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4th year passmedicine by topic > Bleeding Disorders > Flashcards

Bleeding Disorders Flashcards

Pack includes notes on Heparin & Warfarin, Epistaxis, HHT

1
Q

Which factors does Heparin affect?

A

anti thrombin

prevents activation factors 2 and 10

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2
Q

Which factors does Warfarin affect?

A

vitamin K antagonist

affects synthesis of factors 2, 7, 9, 10

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3
Q

Which factors does DIC affect?

A

Factors 1,2,5,8,11

D I C

deux (2)
I - 11, 1
C - 8 and 5 (round numbers)

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4
Q

Which factors does Liver Disease affect?

A

Factors 1,2,5,7,9,10,11

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5
Q

Describe blood clotting results in Haemophilia?

A

APTT increased
PT normal
Bleeding Time normal

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6
Q

Describe blood clotting results in von Willebrand’s disease?

A

APTT increased
PT normal
Bleeding Time increased

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7
Q

Describe blood clotting results in Vitamin K deficiency?

A

APTT increased
PT increased
Bleeding Time normal

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8
Q

What is Warfarin? How does it work?

A

indirect anticoagulant

organic compound 4-hydroxycoumarins

vitamin K antagonist

acts as a cofactor in the carboxylation of clotting factor II, VII, IX and X (mnemonic = 1972) and protein C.

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9
Q

Indications for Warfarin?

A

venous thromboembolism
- target INR = 2.5, if recurrent 3.5

atrial fibrillation
- target INR = 2.5

mechanical ♡ valves
- target INR depends on the valve type and location.
- mitral valves generally require a higher INR than aortic valves.

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10
Q

warfarin monitoring

A

INR (international normalised ration)

ratio of the prothrombin time for the patient over the normal prothrombin time.

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11
Q

Warfarin has a long half-life and achieving a stable INR may take several days.

A

true

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12
Q

Factors that may potentiate warfarin

A

liver disease

P450 enzyme inhibitors: amiodarone, ciprofloxacin

cranberry juice

NSAIDs: displace warfarin from plasma albumin & inhibit platelet function

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13
Q

warfarin side effects

A

haemorrhage

teratogenic: although can be used in breastfeeding mothers

skin necrosis: when first started

purple toes

reduced protein C biosynthesis
- temporary procoagulant state after initially starting warfarin, normally avoided by concurrent heparin administration.

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14
Q

what to do if the patient is on warfarin and having major bleeding?

A

stop warfarin

intravenous vitamin K 5mg

prothrombin complex concentrate
- if not available then FFP

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15
Q

what to do with patients on Warfarin & INR > 8.0

Minor bleeding

A

stop warfarin

intravenous vitamin K 1-3mg
- 24 hrs later: repeat dose if INR still too high

restart warfarin when INR < 5.0

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16
Q

What to do with patients on Warfarin & INR > 8.0

No bleeding

A

stop warfarin

oral vitamin K 1-5mg
- 24 hrs later: repeat dose if INR still too high

restart when INR < 5.0

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17
Q

What to do with patients on Warfarin & INR 5.0-8.0

Minor bleeding

A

stop warfarin

intravenous vitamin K 1-3mg

restart when INR < 5.0

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18
Q

What to do with patients on Warfarin & INR 5.0-8.0

No bleeding

A

withhold 1 or 2 doses of warfarin

reduce subsequent maintenance dose

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19
Q

Drugs which either inhibit or induce the which system may affect the metabolism of warfarin and hence the INR

A

P450

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20
Q

Inducers of the P450 system will affect INR how?

A

INR will decrease

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21
Q

INHIBITORS of the P450 system will affect INR how?

A

INR will increase

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22
Q

Inducers of the P450 system include

A

antiepileptics: phenytoin, carbamazepine
barbiturates: phenobarbitone
rifampicin
St John’s Wort
chronic alcohol intake
griseofulvin
smoking (affects CYP1A2, reason why smokers require more aminophylline)

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23
Q

Inhibitors of the P450 system include

A 
Acute alcohol intake
SSRIs: fluoxetine, sertraline
Antibiotics: ciprofloxacin, clarithromycine/erythromycin
Imidazoles: ketoconazole, fluconazole
Sodium Valproate
Amiodarone
Allopurinol
Cimetidine, Omeprazole
Isoniazid
ritonavir, quinupristin
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24
Q

There are two main types of heparin, these are?

A

unfractionated, ‘standard’ heparin or low molecular weight heparin (LMWH)

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25
Q

Heparins generally act by

A

activating antithrombin III

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26
Q

Unfractionated heparin works by?

A

forms a complex which inhibits thrombin, factors Xa, IXa, XIa and XIIa

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27
Q

LMWH works by?

A

increases the action of antithrombin III on factor Xa

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28
Q

Adverse effects of heparins include:

A

bleeding
thrombocytopenia
osteoporosis and an increased risk of fractures
hyperkalaemia - this is thought to be caused by inhibition of aldosterone secretion

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29
Q

How do you administer standard heparin vs LMWH?

A

standard - Intravenous LMWH - Subcutaneous

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30
Q

Duration standard heparin vs LMWH?

A

standard - short LMWH - long

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31
Q

LMWH heparin has lower risks of what compared to standard heparin?

A

Heparin-induced thrombocytopaenia (HIT)

Osteoporosis

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32
Q

How do you monitor standard heparin?

A

Activated partial thromboplastin time (APTT)

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33
Q

How would you monitor LMWH?

A

Anti-Factor Xa (although routine monitoring is not required)

34
Q

When is standard heparin useful?

A

Useful in situations where there is a high risk of bleeding as anticoagulation can be terminated rapidly. Also useful in renal failure

35
Q

When is LMWH indicated?

A

Now standard in the management of venous thromboembolism treatment and prophylaxis and acute coronary syndromes

36
Q

Heparin-induced thrombocytopaenia (HIT) is a bleeding condition

A

false

despite being associated with low platelets HIT is actually a prothrombotic condition

37
Q

When does HIT usually develop?

A

5-10 days of treatment

38
Q

What is the pathophysiology of HIT?

A

immune mediated - antibodies form against complexes of platelet factor 4 (PF4) and heparin
these antibodies bind to the PF4-heparin complexes on the platelet surface and induce platelet activation by cross-linking FcγIIA receptors

39
Q

What are the features of HIT?

A

features include a greater than 50% reduction in platelets, thrombosis and skin allergy

40
Q

How would you address Heparin overdose?

A

Heparin overdose may be reversed by protamine sulphate, although this only partially reverses the effect of LMWH.

In HIT address need for ongoing anticoagulation:
direct thrombin inhibitor e.g. argatroban
danaparoid

41
Q

How is Haemophilia inherited?

A

X-linked recessive disorder of coagulation

Up to 30% of patients have no family history of the condition.

42
Q

Haemophilia A is due to?

A

deficiency of factor VIII

43
Q

Haemophilia B is due to?

A

(Christmas disease) there is a lack of factor IX

44
Q

Symptoms of haemophilias?

A

haemoarthroses, haematomas

prolonged bleeding after surgery or trauma

45
Q

Blood tests in Haemophilias/

A

prolonged APTT

bleeding time, thrombin time, prothrombin time normal

46
Q

Up to 10-15% of patients with haemophilia A develop antibodies to factor VIII treatment.

A

true

47
Q

What is the most common inherited bleeding disorder?

A

Von Willebrand’s disease

48
Q

The majority of VWD cases are inherited in which pattern?

A

autosomal dominant

49
Q

Symptoms of VWFD?

A

characteristically behaves like a platelet disorder i.e. epistaxis and menorrhagia are common whilst haemoarthroses and muscle haematomas are rare

50
Q

What is the role of VWF?

A

large glycoprotein which forms massive multimers up to 1,000,000 Da in size
promotes platelet adhesion to damaged endothelium
carrier molecule for factor VIII

51
Q

What are the 3 types of VWFD?

A

type 1: partial reduction in vWF (80% of patients)
type 2*: abnormal form of vWF
type 3**: total lack of vWF (autosomal recessive)

52
Q

What will investigations show in VWFD?

A

prolonged bleeding time
APTT may be prolonged
factor VIII levels may be moderately reduced
defective platelet aggregation with ristocetin

53
Q

Management of VWFD?

A

tranexamic acid for mild bleeding
desmopressin (DDAVP): raises levels of vWF by inducing release of vWF from Weibel-Palade bodies in endothelial cells
factor VIII concentrate

54
Q

type 3 von Willebrand’s disease (most severe form) is inherited as an autosomal recessive trait

A

true

55
Q

What is the commonest type of VWFD?

A

80% of patients have type 1 disease

56
Q

What is Hereditary haemorrhagic telangiectasia?

A

autosomal dominant condition characterised by (as the name suggests) multiple telangiectasia over the skin and mucous membranes

57
Q

In HHT twenty percent of cases occur spontaneously without prior family history.

A

true

58
Q

How is HHT diagnosed?

A

There are 4 main diagnostic criteria.

If the patient has 2 then they are said to have a possible diagnosis of HHT.

If they meet 3 or more of the criteria they are said to have a definite diagnosis of HHT

59
Q

What are the diagnostic criteria of HHT?

A

Epistaxis : spontaneous, recurrent nosebleeds

Telangiectases: multiple at characteristic sites (lips, oral cavity, fingers, nose)

Visceral lesions: for example gastrointestinal telangiectasia (with or without bleeding), pulmonary arteriovenous malformations (AVM), hepatic AVM, cerebral AVM, spinal AVM

Family history: a first-degree relative with HHT

60
Q

Epistaxis is split into what? How do these arise?

A

anterior and posterior bleeds,
Anterior: visible source of bleeding and usually occurs due to an insult to the network of capillaries that form Kiesselbach’s Plexus
Posterior haemorrhages, on the other hand, tend to be more profuse and originate from deeper structures.

61
Q

Which type of epistaxis is more common in elderly?

A

Posterior

62
Q

Posterior epistaxis has a higher risk of ?

A

aspiration and airway compromise

63
Q

most cases of epistaxis tend to be benign and self-limiting, they may be an indicator of serious pathology

A

true

64
Q

Most common cause of epistaxis?

A

trauma to the nose- this can range from the insertion of foreign bodies, nose picking and nose blowing

65
Q

Causes of epistaxis can include platelet function disorders such as

A

thrombocytopenia, splenomegaly, leukaemia, Waldenstrom’s macroglobulinaemia and ITP

66
Q

Epistaxis In adolescent males could be

A

juvenile angiofibroma is a benign tumour that may bleed as it is highly vascularised.

67
Q

If the nasal septum looks abraded or atrophied, inquire about

A

drug use

inhaled cocaine is a powerful vasoconstrictor and repeated use may result in obliteration of the septum

68
Q

In the elderly, what may cause prolonged nasal bleeding

A

hereditary haemorrhagic telangiectasia

69
Q

If the patient is haemodynamically stable in epistaxis, bleeding can be controlled with first aid measures. This involves:

A

Asking the patient to sit with their torso forward and their mouth open- avoid lying down unless they feel faint. This decreases blood flow to the nasopharynx and allows the patient to spit out any blood in their mouth. It also reduces the risk of aspirating blood.
Pinch the cartilaginous (soft) area of the nose firmly and consistently for at least 20 minutes and ask the patient to breathe through their mouth.

If first aid measures are successful, consider using a topical antiseptic such as Naseptin (chlorhexidine and neomycin) to reduce crusting and the risk of vestibulitis.

70
Q

Naseptin cautions and alternative?

A

peanut, soy or neomycin allergies, and Mupirocin is a viable alternative.

71
Q

In epistaxis Admission and follow up care may be considered in who?

A

patients who have a comorbidity (e.g. coronary artery disease, or severe hypertension) is present

an underlying cause is suspected

if they are aged under 2 years (as underlying causes such as haemophilia or leukaemia are more likely in this age group).

72
Q

If bleeding does not stop after 10-15 minutes of continuous pressure on the nose, consider?

A

cautery or packing

73
Q

When should cautery be used?

A

if the source of the bleed is visible and cautery is tolerated- it is not so well-tolerated in younger children

74
Q

When should packing be used?

A

if cautery is not viable or the bleeding point cannot be visualised. If the nose is packed in primary care, the patient should be admitted to hospital for review.

75
Q

How do you cauterise in nosebleed?

A

Ask the patient to blow their nose in order to remove any clots. Be wary that bleeding may resume.

Use a topical local anaesthetic spray (e.g. Co-phenylcaine) and wait 3-4 minutes for it to take effect

Identify the bleeding point and apply the silver nitrate stick for 3-10 seconds until it becomes grey-white. Avoid touching areas which do not require treatment, and only cauterise one side of the septum as there is a risk of perforation.

Dab the area clean with a cotton bud and apply Naseptin or Muciprocin

76
Q

How do you pack in nosebleed?

A

Anaesthetise with topical local anaesthetic spray (e.g. Co-phenylcaine) and wait for 3-4 minutes

Pack the patient’s nose while they are sitting with their head forward, following the manufacturer’s instructions

Pressure on the cartilage around the nostril can cause cosmetic changes and this should be reviewed after inserting the pack.

Examine the patient’s mouth and throat for any continuing bleeding, and consider packing the other nostril as this increases pressure on the septum and offending vessel.

Patients should be admitted to hospital for observation and review, and to ENT if available

77
Q

Patients with a bleed from an unknown or posterior source (i.e. the bleeding site cannot be located on speculum, bleeding from both nostrils or profuse) should be admitted to hospital.

A

true

78
Q

(epistaxis) Patients that are haemodynamically unstable or compromised should be admitted to the emergency department

A

yes

Control bleeding with first aid measures in the interim.

79
Q

Self care advice for epistaxis?

A

Patients should be informed that blowing or picking the nose, heavy lifting, exercise, lying flat, drinking alcohol or hot drinks should be avoided. The same applies for patients who have just been cauterised, as any strain on the nostril may induce a re-bleed.

80
Q

Common causes of epistaxis in children include:

A

nose picking (most common cause)
foreign body
upper respiratory tract infection
allergic rhinitis

81
Q

Who do kids with epistaxis who are <2yrs need referal?

A

may be secondary to trauma or bleeding disorders.

4th year passmedicine by topic (96 decks)

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