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BM322: Biomedical Pharmacology > Block B Lecture 1 - Stroke and DVT > Flashcards

Block B Lecture 1 - Stroke and DVT Flashcards

1
Q

What is arterial thromboembolism?

A

A condition where a blood clot forms in an artery and then breaks loose, traveling through the bloodstream (embolism) to block another artery

(Slide 8)

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2
Q

What is embolism and how does it differ from thrombosis?

A

Embolism is when blood flow is preventes due to debris from elsewhere whereas thrombosis is when blood flow is prevented by a clot

(Slide 7)

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3
Q

What is the primary cause of arterial thromboembolism?

A

Atherosclerosis

(Slide 8)

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4
Q

What are the 3 main types of stroke?

A

Transient ischemic attack without infarction (TIA, also known as a mini-stroke)

Ischaemic stroke (cerebral infarction)

Haemorrhagic stroke (cerebral infarction)

(Slide 9)

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5
Q

What is a transient ischaemic attack?

A

A temporary reduction or cessation of blood flow to the brain

(Slide 10)

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6
Q

What does a temporary reduction or cessation in blood flow to the brain cause?

A

Neurodeficits which last less than 24 hours

(Slide 10)

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7
Q

What is an ischaemic stroke?

A

A prolonged reduction or cessation of blood flow, which can cause infarcted brain tissue which cannot be recovered

(Slide 11)

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8
Q

What are 3 primary types of an ischaemic stroke?

A

Thrombotic Stroke

Embolic Stroke

Hypoxic Stroke

(Slide 11)

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9
Q

What is a thrombotic stroke?

A

When brain blood flow is prevented due to thrombosis (blood clotting) of a cerebral vessel

(Slide 11)

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10
Q

What is an embolic stroke?

A

When debris from elsewhere blocks blood flow through a cerebral vessel

(Slide 11)

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11
Q

What is a hypoxic stroke?

A

A decrease in blood flow to the brain (e.g due to cardiac arrest or respiratory failure)

(Slide 11)

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12
Q

What is a haemorrhagic stroke?

A

A rupture of a blood vessel in the brain, resulting in bleeding

(Slide 12)

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13
Q

What is the difference between an intracerebral and a subarachnoid haemorrhage?

A

An intracerebral haemorrhage is when a haemorrhagic stroke bleeds into the brain parenchyma whereas a subarachnoid haemorrhage is when a haemorrhagic stroke bleeds into the subarachnoid space

(Slide 12)

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14
Q

What is the primary cause of a haemorrhagic stroke?

A

Hypertension

(Slide 12)

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15
Q

What are the signs of a stroke (and the mnemonic behind it)?

A

Balance - Sudden loss of balance
Eyes - Sudden loss of vision

Face - Drooping face
Arm - Weakness or numbness in
their arms
Speech - Slurred or confused
speech
Time - take action now and call an ambulance (not a sign but I guess they were clutching at straws for this mnemonic)

BE FAST

(Slide 13)

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16
Q

What is venous thromboembolism and what does it result in?

A

A clot which blocks blood flow through veins, resulting in pulmonary embolism

(Slide 18)

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17
Q

What is a paradoxical stroke and what causes it?

A

A stroke which occurs when venous blood enters the arterial circulation, usually caused by blood from the right side of the heart entering the left side, usually caused a right-to-left shunt caused by a hole in the wall of the heart

(Slide 19)

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18
Q

What is deep vein thrombosis?

A

Clotting in the deep veins

(Slide 20)

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19
Q

What is the difference between deep and superficial veins?

A

Deep veins carry blood back to the heart whereas superficial veins carry blood from tissue to the deep veins

(Slide 20)

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20
Q

What are 3 primary causes of deep vein thrombosis?

A

Venous stasis - slowed blood flow

Hypercoagulation - increased clotting

Damage to blood cells (physical damage or endothelial cell activation)

All 3 of these factors make up Virchow’s triad
(Slides 20 - 22)

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21
Q

What is haemostasis?

A

The process which the body uses to stop bleeding (haemorrhage) after vascular injury while maintaining normal blood flow in the circulation

(Slide 23)

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22
Q

What are primary and secondary haemostasis?

A

They are both steps in the haemostasis process.

Primary haemostasis: Injury triggers the release of clotting factors and vasoconstrictors. Vasoconstriction then limits blood flow and platelets form a plug. During this clotting factors also convert prothrombin into thrombin, which then converts fibrinogen into fibrin.

Secondary haemostasis: Fibrin then strengthens the blood clot

(Slide 23)

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23
Q

What are some risk factors for each part of Virchow’s triad?

A

Venous stasis - bed rest, long flights and pregnancy

Damage to blood cells - the BAD HEART mnemonic and infection

Hypercoagulation - genetics, surgery and medications

(Slide 24)

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24
Q

What are 3 types of drugs used to treat thromboembolic disorders?

A

Anti-platelet drugs (such as COX inhibitors)

Anti-coagulants (prevent clots forming)

Thrombolytics (clot busters)

(Slide 13)

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25
What are 3 examples of anti-coagulant drugs?
Answers Include: Warfarin COX-1 inhibitors (such as aspirin) - ADP Receptor inhibitors Phosphodiesterase Inhibitors (Slide 32)
26
How do COX-1 inhibitors help prevent clotting?
They irreversibly inhibit the enzyme (COX1) responsible for the synthesis of thromboxane precursors, reducing thromboxane levels, which is needed for platelet aggregation and activation, leading to less clotting (Slide 32)
27
How do phosphodiesterase inhibitors prevent blood clotting?
Their metabolites interfere with platelet function by increasing cAMP or cGMP levels (Slide 32)
28
What is an example of a phosphodiesterase inhibitor?
Dipyridamole (Slide 32)
29
What are 2 examples of classes of anti-platelet drugs?
Also COX-1 inhibitors and ADP receptor inhibitors! (Slide 33)
30
What are the pharmacokinetics of COX-1 inhibtors?
They are rapidly onsetting (~1 hour) but have a short half life (Slide 33)
31
Is a high or low dose of COX-1 inhibitors used and why?
A low dose used for secondary preventing of a stroke or myocardial infarction (Slide 33)
32
What are some contraindications of COX-1 inhibitors?
They should not be given to patients who are actively bleeding, have a liver / renal impairment or have an aspirin allergy (Slide 33)
33
What is the mechanism of action of ADP receptor inhibitors for blocking platelet function?
Their metabolites block the P2Y12 receptor present on platelets, reducing platelet activation and aggregation (Slide 34)
34
What are the pharmacokinetics of ADP receptor inhibitors?
They can either be rapidly onsetting (~1 hour) and reversible or slow, irreversible prodrugs (Slide 34)
35
What drug are ADP receptor inhibitors combined with to prevent a stroke or myocardial infarction?
Aspirin (Slide 34)
36
What type of ADP receptor inhibitor is given is the patient has a high bleeding risk?
Clopidogrel (one of the slow acting irreversible prodrug versions of ADP receptor inhibitors) (Slide 34)
37
What are some contraindications of ADP receptor inhibitors?
Active bleeding or liver / renal impairment (Slide 34)
38
What is a risk of COX1 and ADP receptor inhibitors?
They can increase bleeding risk (Slides 33 and 34)
39
What is an example of an ADP receptor inhibitor?
Clopidogrel or Ticagrelor (Slide 34)
40
What is the mechanism of action of warfarin?
It is a vitamin K antagonist which inhibits vitamin K epoxide reductase (VKORC1), preventing the recycling of vitamin K and reducing the synthesis of vitamin K-dependent clotting factors, such as factors II (prothrombin), VII, XI and X, which reduces thrombin generation and fibrin formation, reducing clot formation without the need for antithrombin (Slides 35 - 37)
41
What is antithrombin?
Antithrombin is a natural anticoagulant protein that helps regulate blood clot formation. It inhibits clotting factors, primarily Thrombin (factor IIa) , preventing excessive clotting and reducing the risk of thrombosis. (Slide 37)
42
What are the pharmacokinetics of warfarin?
It is slowly onsetting (2-3 days) to deplete functional clotting factors and has a long half life which requires monitoring (Slide 37)
43
What are the dosage / usage of warfarin?
Dosage is individual titration and it's used to treat deep vein thrombosis (DVT) and pulmonary embolism (Slide 37)
44
What are some contraindications for warfarin?
If the patient is actively bleeding, have a liver impairment or are pregnant (Slide 37)
45
What do patients need to be cautious about when on warfarin?
That they don't consume excessive amounts of vitamin K (so no leafy greens) (Slide 37)
46
What are the mechanism of actions of unfractionated heparin, low molecular weight heparins (LMWHs) and synthetic heparins?
They all enhance the activity of antithrombin III, which inhibits factor Xa and IIa (thrombin). LMWHs preferentially inhibit Xa and synthetic heparins inhibit Xa only. These result in a reduced thrombin generation and fibrin formation. Note: All heparins work through boosting antithrombin, the lecture slides are wrong here 100% (Slide 38)
47
Order the different types of heparin from shortest to longest half life and state what enzyme metabolises heparins.
unfractionated heparin (1 hour) > LMWHs (4-6 hours) > sythetic heparin (12 hours). They are metabolised by CYP450 (Slide 38)
48
How are heparins administrated and what kind of treatment are they used in?
They are administrated by IV infusion and LWWHs and synthetic heparins are used in outpatient treatment (when patients don't stay overnight) (Slide 38)
49
What is an example of Low-molecular weight heparins and a synthetic heparin?
LMWHs - Enoxaparin or Dalterparin Synthetic heparin - Fondaparinux (Slide 38)
50
What is a contraindication for heparins?
Active bleeding (Slide 38)
51
What is the mechanism of action of oral factor Xa inhibitors?
They directly inhibit factor Xa, preventing the conversion of prothrombin (factor II) into thrombin (factor IIa), reducing thrombin generation and fibrin formation, without the need for antithrombin (Slide 39)
52
What are the pharmacokinetics of oral factor Xa inhibitors?
They are rapidly onsetting (2-4 hours) and are metabolised by CYP450 (Slide 39)
53
What is an example of an oral Xa inhibitor?
Answers Include: Apixaban Rivaroxaban Edoxaban Note: These are also known as Direct Oral Anti-coagulants (DOACs) (Slide 39)
54
What are some contraindications of oral Xa inhibitors?
If the patient is actively bleeding, has a liver impairment or is pregnant (Slide 39)
55
What is fibrinolysis?
A natural process which the body uses to break down blot clots. It involves tissue plasminogen activator (tPA) converting plasminogen to plasmin, which degrades fibrin, resulting in the blood clot weakening (Slide 41)
56
What are alteplase, reteplase and tenecteplase and what are their uses?
They are synthetic versions of tissue plasminogen activator (tPA), with alteplase being used to treat a stroke or pulmonary embolism and reteplase and tenecteplase being used to treat a myocardial infarction (Slide 41)
57
What is the usual immediate treatment for a transient ischaemic attack or ischaemic stroke?
Anti-platelets and thrombolytics but usually not anti-coagulants (as they increase the risk of a haemorrhage occurring). Anti-platelet drugs prevent new clots forming whereas thrombolytics break down existing clots Surgically, a thrombectomy may be used to remove the blood clot from the vessel (Slide 42)
58
What are thrombolytics?
A class of drugs that are used to dissolve blood clots that are obstructing blood flow (Slides 41 and 42)
59
What is the treatment for a haemorrhagic stroke?
Reversal of anti-coagulation therapy (via infusion of prothrombin or vitamin K) and a reduction of blood pressure to under 140 mmHG (systolic), by anti-hypertensive medications DO NOT USE ASPIRIN SERIOUSLY DO NOT USE ASPIN It will fucking kill the patient (Slide 43)
60
What are some long-term preventative treatments for a ischaemic stroke?
Reduction of risk factors by using drugs such as statins, anti-platelets, anti-hypertensitives, anti-DM (anti-diabetes medication) and via lifestyle changes, such as maintaining a healthy diet, exercise and quitting smoking (Slide 44)
61
What is the immediate treatment for deep vein thrombosis or thromboembolism?
Small clots may resolve on their own as the body makes and breaks clots frequently. For any clots that don't auto-resolve an anti-coagulant (such as a low molecular weight heparin) is injected, and a thrombolytic therapy (tPA, alteplase etc) may be used in healthier patients Surgical interventions may be used, namely a thrombectomy or an inferior vena cava filter (Slide 45)
62
What is a thrombectomy and when is it used?
A thrombectomy is when a clot is removed surgically using a catheter. It is used to treat deep vein thrombosis or thromboembolism if the clot is large, resistant to pharmacological interventions or if it is in a critical area where it may cause significant complications (Slide 45)
63
What is an interior vena cava filter?
An inferior vena cava (IVC) filter is a small, mesh-like device that is implanted into the inferior vena cava which is designed to trap blood clots which have broken loose from the deep veins before they reach the lungs, causing a pulmonary embolism. (Slide 45)
64
When is an interior vena cava filter used?
When patients cannot take anti-coagulants for any reason, such as them having liver impairment, or if anti-coagulant therapy is not effective. (Slide 45)
65
What are 3 methods / drugs which can contribute to long-term preventative treatment for deep vein thrombosis or thromboembolism?
Oral anticoagulants (vit K inhibitors like warfarin or factor X inhibitors like apixaban / rivaroxaban) In pregnancy, an anticoagulant such as heparin is injected. Low doses of aspirin can be used to prevent formation of new clots (doesn't treat existing condition) Mechanical methos (such as compression, venous foot pump or exercise) (Slide 45)

BM322: Biomedical Pharmacology (14 decks)

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