ACS and stroke Flashcards

Question

Most serious type of stroke?

Answer 1

haemorrhagic stroke

Answer 2

Face: the person's face will droop on one side Arms: they will have weakness in their arms (usually on one side) Slurred speech Time to call 999

Answer 3

- "thunderclap" headache -nausea - vomiting -seizures - lose consciousness

Answer 4

the brain region affected and the degree of damage

Answer 5

- weakness or paralysis in one side of the body - difficulties understanding or producing language, and cognitive problems

Answer 6

the brain has only very limited capacity to repair the damage caused by a stroke

Answer 7

brain equivalent of stable angina period of temporary ischaemia during which the person experiences symptoms similar to a full-blown stroke but less severe A TIA can last from minutes to hours but there is no permanent damage like the relationship between stable angina and a myocardial infarction, a TIA is a warning sign that the person may eventually suffer a full-blown stroke

Answer 8

caused by a small thrombus or embolus

Answer 9

once the thrombus dissolves or the piece of debris moves

Answer 10

depriving brain tissue of its oxygen supply will cause cells to become ischaemic and die Ischaemic neurons ALSO release their stores of the excitatory neurotransmitter glutamate Glutamate acts on NMDA and AMPA receptors on neighbouring neurons causing them to become overloaded with calcium and die the immune system moves in and tries to clean up the mess but this can cause even more damage because it triggers inflammation

Answer 11

process of spreading out from the initial focus in a chain reaction of neurons killing their neighbours

Answer 12

"Time" is critical in stroke care: Up to 2 million neurons and 14 billion synapses are lost every minute during an ischaemic stroke, so rapid treatment is essential. Stroke type must be identified first: It’s crucial to determine whether the stroke is ischaemic or haemorrhagic, as incorrect treatment can be fatal. Limited treatment options: The main goal in ischaemic stroke is to restore blood flow to minimize damage. Thrombolytic drugs: Commonly used to dissolve the clot causing the stroke. Antiplatelet drugs: Given to reduce the risk of another stroke, and used long-term. Statins: Often prescribed if the patient isn’t already on one. Research limitations: We still can't effectively target the excitotoxic and inflammatory processes that cause much of the brain damage after a stroke.

Answer 13

Myocardial infarction and stroke are leading causes of death in the UK, causing 25,000 and 34,000 deaths per year, respectively. Significant progress has been made: Between 1971 and 2021, stroke deaths declined by 82% and heart attack deaths by 80%. Improvements are due to better treatments and greater public awareness of risk factors. Regional disparities remain: Death rates from circulatory diseases vary widely, from 230 per 100,000 in the East of England to 329 per 100,000 in Scotland — a more than 40% difference depending on location.

Answer 14

Lifestyle factors significantly increase the risk of acute coronary syndrome (ACS) and stroke, many overlapping with those for hypertension. Major modifiable risk factors (in order of risk): Hypertension poor diet (e.g. excess salt, sugar) Diabetes High LDL cholesterol Obesity (high BMI) Smoking Poor kidney function Lack of exercise Hypertension and hyperlipidaemia are particularly important because they are direct risk factors for both ACS and stroke.

Answer 15

Blood clotting is a normal and essential process that, along with vasoconstriction, prevents blood loss after vessel injury—this is called haemostasis. When clots form inappropriately and in the wrong place, it's called thrombosis. Thrombosis can lead to serious conditions like deep vein thrombosis, embolism, stroke, and heart attacks.

Answer 16

Haemostasis has two phases: primary and secondary Platelets are short-lived cell fragments from megakaryocytes, continuously produced. Haemostasis functions as a chain reaction, with each step triggering the next. The body uses natural anticoagulants and signalling molecules to regulate the process and prevent widespread clotting.

Answer 17

Stabilizes the platelet plug by forming a fibrin mesh via the coagulation cascade.

Answer 18

Involves vasoconstriction and platelet activation. Platelets adhere to damaged vessels and aggregate using fibrinogen.

Answer 19

Fibrinolysis (or thrombolysis) is the process of removing blood clots after vessel repair. It is carried out by the plasmin system, where plasmin breaks down fibrin into degradation products. Plasmin is formed by the activation of plasminogen via tissue plasminogen activator (tPA). The plasmin system is a key target for anti-thrombotic drugs used to treat thrombosis.

Answer 20

Thrombosis occurs when a thrombus (blood clot) forms inside a vessel and blocks blood flow, reducing oxygen supply to tissues. A thrombus is made of fibrin, platelets, and blood cells, similar to normal haemostatic clots. It typically begins attached to the vessel wall. Thrombosis is classified by vessel type: Venous thrombosis: Coagulation plays the dominant role. Arterial thrombosis: Platelets are more critical, though coagulation also contributes. The type of thrombosis affects treatment choice, as different drugs target different aspects of clot formation.

Answer 21

An embolism is a complication of thrombosis, occurring when a thrombus or its fragment detaches and travels through the bloodstream as an embolus. The embolus can lodge in another vessel, blocking blood flow and causing an embolism. Embolisms can be caused by any circulating material (e.g. air embolism), not just blood clots. When the embolism originates from a thrombus, it is specifically called a thromboembolism.

Answer 22

The effects of thrombosis and embolism vary by location. They can cause heart attacks, strokes, DVT, pulmonary embolism (clot in lungs), or limb infarction (blocked blood flow to a limb, causing tissue death).

Answer 23

Preventing thrombosis and embolism is crucial to lower the risk of heart attacks and strokes, both before and after they occur. Dissolving clots could also reduce tissue damage. However, since clotting is essential for normal haemostasis, the challenge is to prevent harmful clots without disrupting necessary clotting, to avoid dangerous bleeding.

Answer 24

Thrombosis can be reduced without disrupting normal haemostasis. There are two main strategies: Antiplatelet therapy – best for arterial thrombosis Anticoagulant therapy – best for venous thrombosis If prevention fails, thrombolysis (using "clot-buster" drugs) or surgical removal of the clot may be used. Drug choice depends on whether the clot is in a vein or artery.

Answer 25

Platelets are cell fragments (not tiny cake holders!) that rapidly respond to blood vessel damage by changing shape and function. Their signalling pathways are crucial to their role—and are key targets for drugs that block platelet activity.

Answer 26

During primary haemostasis, platelets form a plug at the site of blood vessel damage by recognizing, binding to, and recruiting more platelets. In their inactive state, platelets are small, disc-shaped cell fragments from megakaryocytes in the bone marrow and lack a nucleus, which is important later. 3 steps: adhesion, activation of neighboring platelets, and aggregation

Answer 27

When a vessel wall is damaged, connective tissue containing collagen is exposed. The blood does not normally encounter collagen and platelets recognize this as damage to the vessel wall. A glycoprotein receptor called GPIb-IX-V in the platelet binds to collagen via a blood protein called von Willibrand's factor (VWF). The platelet now activates and undergoes a dramatic change to a spider-like shape.

Answer 28

When activated, platelets release signaling molecules like thromboxane A2 (TXA2) and ADP, which activate nearby platelets to help form a clot.

Answer 29

When platelets activate, they express GPIIb/IIIa receptors, which bind fibrinogen and link activated platelets. This activation follows a positive feedback loop, with platelets releasing ADP and TXA2 to recruit more platelets. However, the intact endothelium releases prostacyclin, which inhibits platelet activation and prevents the activation from spreading throughout the circulation.

Answer 30

The coagulation cascade generates the fibrin net that forms blood clots. It involves a series of proteolytic enzymes activating precursor proteins to produce the final product. It's more complex than the renin-angiotensin-aldosterone system, as some enzymes in the pathway activate others downstream. You only need to understand the general cascade process and the drug targets related to it.

Answer 31

two initiation pathways

Answer 32

faster and triggered by tissue factor (TF), which is exposed when tissues are damaged (e.g., by atherosclerotic plaque rupture).

Answer 33

slower and involves components from within the bloodstream

Answer 34

Both pathways converge on the common pathway, which begins with the activation of Factor X to Factor Xa. Factor Xa activates prothrombin (Factor II) to produce thrombin (Factor IIa), which then converts fibrinogen (Factor I) to fibrin. Fibrin forms cross-linked strands, creating a clot. Coagulation is tightly regulated, with antithrombin III (ATIII) inhibiting Factor Xa and thrombin. The focus for drug targets is mainly on the common pathway, involving Factors X, II, I, and ATIII.