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Year 3 Human Disease > Blood Coagulation and Bleeding Disorders > Flashcards

Blood Coagulation and Bleeding Disorders Flashcards

1
Q

% make up of blood (plasma, WBC/ platelts, RBCs)

A

plasma: 55%
RBCs: 45%
WBC and platelets:

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2
Q

stages when there is damage to blood vessel wall (see diagrams) 7

A
  1. collagen and tissue factor TF exposed
  2. von willebrand factor VWF binds collagen
  3. platelets adhere to VWF-collagen
  4. platelets are activated (PRIMARY HAEMOSTASIS, PLATELET PLUG)
  5. TF and platelets activate clotting factors to make thrombin (CLOTTING CASCADE)
  6. thrombin converts fibrinogen to fibrin clot
  7. stable fibrin-platelet clot is formed
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3
Q

consequences of failure of haemostasis

A

inc bleeding

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4
Q

2 things that increase bleeding in mouth

A
  • oral mucosa highly vascular

- saliva contains fibrinolytic substances and rich in bacteria

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5
Q

2 categories of things that can go wrong with haemostasis

A
  • abnormal primary haemostasis (less platelet number/ function or less VWF)
  • abnormal coagulation pathway (reduced clotting factors)
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6
Q
  • identify causes of pictures*
    a. what are petechiae
    b. what is epistaxis
    c. what is menorrhagia
A

a. small bruises
b. nose bleeds
c. abnormally heavy periods

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7
Q 
p= primary haemostasis disorders
c= coagulation factor disorders
write p, c or both for these symptoms:
a. bleeds in to joints
b. soft tissue joints
c. petechiae/ bruising
d. epistaxis
e. gum bleeding
f. menorrhagia
g. GI/ CNS
A

a. bleeds in to joints: c
b. soft tissue joints: c
c. petechiae/ bruising: p
d. epistaxis: p
e. gum bleeding:p
f. menorrhagia: p
g. GI/ CNS: c+p

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8
Q

3 parts of clinical evaluation to identify patients with abnormal haemostasis

A
  • bleeding history after previous dental tx/ surgery/ minor trauma
  • general medical history
  • drug history (anticoagulants)
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9
Q

2 lab tests used to identify patients with abnormal haemostasis

A
  • full blood count (counts platelets BUT not function- could miss some abnormalities)
  • clotting screen (proothrombin time PT and aPTT)
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10
Q

does abnormality inc or dec PT and aPTT

A

increase

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11
Q

what is INR ratio of

A

patient PT to normal PT

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12
Q

name 2 heritable disorders

A
  • von willebrand disease

- haemophilia A (factor VIII deficiency)

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13
Q

name 4 acquired disorders

A
  • reduced platelet number (eg AITP, leukaemia)
  • liver disease
  • kidney disease
  • anti-coagulant/ antiplatelet drugs
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14
Q

inheritance ofVWs disease

A

autosomal –> 1/100, M=F

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15
Q

treatment of VWs disease 3

A

-desmopressin (DDAVP)- releases endogenous fVIII/ VWF. sc or in
-tranexamic acid- reduces clot breakdown. po or mouthwash
exceptional circumstances: VWF transfusion

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16
Q

usual cause and explain immune thrombocytopenia

A

idiopathic or 2’ eg infection

autoantibodies attack platelets –> reduced platelet number –> abnormal primary haemostasis

17
Q

common symptom of immune thrombocytopenia

A

skin purpura on lower limbs

18
Q

what causes a purpura

A

capillary-level bleed in to skin

19
Q

2 categories of treatment of immune thrombocytopenia and examples

A
  • long term disease control (immunosuppression with steroids/ iv immunoglobulin, splenectomy)
  • treatment of bleeding: tranexamic acid, platelet transfuion (emergencies only, will just be destroyed by autoantibodies)
20
Q

how does immunoglobulin work to treat immune thrombocytopenia

A

coats reticuloendothelial cells in spleen –> prevents binding and destruction of platelets

21
Q

effects of liver disease in blood coagulation

A

EVERYTHING:

  • reduced production of all coagulation factors
  • low platelet count
  • abnormal primary haemostasis
  • abnormal coagulation pathway
22
Q

treatment of bleeding in liver disease 3

A

-tranexamic acid
-vit K
fresh frozen plasma for emergency tx of bleeding

23
Q

2 types of drugs that affect haemostasis and how they work and diseases they’re used with

A

PLATELETS-ARTERIES, COAG-VEINS

  • anti-platelets: inhibit arterial thrombosis (IHD, PVD, CD)
  • anti-coagulants: inhibit coagulation pathway/ venous thrombosis (DVT, PE, CVA in AF, CVA from mechanical heart valves, CPB
24
Q

name antiplatelet types 2/ examples

A
  • permanently inhibit platelet activation: aspirin/ clopidogrel
  • unintentional platelet effects: NSAIDS, SSRIs, statins etc
25
Q

how to overcome antiplatelet effect of drugs when not wanted

A

stop medication and wait 5-7 days for synthesis of new platelets

26
Q

name main anticoagulant and how it works

A

warfarin

prevents synthesis of clotting factors II, VII, IX, X –> inc PT, aPTT

27
Q

what is warfarin used to control

A

long term tx / prevention of venous and arterial thrombosis

28
Q

what should INR be between

A

2-3

29
Q

how often is INR checked

A

4-6 weekly

30
Q

what INR is too high

A

5

31
Q

what is LMW and unfractioned heparin used for

A

prevention of venous and arterial thrombosis (urgent tx and pregnancy)

32
Q

how are the following administered

a. LMW heparin
b. unfractioned heparin

A

a. LMW heparin: subcutaneous injection

b. unfractioned heparin: IV

33
Q

how are the following monitored

a. LMW heparin
b. unfractioned heparin

A

a. LMW heparin: does not require monitoring

b. unfractioned heparin: using aPTT

34
Q

how do LMW heparin and unfractioned heparin work

A

inhibit coagulation factors

35
Q

3 dental procedures relevant to pts with bleeding disorders

A
  • multiple extractions
  • ID block
  • maxillofacial surgery
36
Q

what to do differently with warfarinised pts

A

INR 2-3 normally fine

37
Q

what to do differently for pts with inherited haemostatic disorders

A

discuss with haematologist and devise management plan

Year 3 Human Disease (28 decks)

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