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resit part 2c > thrombotic disease > Flashcards

thrombotic disease Flashcards

1
Q

what is stroke?

A

Stroke occurs when there is a rapid death of brain tissue due to a disturbance in blood supply

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2
Q

what is TIA

A

TIA is defined by ‘stroke (mini stroke) symptoms that resolve completely within 24 hours’ (WHO)

Stroke must be differentiated from Transient Ischaemic Attack (TIA) (or acute ischaemic cerebrovascular syndrome)

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3
Q

what are the risk factors for stroke?

A
  • age
  • family history
  • HBP
  • heart disease
  • diabeties
  • smoking
  • obesity
  • HRT
  • previous stroke or TIA
  • inactivity
  • binge drinking
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4
Q

Blood supply in the brain

where does the Carotid arteries supply

A

Anterior supply for front and middle regions of the brain

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5
Q

Blood supply in the brain

where does the Vertebral arteries supply

A

Posterior supply to brain stem and rear regions of the brain

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6
Q

Blood supply in the brain

where does the Basilar artery: supply

A

Basilar artery: two vertebral arteries joins together

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7
Q

Blood supply in the brain

where does the Communicating arteries supply

A

Posterior (basilar-carotid) & Anterior

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8
Q

what are the different types of strokes ?

A

-Ischemic Stroke
Haemorrhagic Stroke
Transient Ischemic Attack (TIA) – Mini stroke

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9
Q

what are the causes of ischemic stroke?

A

Changes can be observed within 2-3 hours of ischemia
Complete death of brain tissues can occur within 6-24 hours

Thrombosis (large/small arteries)
Large arteries: carotid, vertebral & basilar
Larger branches: anterior, middle & posterior cerebral arteries
Small arteries: small branches from the above large branches

Damage caused by:
Atherosclerotic plaque rupture leads to thrombosis
Interrupts blood supply (oxygen, glucose & other nutrients) to neurons
Rapid death of brain tissues leads to loss of brain function

Embolism
Obstruction (clots) from some other upstream arteries or heart
Heart is the common source of emboli to the brain
Common conditions to form clots in left ventricle: congestive heart failure and heart attack (MI)
Ejection fraction of left ventricle: normally 55-70% but during CHF & MI low ejection fraction (blood stasis at apex)
Blood stasis leads to thrombosis (blood clots)
Thrombus may stick to ventricle wall & become embolised
Emboli can break up to pieces & block arteries results in stroke

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10
Q

what is atrial fibrillation?

A

Atrial fibrillation: left atrium is less effective in ejection of blood
Blood stasis in left atrial appendage and thus leads to formation of blood clots subsequently to emboli & stroke

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11
Q

what is endocarditis?

A

Endocarditis: fungal or bacterial growth (septicaemia) in heart valves forms clumps/vegetation and emboli to the brain

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12
Q

how is Haemorrhagic Stroke caused?

A

Divided into intracerebral & subarachnoid bleeding

Intracerebral (within brain): due to hypertension, trauma, bleeding disorders & vascular defects
Arteriovenous malformation: feeder artery to NIDUS (nest of small arteries) and lead to collection vein
High pressure in AVM causes rupture and bleeding forms haematoma
Haematoma compress/ rupture/ damage neurons – irreversible damage

Subarachnoid (surface of brain): due to aneurysm rupture
Most of the aneurysm occur in circle of Willis
Risks: smoking, alcohol, hypertension, genetic, drug abuse, therapeutic drugs-anticoagulants, etc.
Occurs in circle of Willis such as at the junctions of anterior communicating & anterior cerebral arteries
Two types: saccular (berry) & fusiform
Damages: compression of tissue from expanding haematoma
direct toxic effects of blood cells (free iron)
interruption of blood supply to neurones
Surgical intervention required

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13
Q

what are the causes of TIA?

A

Transient Ischemic Attack (TIA) – Mini stroke

Temporary blockage of blood supply due to small blood clots

May overcome either in 30-60 minutes or 24 hours

Could occur repeatedly or in multiple regions

Leads to major ischemic stroke

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14
Q

Assessment of the risk for a stroke following TIA

A

ABCD2, a prognostic score to identify people at high risk of stroke after a TIA

A - age: 60years of age or more = 1point
B- blood pressure at presentation: 140/90mmHg or greater = 1point
C- clinical features: unilateral weakness = 2points;
speech disturbance without weakness = 1point
D- duration of symptoms: 10 - 59minutes = 1point; 60 minutes or longer = 2points
presence of diabetes: 1point

ABCD2 score ≥ 4 = high risk of stroke
aspirin (300 mg daily) started immediately
specialist assessment
investigation within 24 hours of TIA symptoms

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15
Q

what are the limitations of ABCD2

A

Limitations: cannot be used in patients with recurrent TIA or on
anticoagulant treatment

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16
Q

what are the symptoms of stroke?

A

right side of the brain controls the left side of the body
left side of the brain controls the right side of the body

left of the body:

  • loss of consciousness/ coma
  • worst headache
  • double vision/ lost of vision
  • slurred speech/loss of speech

right of the body

  • numbness of face, arm, legs on one side
  • weakness of face, arm, leg on one side
  • loss of balance/ coordination
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17
Q

what is the simple recognition of stroke?

A

FAST

Facial weakness: can the person smile? Has their mouth or eye drooped?
Arm weakness: can the person raise both arms?
Speech problems: can the person speak clearly and understand what you say?
Time to call 999

18
Q

what is the pharmacological management after TIA?

A

ABCD2 High Score = ≥ 4
Aspirin 300 mg daily start immediately
Specialist assessment & investigation within 24 hours following onset of symptoms
Measures for secondary prevention including the assessment of individual risk factors
Crescendo TIA (≥ 2/week) should be treated as high risk even if the score is <4

ABCD2 Low Score = < 4
Specialist assessment within a week following onset of symptoms
Referral to brain imaging if needed

19
Q

Pharm management of ischemic stroke

A

Alteplase given within 4.5 hours, 900 microgram/kg/over 60 minutes and in specialist stroke centre (to ensure correct delivery and management) or by trained staff

Aspirin started within 24 hours, 300 mg daily for 2 weeks (oral or via rectal/enteral tube, if dysphagic; if history of dyspepsia, give proton pump inhibitor) or clopidogrel 75 mg daily as alternative (if aspirin-intolerant)

Modified-release dipyridamole in combination with aspirin if clopidogrel is contraindicated or not tolerated

Others include anticoagulants, anti-hypertensives, statins, surgeries to remove blockages and place stent

Thrombolytic agents
Tissue Plasminogen Activator (tPA)
Example : Alteplase (900 µg/kg/1 hour)
Promotes the breakdown of fibrin (lysis of the blood clot)
IV administration within 4.5 hours of stroke improves clinical outcome (death or disability)

NOTE:
Can not be used in haemorrhagic stroke
Surgery to remove the plaques 
-cartoid anioplasty 
-Carotid endarterectomy
20
Q

Pharm management of haemorrhagic stroke

A

Removal or clipping of aneurysm
Anti-hypertensives
Reversing anticoagulants (if any)
Surgery (craniotomy) to remove blood or haematoma
Surgery to treat hydrocephalus (to drain CSF)

21
Q

Long-term management of stroke

A

Long-term Clopidogrel 75 mg/daily
Note: Clopidogrel can be used in other cardiovascular conditions/diseases if aspirin is contraindicated/not tolerated

Modified Release (MR) dipyridamole (200 mg twice daily) in combination with aspirin (75 mg/once daily) should be used in people who have had a TIA

Ischemic stroke and Clopidogrel is contraindicated/not tolerated

22
Q

Rehabilitation for Stroke Patients

A

Restoration of function (re-learning skills and abilities)
Physiotherapy (e.g. learning to walk)
Speech and language therapy (e.g. learning to talk)
Occupational therapy (e.g. shopping)
Psychologist/Psychiatrist (e.g. to adapt psychologically)

Learning new skills
e.g. occupational therapy

Adapting to some of the limitations (caused by a stroke)
e.g. smaller meals to avoid choking, physical changes to home, wearing incontinence pads, communicating in different ways, mobility aids

Support network
patience, positive, carers strike a balance between taking over and full independence

23
Q

Peripheral arterial disease (PAD)

A

Atherosclerotic plaques in lower extremities (e.g. legs)

Hardening of arteries supplying blood to legs

Block the blood supply and lead to ischemia

Results in myocytes death

More common in men than women

Mostly occur in diabetes, smokers

Can cause serious complications

Symptoms could be anywhere in legs

24
Q

what are the causes of PAD

A
  • diabetics
  • smoking
  • obesity
  • infection
  • damage to the vessels
  • sedentary lifestyle
  • HBP
  • nutritional deficiencies
  • emboli
  • inflammation of blood vessels
25
Q

what are the causes of PAD

A
  • diabetics
  • smoking
  • obesity
  • infection
  • damage to the vessels
  • sedentary lifestyle
  • HBP
  • nutritional deficiencies
  • emboli
  • inflammation of blood vessels
26
Q

what are the symptoms of PAD?

A
  • none at first
  • coolness of skin
  • infections which dont heal
  • poor nail and skin health
  • pain while walking and stops with rest
  • discolouration - pale
27
Q

what are the methods of diagnosis of PAD?

A
  • angiography
  • doppler ultrasound
  • blood pressure at arms and legs
  • pulse palpation at ankles

-Ankle-brachial index (ABI)

Blood pressure in ankle and arm should be measured 

Systolic blood pressure in ankle / arm = 0.9 - 1 (normal)

<0.9 : represents PAD

0. 71 - 0.9 : mild PAD
0. 41 - 0.7 : moderate PAD

<0.4 : severe PAD
28
Q

what are the treatment for PAD?

A

Change of lifestyle: regular exercise, smoking cessation, weight reduction for obese & reduce alcohol consumption

Medications for hyperlipidaemia, hyperglycaemia/diabetes & hypertension

Anti-platelet drugs: e.g. aspirin (75 mg daily)

Naftidrofuryl oxalate (vasodilator) (100-200 mg/ 3 times a day) alleviates symptoms of intermittent claudication and improve pain-free walking distance in moderate cases

Cilostazol (PDE inhibitor-vasodilation and inhibits platelet activation) is for second-line treatment where lifestyle modifications and other interventions failed

Surgical procedures: angioplasty and endartectomy

29
Q

what is DVT

A

Occurs in deep veins in lower extremities (legs)
Blood flows back to heart due to muscle movement
Reduced/nil movement or injuries diminishes or stops blood flow in veins
So accumulation of platelets & plasma proteins leads to clotting
The clot could be smaller, so it can break up easily by fibrinolysis
Large clots can occlude the veins and prevent the blood flow permanently
Dislodged clots can travel to heart and then lodge in lungs (called pulmonary embolism)
Can cause serious complications if untreated

30
Q

what are the causes of DVT?

A

Inactivity – immobile for a long period (e.g. during/after surgeries, due to other illness or long journeys

Stay at hospitals – long staying at hospitals with reduced activity

Blood vessel damage – injury to the blood vessels can narrow or block the blood flow. Vasculitis, varicose vein and certain medications can also damage the blood vessels

Medical conditions – can increase the clotting activity (cancer treatments – chemo & radiotherapy; heart & lung diseases; infectious diseases, e.g hepatitis

Genetic conditions – thrombophilia – blood is more likely to clot; Hughes syndrome – blood is abnormally sticky

Pregnancy – makes blood to clot quickly

Combined contraceptive pills & hormone replacement therapy (increased oestrogen can cause blood to clot easily)

Previous DVT, obesity, smoking, age (>60) and dehydration

31
Q

what are the symptoms of DVT?

A

Sometimes asymptomatic

Pain, tenderness and swelling in one of the legs

Heavy pain in the affected area

Warm skin in the area of the clot

Redness of the skin at the back of leg below the knee

If untreated, can lead to pulmonary embolism

Breathlessness

Chest pain – gets worse during breathing

Sudden collapse

32
Q

what are the diagnosis method of DVT?

A
  • blood test for D-dimer levels
  • ultrasound scan
  • venogram
33
Q

what are the treatment option for DVT?

non and pharmacological

A

Anticoagulants to prevent the clots getting bigger and breaking off

Heparin (low molecular weight (mostly used form) & standard unfractionated) – an anticoagulant and inhibitor of thrombin

IV infusion or intermittent subcutaneous injection (Low molecular weight)

IV infusion, injection or subcutaneous injection – standard heparin

Warfarin sodium (oral anticoagulant-tablet) – should be started same time as heparin – prevents further clotting 
Not recommended for pregnant women

Rivaroxaban (Factor Xa inhibitor)

Apixaban (thrombin inhibitor)

Compression stockings – to prevent formation of new clots or post-thrombotic syndrome
Waking exercise, raising legs at resting

Inferior vena cava filters when anticoagulants are not suitable

Small mesh device – prevent large clots travelling to heart and lungs
Placed into the vein using a catheter and ultrasound scan

34
Q

what are the mode of action of antiplatelets?

examples

A

Drugs to inhibit platelet function (mostly in arterial thrombosis)

E.g. Aspirin, clopidogrel and dipyridamole

Mainly used for the prevention of arterial thrombotic diseases (MI, stroke, etc.)

Platelet activation

35
Q 
What is the 
drug class
MoA
role 
counselling and caution points 
of ASPIRIN?
A

Drug class: Anti-platelet drug (a NSAID)

Mechanism: Irreversibly binds to cyclooxygenase (COX) enzyme in platelets, inactivating COX and preventing the production of thromboxane A2, which activates platelets and increases aggregation.

Role: Secondary prevention of CV events (dose vary)

Counseling and cautions:
Avoid if patient has history of hypersensitivity to aspirin and other NSAIDs
Use with caution (or avoid) in patients with history of peptic ulceration
Use with caution if patient has asthma
Use with caution if using concomitantly with drugs that increase bleeding risk
Use with caution in elderly with other medications or conditions

36
Q 
What is the 
drug class
MoA
role 
counselling and caution points 
of CLOPIDOGREL?
A

Drug class: Anti-platelet drug

Mechanism: Pro-drug of an active metabolite irreversibly binds to ADP receptor (P2Y12) on platelets, which prevents ADP–mediated activation of platelets and aggregation.

Role: Secondary prevention of CV events (dose vary) \

Counseling and cautions:
Use with caution in patients at increased risk of bleeding or taking concomitantly with drugs that increase bleeding risk
Discontinue use 7 days before elective surgery if anti-platelet effect is not desirable
Caution if history of hypersensitivity to thienopyridines (i.e. antiplatelet drug, prasugrel)

37
Q 
What is the 
drug class
MoA
role 
counselling and caution points 
of Dipyridamole
A

Drug class: Anti-platelet drug

Mechanism: Inhibiting phosphodiesterase (PDE), it prevents the hydrolysis of cAMP and cGMP and thus increase their levels to inhibit platelet activation.

Role: Secondary prevention of CV events (dose vary)

Counseling and cautions:
Use with caution in patients taking it concomitantly with drugs that increase bleeding risk
May exacerbate migraine
Use with caution in case of certain CV conditions i.e. worsening angina or recent MI

38
Q

What is the drug class of heparin and uses and side effects

A

A group of sulphated glycosaminoglycans (long unbranched polysaccharides with repeating disaccharides + amino sugar)
Highly, negatively charged biomolecule in the body
Commercial preparations are normally extracted from beef lungs or porcine intestine
Unfractionated/standard heparin is a mix of polymers with varying lengths of side chains
UF heparin activates antithrombin III and thereby inactivates thrombin, factor Xa and others
Low molecular weight heparins are fractionated form and only contain small side chains (e.g. dalteparin & enoxaparin)
LMW heparin inhibits mainly factor Xa via ATIII

LMW heparin (e.g. dalteparin, enoxaparin & tinzaparin) or synthetic pentasaccharide (e.g. fondaparinux) are associated with less side effects compared to the UF heparin
Heparin should be given as IV or subcutaneous injections
Provides acute effects and half life is 40-90 minutes
Effects can be terminated by stopping the infusion
INR for clotting should be tested regularly

Common side effects
Haemorrhage – if bleeding occurs stop heparin and give protamine sulfate which inactivates heparin
Thrombocytopenia – decrease platelet numbers
Hyperkalaemia
Osteoporosis (in prolonged use >6 months)

39
Q

what is hidurin and moa

A

Hirudin – an anti-coagulant peptide (65 aa) present in leech saliva
A potent natural inhibitor of thrombin
Binds to thrombin surface directly and inhibit its activity
Recombinant hirudins are commonly used
E.g. Lepirudin used in patients with heparin-induced thrombocytopenia but require anti-coagulation therapy
E.g. Bivalirudin used by cardiologists for patients undergoing PCI
Mainly used in unstable angina or NSTEMI

40
Q 
What is the 
drug class
MoA
role 
counselling and caution points 
of wafarin
A

Drug class: Anti-coagulant

Mechanism: Prevents blood clot formation by inhibiting vitamin K reductase and depleting levels of the reduced form of vitamin K, a co-factor for the production of vitamin K-dependent clotting factors II (pro-thrombin), VII, IX and X

Indication and dose:
Prophylaxis and treatment of venous thrombosis and pulmonary embolism, Prophylaxis after insertion of prosthetic heart valves, transient ischaemic attacks or atrial fibrillation

Counseling and cautions:
Monitoring is essential
Use with caution in patients taking it concomitantly with drugs that increase bleeding risk, history of GI bleeding or peptic ulcers, surgery etc.
Check for possible interactions with other medicines
Advise on possible interactions with food (i.e. cranberry juice)

resit part 2c (25 decks)

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