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Year 5 Pathology Revision > Haematology 3: Haemostasis And Bleeding Disorders > Flashcards

Haematology 3: Haemostasis And Bleeding Disorders Flashcards

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1
Q

List 4 Pro-coagulant factors in the body?

A

Platelets
vWF
Endothelium
Coagulation cascade

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2
Q

List 4 Anti-coagulant factors in the body ?

A

AT (antithrombin)
Protein S + Protein C
TFPI (Tissue factor pathway inhibitor)
Fibrinolysis

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3
Q

List 2 thrombopoietic factors ?

A

Thrombopoietin
IL-6
IL-12

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4
Q

Which Surface glycoprotein do platelets use to bind to vWF ?

A

GpIb (more important route)

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5
Q

Which glycoprotein do platelets use to bind directly to collagen ?

A

GpIa

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6
Q

Which glycoproteins do platelets use to bind to other platelets when aggregating ?

A

GpIIb/IIIa (fibrinogen receptor)

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7
Q

Which 2 mediators do platelets release when they bind to subendothelial structures (vWF or collagen) to cause platelet aggregation ?

A

ADP

Thromboxane A2

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8
Q

How does Aspirin inhibit platelet aggregation?

A

aspiring irreversibly Inhibits Cyclo-oxygenase (COX)
This prevents Arachidonic acid being converted to cyclic endoperoxides
This prevents formation of thromboxane A2
Less Thromboxane A2 means less platelet aggregation

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9
Q

List 2 drug targets for inhibiting platelet aggregation ?o

A

Thromboxane A2 production - Aspirin

ADP receptors - Clopidogrel

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10
Q

Which pathway is more important for coagulation in the human body ?

A) Intrinsic pathway
B) Extrinsic pathway
C) Contact activation pathway

A

B) extrinsic pathway

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11
Q

Describe the sequence of events in the Initiation phase of the Clotting cascade ?

A

1) Damage to endothelium causes TF to be exposed
2) Factor 7 binds to TF and becomes activated to F7a
3) F7a/TF complex activate F9 and F10 to F9a and F10a
4) F10a binds to F5a –> first step in the coagulation cascade

TF7a - 9a + 10a - 10a+5a

note: people with factor V leiden cannot beind factor 5a to factor 10a

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12
Q

Describe the sequence of events in the amplification phase of the clotting cascade ?

A

1) activated factors 10 + 5 results in formation of a small amount of thrombin
2) thrombin will activate platelets
3) also activates factor 11 which activates factor 9. activated factor 8 and recruits more factor 5a
4) factors 5a, 8a, 9a bind to the activated platelet - last phase of clotting cascade

thrombin - F11a -9a, 8a, 5a - 5a,8a,9a –

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13
Q

Describe the sequence of events in the propagation phase of the clotting cascade ?

A

1) the activated platelet with factors 5,8+9 recruit factor 10a
2) results in generation of large amounts of thrombin (thrombin burst)
3) converts fibrinogen to fibrin
4) enables formation of a stable fibrin clot

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14
Q

Which 4 clotting factors are vitamin K dependent ?

A

10
9
7
2

Think 1972
made in the liver
vitamin K required as a coenzyme for gamma carboxylation of the clotting factors

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15
Q

What is the role of tPA (tissue plasminogen activator) ?

A
  • Converts plasminogen to plasmin
  • Plasmin cleaves The fibrin clot

tPA is produced by the endothelium

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16
Q

Which of these molecules does not promote Plasminogen conversion to Plasmin ?

A) tPA
B) Urokinase 
C) FXIIa
D) FXIa 
E) PAI 1
A

E) PAI1

Plasminogen activator inhibitor inhibits Plasminogen conversion to Plasmin by inhibiting Urokinase and tPA

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17
Q

What does TAFI do ?

A

TAFI (thrombin Activated Fibrinolysis inhibitor) is a Thrombin dependent inhibitor of Fibrin breakdown

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18
Q

Deficiency of which component is the most Thrombogenic ?

A) TAFI
B) FVIIIa
C) AT3
D) vWF 
E) Protein S
A

C) AT3

Deficiency of Antithrombin (AT) is very rare but is the most thrombogenic

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19
Q

What is the role of Protein C and protein S ?

A

Inhibit FVIIIa and FVa

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20
Q

What is the role of Thrombomodulin ?

A

Thrombomodulin is an endothelial receptor for Protein C
It first needs to be activated by Thrombin.
EPCR is another receptor which helps Thrombomodulin bind to protein C

When Thrombomodulin binds to Thrombin and Protein C the complex is called APC (activated protein C)

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21
Q

What is the role of APC (activated protein C) ?

A

APC inactivates FVa and FVIIIa

Requires protein S as cofactor

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22
Q

What is different in the interaction between APC and FVa in people with Factor V Leiden ?

A

People with Factor V Leiden have APC resistance.

This means activated factor V is not inactivated by APC.

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23
Q

What is the physiological role of TFPI as an anticoagulant ?

A

TFPI neutralises the TF/FVIIa complex.

TFPI is produced as a result of TF/FVIIa complex formation in order to stop activation by the extrinsic pathway. (TF/FVIIa is only required for a very short time to activate FX and FIX)

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24
Q

What disease is associated with large platelets ?

A

grey platelet syndrome

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25
What is ITP (immune thrombocytopenia purpura) ?
Autoantibodies against platelets | This causes the platelets to b e removed and destroyed by the immune system
26
List 2 common inherited disorders of coagulation (bleeding disorders) ?
Haemophilia A / B | Von willibrand disease
27
Which coagulation factors are deficient in: Haemophilia A Haemophilia B
Haemophilia A - Factor 8 | Haemophilia B - Factor 9
28
What is the inheritance pattern of haemophilia A /B ?
X-linked
29
What happens to APTT and PT in Haemophilia A/B ?
APTT - INCREASED PT- normal APTT Is a measure of the intrinsic pathway
30
List 3 clinical features of haemophilia A/B ?
Haemarthroses (bleeding into joints) Prolonged bleeding after surgery Ecchymoses
31
How is vWD inherited ?
Autosomal dominant
32
What are the differences in type1, type 2 and type 3 vWD ?
Type 1- partial quantitative defficiency in vWF Type 2- Partial Qualitative decency in vWF Type 3- Complete quantitative deficiency in vWF
33
How does most of vWF circulate in the blood ?
Most of it is bound to factor 8
34
What happens to APTT, PT, TT and fibrinogen in DIC ?
APTT- prolonged PT- prolonged TT- prolonged Fibrinogen- decreased
35
What are 3 treatments of Vitamin K deficiency ?
I.V Vitamin K FFP PCC (Prothrombin complex concentrate) Vit K dependent coagulation factors
36
List 3 differences in clinical presentation of Coagulation and platelet disorders ?
Platelet disorders - Superficial bleeding (petechia) - mucous membrane bleeding - epistaxis, gym, vaginal, GI - bleeding immediately after surgery - small, superficial ecchymoses Coagulation disorders - Deep bleeding into Joints (haemarthroses)/muscles - delayed bleeding after surgery/trauma - no prolonged bleeding after cuts
37
List 2 congenital causes of Vascular defects of coagulation ?
Older-Weber-rendu syndrome | Ehler’s danlos syndrome
38
List 3 acquired vascular defects of coagulation ?
Dengue haemorrhagic fever Scurvy Meningococcal infection
39
What is the treatment of Haemophilia A / B ?
Factor 8 / 9 concentrates replacement therapy
40
Which drug is used in the treatment of Haemophilia A ?
Desmopressin (causers increased vWF release from the endothelium. vWF is a factor VIII carrier)
41
Name 1 carrier protein of Factor VIII ?
vWF
42
Describe how you can used Ristocetin to test for vWD ?
Add Ristocetin to the patients vWF and platelets in a test tube. Ristocetin normally causes vWF to find to Gp1b on platelets causing platelet aggregation. If there is no platelet aggregation then this means there is a qualitative defect in vWF or Gp1b (Bernard soulier syndrome).
43
what 3 responses does vessel injury stimulate
vasoconstruction platelet activation activation of the coagulation cascade
44
what is the role of the endothelium in coagulation
``` barrier produce: - prostaglandins - vWF - plasminogen activators - thrombomodulin ```
45
where do platelets originate from
bone marrow made by megakaryocytes life span of 10 days production regulated by thrombopoietic factors (thrombopoietin, IL-6, 1L-12)
46
describe the structure of platelets
glycoproteins - cell surface proteins use dto interact with the endothelium, vWF and other platelets dense granules - contain energy stores (ATP, ADP) open canalicular system, microtubules, actomyosis - pl can expand their surface area
47
how are aspirin and NSAIDs different
NSAIDs reversibly inhibit COX | aspirin reversibly blocks COX
48
role of prostaglacyclin PGI2 in platelet function
inhibits platelet aggregation
49
what other receptor is also important for platelet aggregation
ADP receptors | inhibitors = clopidogrel, ticagrelor
50
what is the rate limiting step for fibrin formation
factor Xa
51
what are the 5 main effects of thrombin
``` activates fibrinogen activates platelets activates pro-cofactors (5 and 8) activates zymogens (7,11,13) all link together to form a prothrombinase complex - activates prothrombin to thrombin ```
52
what is the role of the prothrombinase complex
made up of factor 10a and factor 5a | converts prothrombin - thrombin
53
what are some causes of vitamin K deficiency
most common = warfarin antibiotics obstruction of biliary tree
54
describe the process of fibrinolysis
plasminogen - plasmin - fibrin --> fibrin degradation products tPA - made by endothelium and converts plasminogen to plasmin urokinase can also activate plasminogen to plasmin tPA and urokinase are inhibited by plasminogen activator inhibitor 1+2 plasmin is inhibited by alpha 2 antiplasmin + alpha 2 microglobulin TAFI (thrombin-activatable fibrinolysis inhibitor) is an important inhibitor of fibrin breakdown
55
describe the action of physiological anticoagulants
ANTITHROMBINS: - bind thrombin 1:1 then excreted in the urine - most active = AT III - lack or deficiency = the most thrombogenic condition PROTEIN C+S: - to stop thrombin generation, f 5 and 8 need to be inactivated - trace amounts of thrombin generated at the start of the cascade activate thrombomodulin opens up the receptor for thrombomodulin to bind protein C through EPCR - forms APC - APC, in the presence of protein S fully activates protein C - inactivates factor 5a and 8a TISSUE FACTOR PATHWAY INHIBITOR: - as soon as tissue factor and factor 7 released in the first step of the coagulation cascade - TFPI is activates to neutralise the TF-F7a complex
56
what are two causes of APC resistance
mutated factor 5 (eg factor V leiden) - factor 5a resistant to breakdown by APC --> prothrombotic state high levels of factor 8
57
list some genetic causes of excessive bleeding
platelet abnormalities vessel wall abnormalities clotting deficiencies excess clot breakdown
58
list some inherited causes of excessive bleeding
``` liver disease vitamin K deficiency AI disease trauma anticoagulants/antiplatelets ```
59
what causes pseudothrombocytopaenia
platelets clump together
60
list different platelet disorders
decreased number (thrombocytopaenia): - decreased production - decreased survival (ITP) - increased consumption (DIC) - dilution defective platelet function: - acquired (aspirin, end-stage renal failure) - congenital (thrombasthenia) - cardiopulmonary bypass
61
list things that can cause thrombocytopaenia
IMMUNE: drug induced -quinine, rifampicin, vancomycin rheumatoid arthritis, SLE sarcoidosis NON-IMMUNE : DIC MAHA IDIOPATHIC THROMBOCYTOPAENIC PURPURA
62
describe features of ITP
autoantibodies generated against platelets platelets then destroyed in the reticuloendothelial system (spleen, liver, bone marrow - anywhere with macrophages) childhood ITP - acute following illness, self-limiting adult - chronic and indolent hematomas and subconjunctival haemorrhages
63
how can we treat ITP
depends on platelet count and symptoms steroids IVIG - cometes with anti-platelet antibodies
64
list inherited and acquired coagulation factor disorders
inherited: - haemophilia A dn b - vWD acquired: - liver disease - vitamin K deficiency/warfarin - DIC
65
what is haemophilia
congenital deficiency of factor 8 or 9 deep bleeding into joints and muscles x-linked recessive abnormality of intrinsic pw so get PROLONGED APTT , NORMAL PT need clotting factor replacement for life haemophilia A - factor 8 deficiency, B - factor 9 deficiency
66
clinical features of haemophilia
haemarthroses (most common) soft tissue haematomas prolonged bleeding after surgery or dental extractions
67
describe features of VWD
most common coagulation disorder autosomal dominant mucocutaneous bleeding measure vwf antigen/ vwf activity/multimer
68
classification of VWD
type 1 - partial quantitative deficiency 2 - qualitative deficiency 3 - total quantitative deficiency
69
describe vitamin K deficiency `
sources: green veg and intestinal flora factors 1972 and protein C,S,Z need vit K causes: malnutrition, biliary obstruction, malabsorption, antibiotic therapy treat: vit K and FFP
70
features of DIC
``` emergency activation of coagulation and fibrinolysis triggered by: - sepsis - trauma - obstetric complications - malignancy - vascular disorders - reaction to toxins eg snake venom ``` systemic activation of coagulation - deposition of fibrin in small vessels - kidney damage, brain damage, damage to extremities
71
clotting study results in DIC
``` prolonged APTT prolonged PT prolonged TT decreased fibrinogen decreased FDP decreased platelets schistocytes ```
72
treatment of DIC
``` treat underlying disorder anticoagulation with hepatin platelet transfusion FFP coagulation inhibitor concentrate (APC concentrate) ```
73
why does liver disease lead to bleeding disorders
``` decreased synthesis of 2,7,9,10,11 and fibrinogen dietary vitamin K deficiency dysfibrinogenaemia enhanced haemolysis DIC thrombocytopenia due to hypersplenism ```
74
describe treatment for prolonged PT/PTT
vitamin K 10mg od | FFP
75
treatment for low fibrinogen
cryoprecipitate
76
list some new anticoagulants
``` tissue factor pathway inhibitors factor 9a inhibitors protein C activators factor 10a inhibitors - fondaparinux, rivaraxaban, apixaban thrombin inhibitors ```
77
key features of the intrinsic pathway
APTT monitor heparin therapy starts with factor 12 ( - 11 - 9 - 8 - 10 )
78
key features of the extrinsic pathway
PT monitor warfarin therapy (INR) starts with factor 7
79
key features of the common pathway
TT | starts with activated factor 5
80
diagnosis and treatment of haemophilia A
high APTT, normal PT, low factor VIII assay avoid NSAIDs and IM injections, factor VIII concentrate replacement life-long
81
diagnosis and treatment of haemophilia B
clinically similar to haemophilia A | treat with factor IX concentrates
82
diagnosis of vWD
low platelet function low factor VIII (vWF faces factor VIII in the circulation) mainly AD high APTT, high bleeding time, low factor VIII, low vWF, normal INR and platelets
83
diagnosis of DIC
low platelets, low fibrinogen, high FDP/D-dimer, long PT/INR

Year 5 Pathology Revision (106 decks)

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