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Year 4 > Haematology > Flashcards

Haematology Flashcards

1
Q

How does warfarin work?

A

It antagonises vitamin K

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2
Q

What is warfarin used for?

A

Mechanical heart valves
Valvular atrial fibrillation
End-stage renal failure

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3
Q

What are the warfarin dependent clotting fcators?

A

2 + 7 = 9, not 10

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4
Q

What are the indications for warfarin use?

A
  • Treatment of DVT and PE
  • Prophylaxis for emboli in AF, rheumatic heart disease, mechanical heart valves, mitral valve disease
  • Symptomatic thrombophilia
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5
Q

What are the contraindications for warfarin?

A
  • Malignancy, heparin or a DOAC must be used instead
  • Known hypersensitivity
  • Any condition that increases risk of major bleed
  • Pregnancy but breast feeding allowed
  • Uncontrolled severe hypertension
  • Patient factors (e.g. uncooperative, unreliable and/or high risk of repeated falls)
  • Drugs with which there is a significantly increased risk of bleeding
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6
Q

What is the warfarin INR target?

A

INR 2 – 3: for VTE, AF, mitral valve disease and inherited symptomatic thrombophilia

INR 2.5 – 3.5: for mechanical heart valves

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7
Q

How long does Warfarin take to reach therapeutic effects?

A

5 days to achieve an INR within therapeutic ranges

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8
Q

Why is heparin administered until warfarin can reach therapeutic range?

A

Warfarin induces a hypercoagulable state because the suppression of protein C occurs much quicker than the coagulation factors due to protein C having a short half-life of 8 hours

So heparin is considered for at least five days until the INR is within the therapeutic range

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9
Q

How can warfarin be reversed?

A
  • Withholding warfarin
  • Vitamin K, either orally or intravenously
  • Prothrombin complex concentrate (PCC): contains vitamin-K dependent clotting factors; PCC containing factors II, VII, IX and X is known as 4-factor PCC whilst PCC without factor VII is known as 3-factor PCC
    -If PCC unavailable, give fresh frozen plasma (FFP) which contains normal levels of all coagulation factor

Often a combinations of reversal agents is given

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10
Q

What does warfarin interact with?

A

Enzyme inducers: decrease the amount of active warfarin
Eg. St John’s wort, phenytoin, and carbamazepine

Enzyme inhibitors: increase the amount of active warfarin
Eg. Amiodarone, metronidazole, clarithromycin, cranberries

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11
Q

Where is warfarin metabolised?

A

Cytochrome P450 system in the liver

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12
Q

How long does warfarin need to be held for before surgery?

A

5 days

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13
Q

Which type of Heparin is used to bridge the therapeutic effect before warfarin starts working?

A

LMWH because it has predictable pharmacokinetic properties

UFH can be used in severe renal impairment and patients at extremes of weight

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14
Q

What is the structure of warfarin councelling?

A
  • ICE
  • How does warfarin work?
  • Monitoring through INR
  • How to take warfarin
  • Side effects: bleeding risk, mild rash, alopecia, jaundice, skin necrosis
  • Diet to avoid cranberries and limit alcohol
  • INR monitoring booklet and patient alert card
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15
Q

How is warfarin to be taken?

A
  • Taken at the same time each day
  • Tablets have different colours depending on the strength
  • If you miss a tablet, take it as soon as possible. Never take 2 doses together and inform the doctor this happened
  • Let the doctor know about any changes in medication
  • Not safe during pregnancy
  • Don’t suddenly stop
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16
Q

What is the pathophysiology of AF?

A

AF is a type of supraventricular cardiac arrhythmia

There is chaotic electrical activity with the atria resulting in ineffective atrial contraction causing blood stasis which increases the risk of thrombosis

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17
Q

What are the causes of AF?

A

Hypertension
Obesity
Alcohol

Heart failure (e.g. secondary to myocardial infarction)
Structural pathology (e.g. valve stenosis or valve regurgitation)
Congenital heart disease
Atrial or ventricular dilation
Atrial or ventricular hypertrophy
Pre-excitation syndromes (e.g. Wolff-Parkinson-White syndrome)
Sick sinus syndrome
Inflammatory conditions (e.g. pericarditis or myocarditis)
Infiltrative conditions (e.g. amyloidosis)

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18
Q

What are the symptoms of AF?

A

-Breathlessness
-Chest discomfort
-Palpitations
-Light-headedness
-Reduced exercise tolerance
-Syncope: due to bradycardia, particular in paroxysmal AF when sinus rhythm is restored because the SAN can take a few seconds to wake up

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19
Q

What is the treatment for AF?

A

Rhythm in new-onset AF
- Most cardiovert spontaneously
- Defibrillator pads can be used to cardiovert or flecainide or amiodarone

Rate control in non-acute AF
- Used in on-going symptoms where rate control has been unsuccessful
- Cardioversion can be done only when anticoagulation has been achieved
- Beta-blockers are 1st line for rhythm control

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20
Q

What is acrdioversion?

A

A medical procedure that uses quick, low-energy shocks to restore a regular heart rhythm

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21
Q

How does Flecainide work?

A

A class 1c antiarrhythmic drug that blocks sodium channels within the heart and thereby raises the threshold for depolarisation

It should not be used in patients with evidence of structural or ischaemic heart disease because of the risk of sudden cardiac death

Given orally or IV

22
Q

How does Amiodarone work?

A

A class 3 antiarrhythmic drug that blocks potassium channels within the heart and thereby prolongs the refractory period of the myocardium.

Can be used in patients with evidence of structural heart disease
May prolong the QT interval and should be avoided in patients with QT prolongation

23
Q

What does the CHA2DS2VASc tool do?

A

Calculates the risk of stroke in AF

24
Q

What is the ORBIT tool used for?

A

Previously was HAS-BLED score is used alongside CHA2DS2VASc to make decisions about anticoagulation

0-2: low
3: medium
4-7: high

25
Q

Which anticoagulants are used in AF?

A

Apixaban
Dabigatran
Edoxaban
Rivaroxaban
Warfarin

26
Q

What are some forms of invasive managements of AF?

A
  • Left atrial ablation
    Creating small scars within the myocardium to block abnormal electrical signals and restore sinus rhythm

Pace and ablate strategy
A pacemaker is inserted and ablation of AVN is done

27
Q

What are some risk factors for DVT and PE?

A
  • Recent surgery, Fractures, or immobility
  • Personal or family history of a clotting disorder or PE/DVT
  • Obesity
  • Malignancy
  • Infection
  • Pregnancy
  • Medications such as the COCP or HRT
28
Q

What is a CTPA?

A

A CT pulmonary angiogram, a CT scan that looks for blood clots in the lung

28
Q

What are some symptoms of PE?

A
  • SOB
  • Pleuritic chest pain: with each breath, the pleura comes into contact with an ischaemic area of the lung.
  • Cough
  • Haemoptysis: secondary to infarcted lung tissue.
  • Dizziness or syncope: due to haemodynamic instability (i.e. right ventricular strain)
29
Q

What is the Wells score used for?

A

Determines if its a PE or not

30
Q

How is a PE treated in secondary care?

A
  • Fondaparinux
  • LMWH
  • LMWH followed by an oral anticoagulant (dabigatran or edoxaban).
  • Oral anticoagulant treatment (warfarin, apixaban, or rivaroxaban).
  • Unfractionated heparin.
  • Mechanical (or physical) interventions like
    Inferior vena cava (IVC) filters
  • Thrombolytic therapy
  • Open pulmonary embolectomy
31
Q

What is Kaposi’s sarcoma?

A

A cancer caused by a virus. Most common in poorly controlled HIV

32
Q

How does Kaposi’s sarcoma present?

A

Patients present with purple skin lesions

The cancer cells are found in the skin or mucous membranes that line the GI tract but those can’t be seen

Can spread to lymph nodes and the lung

33
Q

Why is endocarditis associated with central lines?

A

The line can become colonised with staphylococcus and spread in the heart

The insertion of the central line can also damage the valves which can predispose patients to endocarditis

34
Q

What is Endocarditis?

A

An inflammation of the inside lining of the heart chambers and heart valves (endocardium

35
Q

How is rheumatic fever linked to strep throat?

A

Rheumatic fever may develop if strep throat or scarlet fever infections are not treated properly or after strep skin infections (impetigo)

Both are caused by group A Streptococcus

36
Q

What is Hydroxycarbamide used for?

A

Used to treat CML, myeloproliferative disorders, and other cancers, like cervical cancer

Used in sickle cell to increase the amount of HbF which helps the RBC’s to remain more round and normal

37
Q

When is haemophilia described as severe?

A

When factors levels are below 1%

moderate 1-5%
Mild 5-50%

38
Q

On which chromosome is the haemophilia gene found on?

A

On the X chromosome

It’s recessive, so men get the disease but women are only carriers

39
Q

Other then genetic, what are the other causes of haemophilia?

A

Acquired when autoantibodies develop or as a result of malignancy

40
Q

What is Henoch-Schönlein purpura (HSP)?

A

IgA vasculitis which commonly presents with glomerulonephritis, abdominal pain, arthralgia and purpura

The most common type of vasculitis in children

41
Q

What are some causes for reduced platelet production?

A
  • Viral: herpes simplex virus, cytomegalovirus, varicella-zoster virus, Epstein-Barr virus, rubella, enterovirus, mumps, hepatitis, and HIV
  • Chemotherapy: causes direct bone marrow toxicity, inhibiting the production of platelets
  • Aplastic anaemia
  • Haematological malignancy or metastasis
  • B12 and folate deficiency: causes macrocytic anaemia and in some cases thrombocytopenia
  • Excess alcohol intake: results in direct bone marrow toxicity and liver cirrhosis
  • Congenital conditions including Fanconi’s anaemia, Wiskott-Aldrich syndrome (WAS)
42
Q

What is Fanconi’s anaemia?

A

An inherited bone marrow failure syndrome. It leads to gradual bone marrow failure

Can be associated with birth defects

43
Q

What is Wiskott-Aldrich syndrome (WAS)?

A

A genetic immunodeficiency

It also makes it difficult for a child’s bone marrow to produce platelets

It occurs mostly in males

44
Q

What are some immune-mediated causes for low platelet count?

A
  • Idiopathic thrombocytopenic purpura (ITP)
  • SLE
  • Rheumatoid arthritis
  • Sarcoidosis
  • Antiphospholipid syndrome
45
Q

What is idiopathic thrombocytopenic purpura (ITP)?

A

Autoimmune destruction of platelets

46
Q

What is sarcoidosis?

A

A condition that causes small patches of swollen tissue (granulomas) to develop in organs

It often affects the lungs, lymph nodes, and skin

47
Q

What is Antiphospholipid syndrome?

A

An autoimmune disorder that causes abnormal blood clots to form

48
Q

What are some non-immune causes of decreased platelet survival?

A
  • Medications e.g. heparin, carbamazepine, ibuprofen, rifampin, trimethoprim, vancomycin
  • Splenomegaly: the spleen sequesters more platelets than normal, decreasing the total circulating number of platelets.
  • Haemolytic uraemic syndrome (HUS): toxins from E.coli cause increased thrombogenicity of the vascular endothelium which results in the consumption of platelets due to thrombotic microangiopathy
  • HELLP syndrome: platelets are consumed due to increased exposure to von Willebrand’s factor resulting in widespread thrombotic microangiopathy
    Thrombotic thrombocytopenic purpura (TTP): reduction in the function of the enzyme ADAMTS13 normally responsible for the breakdown of von Willebrand’s factor results in platelets being excessively consumed due to a similar mechanism as that described in HELLP syndrome
49
Q

What is Pseudothrombocytopenia?

A

When platelets undergo a phenomenon called ‘clumping’, in which they stick together causing a false low reading when passed through an auto-analyse

50
Q

How is a low platelet count treated?

A

Corticosterois help increase platelet counts
Eg. Prednisalone or Dexathasone

Year 4 (100 decks)

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