontaneous bleeding: <20 x 10^9/L (severe and life-threatening)

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23
Q

What is ITP and what are the clinical features?

A
  • immune thrombocytopenic purpura
  • autoimmune disorder –> IgG Ab against plts –> plts destroyed in spleen –> thrombocytopenia

CF’s:

  • petichiae
  • purpura
  • ecchymosis
  • easy bruising
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24
Q

What are the 2 types of ITP?

A
  1. acute
    - children, post-infection, self-limited
  2. chronic
    - F (20-40yrs)
    - chronic + severe
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25
What are the lab. findings in ITP?
CBC: - thrombocytopenia - giant immature plts PT/PTT: -normal (coagulation is normal) BM: -immature megakaryocytes increased --> compensatory in response to loss of plts.
26
What are the common causes of viral haemorrhagic fevers and what is the pathogenesis?
Causes: -dengue, chikungunya, measles, malaria, yellow fever, Ebola, etc Patho: -endothelial damage by virus +/or anti-viral Abs --> vasculitis --> plt. activation --> thrombocytopenia --> bleeding *PT/PTT usually normal
27
What coag. factor deficiency is present in hemophilia A + B?
A --> FVIII | B --> FIX
28
What type of genetic abnormality is hemophilia + what does this mean?
x-linked recessive - increased in females (carriers) - increased in males (affected)
29
True or False? | -hemophilia A/B results in petichiae/purpura/ecchymosis
False - as coag. factors (NOT plts) are affected, bleeding is deep NOT superficial - increased wound bleeding and deep hematoma - joint bleeds (skin/mucosal bleeding in severe)
30
What is the therapy for hemophilia?
DDAVP -releases factors from endothelium FVIII/FIX concentrate
31
Where is vit. K found and what is it necessary for?
- green leafy veggies + intestinal bacteria | - necessary for carboxylation of factors 2, 7, 9, 10 in the liver
32
What are the causes of vit. K deficiency?
- diet - drugs - liver disease - warfarin inhibits vit. K action (to prevent thrombophilia)
33
Why is PT increased and PTT normal until late in vit. K deficiency/warfarin Tx.?
-factor VII (extrinsic pathway - PT) has the shortest half-life --> warfarin affects this factor first
34
What is vWD?
- von willebrand disease - low vWF --> deficiency of both platelet adhesion to damaged endothelium AND deficiency in FVIII - both plt. and coag. = abnormal --> superficial and deep bleeds
35
What is vWF produced by?
both plts. and endothelial cells
36
True or False? | -vWD is an x-linked recessive disorder
False - autosomal dominant - both males + females affected
37
Why is there increased BT despite normal plt. count in vWD?
- low vWF in vWD | - plts cannot function without vWF (cannot bind to collagen in endothelial defects) --> increased BT
38
Why is normal PT but PTT increased in vWD?
- vWF carries + protects FVIII | - no vWF in vWD = FVIII deficiency --> increased PTT
39
What is therapy for vWD?
fresh frozen plasma (FFP)/cryoprecipitate which contain vWF
40
What is DIC?
Disseminated Intravascular Coagulation | -systemic activation of coagulation --> consumption of coag. factors + plts --> severe bleeding
41
What is the cause/etiology of DIC?
-infection/trauma/cancer -release of tissue factor into circulation --> trauma OR -widespread endothelial damage --> infection
42
What is the pathogenesis of DIC?
activation of coagulation --> microthrombi --> infarction --> consumption of hemostatic factors --> bleeding --> activation of fibrinolysis --> excess fibrin breakdown
43
What are the clinical features of DIC?
- thrombosis - severe bleeding - shock - renal failure
44
What are lab Dx. for DIC?
- decreased coag. factors (deep) + plts (superficial) --> ALL tests abnormal - FDP + D-Dimer increased * life-threatening
45
What are the 2 clinical syndromes of thrombotic microangiopathy? and how do they differ to DIC?
1. thrombotic thrombocytopenic purpura (TTP) - adults 2. hemolytic uremic syndrome (HUS) - children - unlike DIC, coagulation factors remain normal or mild decrease - ONLY activation of plts.
46
What is thrombotic microangipathy?
- widespread thrombosis in microcirculation leading to organ infarctions + microangipathic hemolytic anemia (fragmented RBCs) * TTP + HUS
47
What are the predominant consequences of TTP + HUS?
TTP --> neurologic defects/strokes | HUS --> kidney failure
48
What enzyme is deficient in TTP? What is its normal function and how can one be deficient in it?
ADAMTS13 - protease which normally breaks down vWF multimers to stop plt activation - essentially, TTP is opposite to vWD as there is increased vWF --> increased plt. activation + loss --> extensive systemic thrombosis Acquired: -Ab to ADAMTS13 --> deficiency Congenital: -mutation --> ADAMTS13 deficiency
49
How is TTP treated?
-plasma exchange with fresh frozen plasma or cryoprecipitate to remove Ab or replace ADAMTS13 (previously 90% fatal)
50
True or False? | ADAMTS13 levels are decreased in childhood HUS
False - normal levels - E. coli/shigella infection + shiga toxin causing extensive endothelial damage --> plt activation
51
What is adult HUS?
TTP with predominant renal failure
52
What are the natural anticoagulants?
Protein C + S --> inhibit FVIIIa + FVa | Heparin --> inhibits thrombin (FIIa)
53
What is the most common anticoagulant drug + what does it inhibit?
warfarin - inhibits vit. K reductase - decreased vit. K dependent coag factors (2, 7, 9, 10)
54
What are the hereditary causes of hypercoagulability?
Factor V Leiden mutation - Factor V is resistant to protein C inhibition - uncontrolled factor V activation Protein C/S deficiency -decreased inhibition of FVa + FVIIIa
55
What are acquired causes of hypercoagulability?
- trauma, inflamm., cancer - heart disease, atherosclerosis, HTN, DM, etc - stasis of blood - drugs, Abs --> antiphospholipid antibody syndrome (AAS) * *Virchow's Triad (Blood - BV - Blood Flow)
56
What are clinical features of hypercoagulability?
THROMBOSIS - vein --> DVT (potential PE) - artery --> thrombosis; stroke - placenta (pregnancy) --> abortion
57
What is AAS + what Abs are involved?
antiphospholipid antibody syndrome - Abs to plt. phospholipids: 1. anticardiolipin 2. lupus anticoagulant N.B. following infection in children/pts with autoimmune dis./drugs
58
What % of SLE pts develop AAS?
30%
59
How does AAS differ clinically from in the laboratory?
- clinically, autoantibodies activate coagulation in body | - in lab. autoantibodies bind to phospholipid part of reagent --> prolong PTT
60
What is the lab Dx. of AAS?
- normal PT but prolonged PTT --> looks like deficiency but is hypercoagulability - PTT remains prolonged even after adding 50% normal plasma --> unlike factor deficiency
61
What is contained in fresh frozen plasma + cryoprecipitate and what are the indications for transfusion?
FFP --> all coag. facotrs --> bleeding cryoprecipitate --> factor 1, 8, 9, vWF --> specific deficiency *factor 1 = fibrinogen
62
What is the shelf-life of platelet concentrate?
5 days
63
Why are RBCs easier to match in transfusions compared to WBCs/plts?
WBCs/plts - have HLA Ag - difficult to match - more reactions/rejections RBCs - no HLA Ag - only major blood groups
64
What are the clinically significant blood group systems + why?
ABO + Rh | -naturally occurring strong IgM antibodies
65
What is the commonest + rarest blood group?
``` commonest = O+ rarest = AB- ```
66
What is Landsteiner Law?
when a person has a blood group Ag, corresponding Ab is ABSENT from plasma
67
What is the substance known as on red cell membranes that is modified by A, B, O genes?
H substance | -A, B, O genes control synthesis of enzymes that modify red cell membrane glycolipid (H substance)
68
What are the 3 genes involved in Rh system?
1. C/c 2. D/d 3. E/e Rh+ = D --> strong/clinically significant Rh- = d -little letter denotes negative
69
What is bombay blood group?
- absence of H substance in ABO blood system - anti-H antibodies present - clinically seen as O group
70
Compare IgG vs. IgM
IgG: - small, monomer - optimum reaction @37degrees - able to cross placenta - coat cells --> no agglutination - main type produced following preg./transfusion (alloantibodies) IgM: - large, pentamer - optimum reaction @-20degrees - does NOT cross placenta - agglutinates - often "naturally occuring" Abs - ABO blood group
71
What is a major + minor cross match?
``` major = donor RBC with pt. plasma minor = donor plasma with pt. RBC ``` --> to prevent hemolytic transfusion reaction
72
What is the purpose of Ab screening?
- many other Ags on donor RBC - additional Ab screening done to detect alloantibodies in pt. plasma with known reagent RBC (post transfusion/pregnancy)
73
What are the 3 main transfusion reactions and what are each caused by?
1. allergic --> plasma proteins 2. febrile --> Abs to donor leucocytes 3. hemolytic --> immune/mismatch
74
What are the Sx. of hemolytic transfusion reaction?
- hemoglobinuria - chest pain - apprehension - lower back pain - fever/chills - decr. BP/incr. RR - acute kidney failure*
75
Why is bacterial contamination of blood products more common with plts?
They are kept at increased temp. (22degrees)
76
What is "lookback program"?
-identify + notify recipients of blood products from previously negative/screened donor who is now positive for infectious agent

Pathology Term 3 (6 decks)

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