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Human Diseases > W18 65 non-malignant haematological conditions > Flashcards

W18 65 non-malignant haematological conditions Flashcards

1
Q

What are the 2 stages of haemostasis?

A

Primary haemostasis - formation of a platelet aggregate
Secondary haemostasis - formation of a stable fibrin clot

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2
Q

Describe the whole haemostasis process briefly (PG627)

A

Rupture of a thin fibrous plaque
Initial platelet adhesion
Rolling
Activation and firm adhesion
Platelet aggregation
Formation of a fibrin network
Recruitment of leukocytes
Net formation

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3
Q

What happens in primary haemostasis?

A

Rupture of the vessel wall, damage
Platelets bind to the underlying collagen (via von Willebrand factor)
Platelets are flowing along fast in the vessel wall, and meet the exposed bit of collagen
vWF binds to collagen and acts as an anchor which grabs the platelets out of the flowing vessel, slowing the platelets down so they roll
Collagen receptor can then bind to the platelets, activating them, so they release secondary mediators for their granules to allow other platelets to activate and they start sticking together and to the vessel wall.

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4
Q

What is needed to bind platelets?

A

Fibrin (end product of the coagulation cascade)

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5
Q

What occurs during secondary haemostasis?

A

The common pathway
The extrinsic and intrinsic pathways

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6
Q

What is the common pathway?

A

Factor X is cleaved and activated
Xa cleaves factor II (prothrombin) into thrombin (IIa)
Thrombin cleaves fibrinogen into fibrin
Factor XIII is also activated by thrombin, which cross-links fibrin.

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7
Q

What is the first thing to activate the common pathway?

A

Factor VII (extrinsic pathway)
Trauma to the blood vessels releases tissue factor which cleaves and activates factor VII
This kicks off factor X activation

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8
Q

What is the amplification step?

A

Intrinsic pathway kicking off the common pathway
Damaged cell membrane or thrombin will cleave/activate factor XII, which cleaves and activates factor XI, which cleaves and activates factor IX
Then factor IX causes activation of factor X etc

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9
Q

What else does thrombin do?

A

Feedbacks and activates the intrinsic cascade (via factor VIII)

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10
Q

What is the role of calcium in the clotting cascade?

A

Calcium also plays a role in activating the clotting factors

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11
Q

How do you detect a clot in a lab?

A

Tilt the tube
Mechanical stress device
Photo-optical

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12
Q

Is prothrombin time (PT) or activated partial thromboplastin time (APTT) longer and why?

A

PT should be 12-14 seconds, measures the extrinsic pathway
APTT should be 25-35 seconds, measures the intrinsic pathway

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13
Q

A normal INR or APTT doesn’t mean a patient won’t bleed on you. Take a bleed history - IMPORTANT!. What questions should you ask?

A

Have you bled after previous surgery/dental work/giving birth
Do you have any abnormal bruising?
Does it take a long time to stop bleeding after cutting yourself?
Do you get lots of nose bleeds?
Do you get lots of heavy periods?
Are you on anticoagulants/Antiplatelet drugs?
Do you have a family history of any of the above?
Or any other known bleeding disorder?
(Don’t need to the tests if answers are no).

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14
Q

What are anticoagulants?

A

Drugs used to stop the blood from clotting in those whose blood clots too much or where it would be problematic if their blood clotted in the wrong place etc.

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15
Q

What is warfarin?

A

A vitamin K antagonist

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16
Q

What is the role of vitamin K in the clotting cascade?

A

Vitamin K is a coenzyme needed to make some of the clotting factors - 2,7,9,10.

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17
Q

Where is vitamin K made?

A

In the liver

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18
Q

Which factor will taking warfarin at a normal dose affect?

A

The one with the shortest half-life - factor VII, hence affects the extrinsic pathway. So prolongs the prothrombin time.

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19
Q

Does taking warfarin affect the APTT?

A

Factors 2,7,10 are also part of the intrinsic pathway, but it only prolongs the APTT in really high doses.

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20
Q

What is INR?

A

Patient PT (s) / normal PT time (s)

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21
Q

What does an INR score of 2 mean?

A

A score of 2 means a patients prothrombin time is prolonged by 2 times.

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22
Q

Why do people on warfarin need their INR level checked regularly?

A

Since lots of things interact with it causing the level to go up and down in the blood eg alcohol, antibiotics and other medications

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23
Q

What is the antidote to warfarin?

A

Oral or IV vitamin K

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24
Q

What does unfractionated heparin do?

A

Block both factor Xa and factor IIa (thrombin)

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25
Q

Why is heparin not ideal for use in patients?

A

Since it is IV only, so only for hospital use.

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26
Q

How do you measure heparin?

A

Measure heparin by measuring the APTT. Will also prolong the PT time but not used.

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27
Q

What do low molecular weight heparins (LMWH) do?

A

Inhibits factor Xa (hence more specific)

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28
Q

How are LMWH’s delivered?

A

Given as subcutaneous injections

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29
Q

What are direct-acting oral anticoagulants (DOACs) (with examples)?

A

Directly inhibit clotting proteins. The 2 types:
Anti-Xa drugs - rivaroxaban, apixaban, edoxaban
Direct thrombin inhibitors (dabigatran)

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30
Q

How do you administer DOACs?

A

Can be taken orally

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31
Q

Are DOACs better than warfarin?

A

Don’t have to be monitored with blood tests
Have lower rates of bleeding than warfarin (about the same as LMWH)
Not inferior to warfarin

32
Q

Examples of LMWHs

A

Enoxaparin, dalteparin

33
Q

Is risk of bleeding or risk of clot worse?

A

Risk of bleeding is often outweighed by risk of a clot

34
Q

What is a stable INR?

A

Checked 72hrs before the procedure and ensure it is between 2.5-3.5.

35
Q

What things can be done with a stable INR?

A

Denture construction
Scaling/polishing
Fillings/crowns/bridges
Root canal
LA
Tooth extractions, minor oral surgery
Biopsies
Periodontal surgery, subgingival scaling

36
Q

What can you not do on patients on anticoagulants?

A

Anything more invasive - refer!
Anything on people with poorly controlled INRs
Anything on people with another problem/drug that might cause Anticoagulation problems
(check with haematologists)

37
Q

What extra things can be done to help bleeding?

A

SurgiCel/collagen sponges (strengthens platelet aggregate)
Tranexamic acid mouthwash (stops the breakdown of clots after they are formed)

38
Q

When would you need to monitor levels of LMWHs?

A

If someone has renal failure

39
Q

Should you stop DOACs before a procedure?

A

Miss morning dose of DOAC on the day of the procedure if it is one of the low bleeding risk procedures as described above.

40
Q

What acquired bleeding disorders are there?

A

Vitamin K deficiency
Liver disease
Renal disease
Acquired haemophilia/acquired von Willebrand syndrome

41
Q

What might vitamin K deficiency be caused by?

A

Poor diet (generally alcoholics since made in liver), or poor pancreatic/bile function

42
Q

How will vitamin K deficiency affect the PT time and bleeding?

A

Prolonged PT
Patient probably won’t bleed

43
Q

Why does liver disease affect bleeding?

A

Clotting factors and anticoagulant proteins are made in the liver.

44
Q

What affect does liver disease have on the times and bleeding?

A

Prolonged PT and APTT
But pt may well clot normally

45
Q

Why might renal disease cause bleeding?

A

Uraemia that you get with kidney disease might interfere with platelet function

46
Q

What will renal disease do to the times and bleeding?

A

Normal clotting screen
Patients might bleed

47
Q

What will acquired haemophilia or von Willebrand syndrome do to the times and bleeding?

A

Autoimmune antibody formed against clotting factors of vWF. These clotting factors plummet down to zero. These patients will bleed A LOT!
APTT might be prolonged or normal

48
Q

What is the difference between severe, moderate, mild of haemophilia A and B?

A

Severe - <1% - will bleed a lot, eg spontaneous bleeding
Moderate - 1-5% - will bleed upon minor injury
Mild - 5-30% - bleed upon a fair amount of trauma

49
Q

Where should you treat the difference classes of haemophilia?

A

Severe and moderate should be treated in hospital
Mild can be treated in primary car but with liaison with haematologists
Carries (females with fathers with the disease) should be treated as mild haemophiliacs

50
Q

What is haemophilia A and why does it cause extra bleeding?

A

Deficiency of factor VIII
Factor VIII helps in the process of creating more factor X, forming more clot formation, which creates more thrombin - a positive feedback step
Normal platelets and normal original thrombin, but not positive feedback effect, so causes delayed bleeding.

51
Q

What is haemophilia B and how does it cause extra bleeding?

A

Deficiency of factor IX
Factor IX is involved in the amplification step, intrinsic pathway, measured by APTT test. Increases the time of this test.

52
Q

What are the different types of von Willebrand disease?

A

I - low vWF
II - dysfunctional vWF
III - absent vWF
Can also be mild moderate or severe

53
Q

Will von Willebrand disease affect any of the clotting tests?

A

vWF doesn’t affect any of the clotting cascade or platelet count so it won’t affect any of the clotting tests.

54
Q

What is the role of vWF?

A

vWF allows the platelets to bind to collagen when the vessel surface is damaged. Once they bind to collagen, the platelets activate, release their granules to make more platelets, causing them to stick together.

55
Q

What type of disease is haemophilia?

A

X-linked

56
Q

What type of disease is vW disease?

A

Autosomal dominant

57
Q

What are the acquired platelet defects?

A

Antiplatelet drugs
Other drugs eg anti-epileptics, chemotherapy
Autoimmune (ITP)
Bone marrow failure: leukaemia, aplastic anaemia

58
Q

What do anti-epileptics/chemotherapy drugs, autoimmune conditions like ITP and bone marrow failure conditions, do to the platelet count?

A

These all cause low platelet count

59
Q

What do antiplatelet drugs do to the platelet count?

A

Platelet levels are normal

60
Q

Give examples of antiplatelets.

A

Aspirin, clopidogrel, dipyramidole

61
Q

What does aspirin do?

A

When platelets get activated, they make thromboxane (TXA2), using COX. Aspirin irreversibly inhibits COX, so blocks thromboaxane formation, so the platelets get activated but don’t activate other platelets around them.

62
Q

What does clopidogrel and dipyridamole do?

A

Blocks the platelets ADP receptors. Focusing on platelets positive feedback after platelets have been activated.

63
Q

What are some hereditary platelet defects (don’t need details abt them)?

A

Bernard Soulier syndrome (GP1b deficient)
Glanzamann’s Thrombasthaenia (GPIIb/IIIa deficient)
Grey platelet syndrome (no alpha granules)

64
Q

What procedures can be done on anyone?

A

Examinations
Fissure sealants
Supragingival scaling
Small occlusal restorations without LA

65
Q

What is anaemia?

A

Low haemoglobin - translates to low RBCs

66
Q

What do the signs and symptoms of anaemia correspond to?

A

Signs and symptoms of anaemia correspond with how bad the oxygen carrying capacity has gotten in the blood

67
Q

What are the mild moderate and severe symptoms of anaemia?

A

Mild - very little signs/symptoms
Moderate - fatigue, pale conjunctiva and skin, burning mouth sensation
Severe - breathless, syncope, heart failure, atrophy of filiform papillae, Plummer-Vinson syndrome

68
Q

What blood tests would you do for anaemia?

A

Hb, and mean cell volume

69
Q

What other tests might you do if MCV was low?

A

Ferritin, serum iron, transferrin saturation (most important)
Blood film
Consider GI investigations, haemoglobinopathy screen

70
Q

When is MCV usually low?

A

MCV is low in iron-deficiency anaemia. Causes red cells to be small.

71
Q

What results will be seen in iron-deficiency anaemia?

A

Less haemoglobin (low Hb)
Smaller red cells (decreased MCV)
Less Hb in each red cell (decreased MCH)

72
Q

What might cause anaemia if MCV is normal?

A

Acute blood loss, patients with suppressed bone marrow formation of RBCs due to chronic inflammation

73
Q

What further tests would you do in patients with a normal MCV but low Hb?

A

U&E, CRP/ESR

74
Q

What might cause a high MCV?

A

B12 or folate deficiencies - cause red cells to be too big

75
Q

What extra tests might you do in patients with a high MCV?

A

Alcohol history, B12, folate, LFT, TFT, haemolysis screen, blood film, myeloma screen

76
Q

What else might low B12 and folate cause?

A

Low folate or B12 will cause: fewer red cells so less haemoglobin (lower Hb); big red cells (increased MCV); shorter red cell survival (increased immature RBCs); decreased WCC and platelet count
Lower B12 can also cause high homocysteine levels which is toxic to nerves so can cause peripheral neuropathy.

77
Q

What is the management of anaemia?

A

Treat the cause: stop the bleeding! Replace thyroid hormone. Treat chronic infection. Stop haemolysis. Treat the dietary, or GI disease or pernicious anaemia causing low B12, folate or iron.
Treat the anaemia: replace B12/folate/iron. Blood transfusions for immediate replacement.

Human Diseases (75 decks)

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