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Y3 > Cardiovascular Disease > Flashcards

Cardiovascular Disease Flashcards

1
Q

What is occurring during systole?

A

contraction and emptying of chambers

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2
Q

What is occuring in diastole?

A

relaxation and filling of chambers

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3
Q

Describe the action potential occuring in the pacemaker cells in the heart (sinoatrial node).

A
  • Cells are autorhythmic
  • Cells can initiate and conduct action potentials (self-induced)
  • Has no resting membrane potential, constantly firing
  • Cells slowly drift towards the threshold (~40mV)
  • Sodium induces the action potential (positive charge crossing membrane starts a slow depolarisation)
  • Calcium rushes into the cell which causes rapid depolarisation. The L-type calcium channels will then close when the peak is reached.
  • Repolarisation is initiated by potassium leaving the cell through rectifier channels.
  • This action potential uses: L-type channels (VGCC), T-type channels (VGCC), funny channels (Na) and rectifier channels (K).
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4
Q

Describe the action potential occuring in the cardiomyocyte cells.

A
  • Cells have a resting membrane potential, so are not autorhythmic (~70mV)
  • Cardiomyocytes only use L-type VGCCs
  • Sodium influx induces the action potential. Permeability for sodium increases causing rapid depolarisation.
  • At the peak of the action potential, sodium permeability decreases and potassium permeability is increased allowing for it to leave the cell, which initiates slow repolarisation.
  • Shortly after, L-type channels open allowing Calcium in slowly which causes a plateau.
  • Then the calcium channels shut and potassium leaves the cell rapidly through rectifier channels again causing repolarisation back to the resting potential.
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5
Q

How have each cardiac cell type adapted to fit its function?

A
  • The pacemaker cells in the sinoatrial node have adapted to allow for autorhythmicity, which allows for constant firing of the action potential.
  • The cardiomyocyte has adapted to allow calcium inside the cell during the action potential which allows the muscle cell to contract to push blood out of the heart.
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6
Q

What lifestyle advice can be offered to patients as part of primary prevention?

A
  • behaviour change
  • healthy eating
  • cardioprotective diet
  • physical activity
  • weight management
  • alcohol and smoking
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7
Q

Primary prevention of CVD for people with/without Type 2 DM

A
  • If QRISK3 >= 10%, offer Atorvastatin 20mg daily
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8
Q

Primary prevention of CVD for people with Type 1 DM

A
  • Offer 20mg Atorvastatin daily
  • Offer when: >40y/o, DM for >= 10yrs, establiashed nephropathy, other CVD risk factors
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9
Q

Secondary prevention (after CV event) for people with/without Type 1 or 2 DM

A
  • Offer 80mg Atorvastatin daily
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10
Q

Primary AND secondary prevention for people with CKD

A
  • Offer 20mg Atorvastatin daily
  • If eGFR is >30, dose increase? (renal specialist)
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11
Q

What are the side effects of statin therapy?

A
  • statin related muscle toxicity (SRM) - elevated creatine kinase, symmetrical muscle pain and/or weakness, large proximal muscles
  • GI disturbances, hepatotoxicity, new onset Type 2 DM, intercranial haemorrhage, sleep disturbance
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12
Q

What can be done for intolerance to statins?

A
  • De-challenge (reduce dose)
  • Re-challenge
  • Change statin (hydrophilic = Rosuvastatin, lipophilic = Atorvastatin)
  • Alternate days dosing
  • Alternate drug (Ezetimibe, PCSK9i, Inclisiran)
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13
Q

How are fibrates chemically activated in the body?

A

They are a pro-drug, and the ester group needs to be cleaved before it can be active. The active species has a carboxylic acid group.

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14
Q

Describe the mechanism of action of bile acid sequestrants.

A
  • The drug itself is a chemical drug - it has no biological target.
  • When the patient takes the sequestrant, it travels to the gut where bile acid emulsifies fat, and exchanges anions with the bile acid. In most circumstances, Cl- is exhanged for OH-. The polymer is then excreted with the bile acid attached to it.
  • Increased excretion of bile acids means increased bile acids synthesised from cholesterol meaning reduced overall cholesterol levels.
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15
Q

Describe the mechanism of action of statins.

A
  • competitive, reversible inhibition of HMG-CoA reductase.
  • the enzyme itself is responsible for the inhibition of an early rate-limiting step in cholesterol biosynthesis, the conversion of HMG-CoA to mevalonate (mevalonic acid).
  • as well as this, due to reduced levels of cholesterol in the liver lead to an increased upregulation of LDL receptors in the liver, which lead to increased hepatic uptake of cholesterol.
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16
Q

Why is Aspirin effective as an anti-platelet drug?

A
  • Aspirin inhibits COX-1 irreversibly
  • This means that thromboxane A2 and prostacyclin will both not be formed.
  • Prostacyclin (PGI2) is an inhibitor of platelet aggregation and can be resynthesised in endothelial cells, whereas thrombxane A2 requires new COX regeneration.
  • If thromboxane A2 is inhibited for longer than prostacyclin, this means that at a low dose Aspirin can act as an anti-platelet drug.
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17
Q

Describe the mechanism of action of Clopidogrel.

A
  • it is an irreversible antagonist of the P2Y12 subtype of the ADP receptor found on platelets. This antagonistic effect prevents ADP from binding and activating platlet aggregation.
  • undergoes in vivo metabolism into active species
  • once activated, thiol can form disulphide bond with receptor
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18
Q

Describe the different classes of cholesterol.

A
  • VLDL, IDL, LDL and chylomicrons - bad cholesterol
  • HDL - good cholesterol
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19
Q

What apoprotein is found on chylomicrons?

A

B48 (A,C,E)

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20
Q

What apoprotein is found on VLDL?

A

B100 (A,C,E)

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21
Q

What apoprotein is found on IDL?

A

B100, E

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22
Q

What apoprotein is found on LDL?

A

B100

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23
Q

What apoprotein is found on HDL?

A

AI, AII (C,E)

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24
Q

What are each of the different lipoprotein classes responsible for?

A
  • chylomicrons - lipid transport from gut
  • VLDL, IDL, LDL - transport triglycerides and deposit glycerol and fatty acids in cells
  • HDL - reverse cholesterol transport
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25
Q

What pathways are associated with endogenous lipids?

A
  • Cholesterol (from diet and liver) and newly synthesised TGs travel as VLDL to muscle and adipose tissue
  • TGs hydrolysed by lipase in tissues, fatty acids and glycerol are liberated.
  • Lipoprotein particles become smaller but retain cholesteryl esters and become LDL, which binds to LDL receptors on hepatocytes (LDL receptors recognise ApoB100 on LDL particles)
  • Cholesterol deposited in tissues for cell membranes and other functions
  • Cholesterol can return to plasma and liver for tissues via HDL (reverse cholesterol transport)
  • Cholesterl esterified with long chain fatty acids in HDL and transferred to VLDL or LDL in plasma by cholesteryl ester transfer protein (CETP).
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26
Q

Describe the LDL receptor pathway.

A
  1. LDL approaches the liver hepatocyte and binds to LDL receptor, which initiates receptor mediated endocytosis.
  2. The LDL and its receptor are taken up into a coated vesicle. This then starts to dissociate the LDL from the receptor. There is also a pH drop from 7 to 5.
  3. The vesicle then splits in two smaller vesicles, one containing the LDL and the other containing the receptor.
  4. The vesicle containing the LDL combines with a lysosome. Enzymes from the lysosome cause the release of cholesterol into the cytosol.
  5. The vesicle containing the receptor recycles it back onto the cell surafce via exocytosis.
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27
Q

Describe the pathway of reverse cholesterol transport.

A
  1. HDL is assembled in the liver and intestine (pre-βHDL).
  2. HDL acquires cholesterol from cell membranes in the peripheries via the ABCA1 transporter (ATP-binding casette transporter A1).
  3. Cholesterol acquired by HDL is esterified by lecithin cholesterol acyltransferase (LCAT)
  4. The cholesteryl esters move into the interior of the HDL particle which enlarges it, making it spherical - it is now HDL-3.
  5. Cholesteryl ester transfer protein (CETP) aids the transfer of cholesteryl esters to chylomicrons, VLDL and remnant particles in exchange for triglycerides.
  6. The acquisition enlarges the HDL again into HDL-2.
  7. Cholesterol remaining in the HDL-2 can be carried to the liver. There, HDL-2 can bind to scavenger receptor B1 and transfers cholesterol to the cell membrane.
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28
Q

Describe the enzymes involved with lipid transport.

A
  • ACAT-acyl-CoA (cholesterol acyltransferase) - catalyses intracellular synthesis of cholesteryl esters in macrophages, adrneal cortex, gut and liver
  • LCAT (lecithin cholesterol acyl transferase - catalyses cholesteryl ester synthesis in HDL particles
  • CETP (cholesteryl ester transfer protein) - transfer of cholesteryl esters between HDL to LDL or VLDL
  • PLTP (phospholipid transfer protein) - transfer of triglycerides and cholesterol between different classes of lipoproteins in plasma
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29
Q

Describe the aeitology of primary and secondary dyslipidaemia.

A
  • Primary - combination of diet and genetics
  • Secondary - underlying cause (disease or certain drug)
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30
Q

Describe the stages of Atherosclerosis.

A
  1. Injury occurs to endothelial cells (High BP, smoking, high cholsterol)
  2. Adhesion molecules come to surface and monocytes bind to endothelial cells
  3. LDL becomes oxidised and bind to adhesion molecules and monocytes leading to formation of foam cells
  4. Foam cells stick to the blood vessels underneath endothelial cells. This causes the smooth muscle to move, reducing the diameter of the artery.
  5. Plaque forms, blocking the flow of blood
  6. A necrotic core forms as there is a hypoxic and nutrient-deficient area in the build up
  7. Fibrous cap over build up can thin and eventually rupture causing myocardial infarction and/or stroke
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31
Q

Why is Lipoprotein A considered a risk factor?

A
  • LDL is stronlgy associated with Atherosclerosis
  • Locaslised to atherosclerotic lesions
  • Apo(A) - structurally similar to plasminogen
  • Lipoprotein(A) inhibits binding of plasminogen to receptorrs on endothelial cells - leads to less plasmin generation and promotiom of thrombosis
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32
Q

Describe the mechanism of action of the fibrates.

A
  • Agonists for PPARalpha - subfamily of nuclear receptors that modulate lipid and carbohydrate metabolism and induce differentiation of different adipocytes (lipase - breakdown of VLDL and ApoA1 and ApoA5 - increased HDL production)
  • Increased hepatic uptake of LDL
  • Increased fatty acid uptake and synthesis of acyl CoA, therefore less fatty acids for TG synthesis
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33
Q

Describe the mechanism of action of Ezetimibe.

A
  • Blocks cholesterol absorption, without affecting absorption of fat-soluble vitamins, TGs or bile acids
  • Acts on NCPC1L1 in brush border enterocytes which is responsible, in part, for cholesterol absorption in the GI tract
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34
Q

Describe the mechanism of action of Alirocumab and Evolocumab

A
  • They are mAbs that target proprotein convertase subtilisin/kexin type-9 (PCSK9).
  • By doing this, they can increase receptor number and decrease LDL uptake into hepatocytes.
  • By binding to receptors, they can force lysosomal degradation which prevents uptake of LDL from the blood
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35
Q

Describe the mechansim of action of Inclisiran.

A

Inclisiran is an siRNA treatment that inhibits translation of PCSK9 mRNA (gene silencing).
1. Ga1NaC targets Inclisiran to the heptatocyte ASGP receptor.
2. Endosomal uptake occurs, Ga1NaC cleaved, ASGPR recycled to cell membrane
3. Inclisiran slowly released from endosomes, resulting in sustained therapeutic effect
4. Inclisiran enters the RNA-induced silencing complex (RISC)
5. Inclisiran sense and anti-sense strands separate
6. Inclisiran anti-sense strand directs RISC to bind PCSK9 mRNA strands, triggering catayltic cleavage and reducing production of PCSK9.
7. Reduced PCSK9 results in increased LDL receptor recycling to the hepatocyte surface and increased clearance of circulating LDL.

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36
Q

Describe the mechanism of platelet adhesion, activation and secretion.

A
  1. Endothelial cells exposed to damage, platelets become activated by ADP and TXA2.
  2. Basement membrane becomes exposed to ECM (collagen and Von-Willebrand factor) - they combine and induce platelet aggregation
  3. Platelet aggregation causes platelet activation. Fibrinogen binds to glycoprotein IIb/IIIa receptors on platelet, forming links between platelets causing aggregation.
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37
Q

Describe the mechanism of action of Ticagrelor.

A
  • blocks P2Y12 ADP receptors on platelets
  • acts at a different binding site to ADP so allosterically inhibits
  • blockage is reversible
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38
Q

Describe the mechanism of action of glycoprotein IIb/IIIa receptor antagonists.

A

Inhibits all pathways of platelet activation because drug binds to GP IIb/IIIa receptors, blocking fibrinogen which inhibits aggregation of platelet

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39
Q

Describe the role of thrombin.

A
  • Thrombin cleaves fibrinogen, producing fragments that polymerise to form insoluble fibrin
  • Activated factor XIII (stabilising factor) - strengthens fibrin links
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40
Q

What three things can initiate the intrinsic pathway of the coagulation cascade?

A

collagen, kallikrein, kininogen act on factor XII (hageman factor)

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41
Q

What initiates the extrinsic pathway of the coagulation cascade?

A

damage to endothelial tissue catalyses the conversion of factor III (tissue factor) into factor IIIa

42
Q

Describe the role of the liver and Vitamin K in coagulation.

A
  • The Liver synthesises clotting factors and Vitamin K
  • Vitamin K is required for synthesis of factors II, VII, IX, X
43
Q

Describe the mechanism of action of heparins.

A
  • activate antithrombin III (ATIII)
  • inactivates thrombin and Xa
  • accelerates rate of action of ATIII.
44
Q

Why is the effect of LMWH more predictable then UFH?

A

LMWHs inhibit mainly factor Xa, where as UFHs inhibits both thrombin AND factor Xa. LMWHs effect is more predictable this way.

45
Q

Describe the mechanism of action of Warfarin.

A
  • inhibits vitamin K reductase
  • competitive inhibition
46
Q

What is the fibrinolytic system?

A
  • It is the clot resolution system, which is activated when haemostasis has been restored.
  • Clot removal is spearheaded by plasmin formation, which is a potent proteolytic enzyme which attacks and breaks down fibrin.
  • Plasmin is formed by plasminogen (proenzyme)
  • Plasmin has a biological affinity for fibrin but requires activation by: tissue plasmin activators (tPA), urokinase plasminogen activator (uPA) and kallikrein.
47
Q

What happens in fibrinolysis?

A
  • Plasminogen becomes activated into plasmin by plasminogen activators (tPA, uPA, kallikrein, neutrophil elastase)
  • Plasmin has high affinity for fibrin, and binds itself. This results in degredation of the clot.
  • Fibrin degradation products are remaining after.
48
Q

What drugs are used to stimulate fibrinolysis?

A
  • Streptokinase
  • Human recombinant tPA (Reteplase, Alteplase, Tenecteplase)
  • Urokinase
49
Q

Which fibrinolytic drugs are ‘clot-selective’ and why?

A

Alteplase, Reteplase and Tenecteplase are clot-selective as they are more active on fibrin-bound plasminogen than plasma plasminogen.

50
Q

What anti-anginal agents can be used for treatment of stable angina?

A
  • oragnic nitrates
  • CCB
  • beta-adrenoreceptor antagonists - Bisoprolol, slows the heart which reduced metabolic demand
  • Potassium channel activators - Nicorandil, vasodilator
51
Q

Describe the mechanism of action of nitrates.

A
  • Nitric oxide is released from organic nitrates
  • NO diffuses into smooth muscle and induces Guanylate cyclase
  • Guanylate cyclase then induces the accumulation of cGMP from GTP.
  • This then induces Myosin groups in order to relax smooth muscle and dilate vessels
52
Q

Describe what Class 1a Vaughan-Williams drugs do to the action potential.

A
  • They reduce the rate of rise of phase 0 (Na+ entering cell)
  • Lengthen action potential
53
Q

Describe what Class 1b Vaughan-Williams drugs do to the action potential.

A
  • They reduce the rate of rise of phase 0 (Na+ entering cell)
  • Shorten action potential
54
Q

Describe what Class 1c Vaughan Williams drugs do to the action potential.

A
  • They reduce the rate of rise of phase 0 (Na+ entering cell)
  • No effect on length of action potential
55
Q

Describe what Class 2 Vaughan Williams drugs do to the action potential.

A

Predominant action is on sinoatrial node - increases time between action potential firing

56
Q

Describe what Class 3 Vaughan Williams drugs do to the action potential.

A

Widen duration of action potential

57
Q

Describe what Class 4 Vaughan Williams drugs do to the action potential.

A

Predominant action is on atrioventricular node - shorten plateau phase of action potential.

58
Q

Describe the mechanism of action of Digoxin.

A
  1. Digoxin inhibits Na+/K+ ATPase pump
  2. Na+ conc. increases inside cardiomyocyte
  3. Exchange of Na+ for Ca2+ is increased
  4. Intracellular Ca2+ increases
  5. Influx of Ca2+ from sarcoplasmic reticulum
  6. Increased contractility of cardiac muscle
59
Q

Describe the mechanism of action of Adenosine.

A
  • Adenosine binds to A1 receptor which reduces the conduction time in the AV node
  • Decreased cAMP levels lead to decreased chronotropy and dromotropy
60
Q

Describe each of the Vaughan Williams anti-arrythmics.

A

Class 1a,b,c - Na+ transporter blockers
Class 2 - beta-blockers
Class 3 - K+ channel blockers
Class 4 - Ca2+ channel blockers

61
Q

List the different types of cardiotropic effects.

A

Chronotropy - affecting rate of SA node firing
Inotropy - affecting force of contraction
Dromotropy - affecting conduction in AV node

62
Q

What is Coronary Heart Disease?

A

A condition where vascular supply to the heart is impeded by atheroma, thrombosis or spasm. Inadequate supply of blood to heart results in decreased O2 supply. This can result in stable angina, ACS (MI and unstable angina) and sudden death.

63
Q

What is stable angina?

A
  • narrowing of coronary arteries due to atherosclerotic plaques
  • chest pain occurs during exercise, stress, heavy meals or extreme temperatures
  • relieved by rest (decreased demand on heart) or S/L GTN
  • “demand ischaemia”
64
Q

What management options are available for stable angina?

A
  • symptom control - S/L GTN for acute angina, anti-anginals (1st line: beta blockers, CCBs and 2nd line: long acting nitrate (ISMN), Ivabradine, Nicorandil
  • Secondary prevention - lifestyle changes, anti-platelet (Aspirin), statins
65
Q

What cardiac enzymes are raised in NSTEMI/STEMI?

A
  • troponin T and I
  • creatine kinase (CK-MB)
  • aspartate transaminase and lactate dehydrogenase (not used routinely)
66
Q

Describe the immediate management of a STEMI.

A
  • Oxygen (if indicated)
  • Diamorphine + anti-emetic
  • Aspirin 300mg STAT ASAP
  • Clopidogrel 300mg STAT (or Ticagrelor 180mg, or Prasugrel 60mg)
  • PPCI - angioplasty and stenting
  • OR if PPCI not available, offer fibrinolysis
67
Q

Describe the immediate management of a NSTEMI or unstable angina.

A
  • Oxygen if indicated
  • Diamorphine + anti-emetic
  • Aspirin 300mg STAT ASAP
  • Clopidogrel 300mg STAT (or Ticagrelor 180mg, or Prasugrel 60mg)
  • Also: Fondaparinux until stable
  • NO PPCI OR FIBRINOLYSIS
  • Use GRACE to decide next steps
68
Q

Describe the secondary prevention of all ACSs.

A
  • Dual anti-platelet therapy (DAPT) - Aspirin + Clopidogrel (or Ticagrelor or Prasugrel) - DAPT for 12 months, Aspirin for life
  • Beta-blocker (Bisoprolol, start low go slow)
  • ACEi
  • High intensity statin - Atorvastatin 80mg
  • Lifestyle changes
69
Q

Describe the two causes of the heart to fail.

A
  1. Pump failure - reduction in contractile ability of heart muscle
  2. Overloading - overwork and over stretch of cardiac muscle (excessive after and preload)
70
Q

What is pre-load?

A

Volume of blood present in a ventricle of the heart after passive filling and atrial contraction.

71
Q

What is after-load?

A

The pressure that the chanber of the heart has to generate in order to eject the blood from the chamber.

72
Q

Describe compensated heart failure.

A

Occurs after an MI, contractility of cardiac muscle immediately drops and cardiac output falls. Heart will compensate this change by: enlarging of the heart, arterial constriction to increase perfusion, sympathetic drive increases and salt and water are retained to release Aldosterone which increases pre-load.

73
Q

Describe decompensated heart failure.

A

If MI is very severe, there is extensive damage to cardiac muscle. Damage is too much for heart to compensate and becomes overwhelmed.

74
Q

Describe the oedema features seen in left-sided heart failure.

A
  • pulmonary oedema (dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea)
  • cough/wheeze
  • central cyanosis
  • tiredness
  • breathlessness
75
Q

List some clinical features of heart failure.

A
  • exercise limitation - decreased cardiac output means impaired oxygenation
  • shortness of breath - fluid build-up in lungs from back pressure of failing heart
  • oedema - due to retention of salt and water
76
Q

Describe the oedmea features seen in right-sided heart failure.

A
  • peripheral oedema
  • hepatomegaly (liver enlargement)
  • raised jugular venous pressure
  • fluid and electrolyte retention
77
Q

Describe Class I of the New York Heart Association Classfication of Heart Failure symptoms.

A

No limitation. Ordinary physical activity does not cause fatigue, breathlessness or palpitation.

78
Q

Describe Class II of the New York Heart Association Classfication of Heart Failure symptoms.

A

Slight limitation of physical activity. Such patients are comfortable at rest. Ordinary physical activity results in fatigue, palpitation and breathlessness or angina pectoris (‘mild’ heart failure)

79
Q

Describe Class III of the New York Heart Association Classfication of Heart Failure symptoms.

A

Marked limitation of physical activity. Alrthough patients are comfortable at rest, less than ordinary activity will lead to symptoms (‘moderate’ heart failure)

80
Q

Describe Class IV of the New York Heart Association Classfication of Heart Failure symptoms.

A

Inability to carry on any physical activity without discomfort. Symptoms of congestive heart failure are present even at rest. With any physical activity, increased discomfort is experienced (‘severe’ heart failure)

81
Q

HFrEF

A

Heart failure with reduced ejection fraction (<=40%)

82
Q

HFpEF

A

Heart failure with preserved ejection fraction (>=50%)

83
Q

HFmrEF

A

Heart failure with mid-range ejection fraction (41-49%)

84
Q

chronic heart failure

What is the treatment pathway for HFrEf?

A
  1. Offer ACEi and beta-blocker (Consider mineralcorticoid receptor antagonist if symptoms continue)
  2. Specialist re-assessment - ARNI, Digoxin, Ivabradine, Hydralazine
85
Q

acute heart failure

What should be used if a patient comes into hospital with heart failure symptoms?

A
  • Furosemide IV (no more than 4mg/minute)
  • Metozalone can be used if Furosemide is not effective enough
86
Q

What scoring system is used in stroke prevention for AF?

A

CHA2DS2-VASc. Consider anti-coagulation if score for man >1 or woman >2.

87
Q

What scoring system is used to assess bleeding risk before starting anticoagulation therapy?

A

ORBIT. 0-2 low risk, 3 medium risk, 4-7 high risk.

88
Q

What is first line for rate control in AF?

A
  • Strandard beta-blocker (Bisoprolol) or rate-limiting CCB (Diltiazem, Verapamil, C/I IN HFrEF)
  • Digoxin if sedentary lifestyle
  • If monotherapy is not effective, combine 2 of beta-blocker, Diltiazem or Digoxin.
89
Q

What is first line for rhythm control in AF?

A
  • Electrical cardioversion
  • standard beta-blocker
  • Dronedarone, Amiodarone (esp. in HF)
90
Q

What are the side effects of Amiodarone?

A
  • bradycardia
  • phototoxicity - avoid sunlight
  • slate-grey skin
  • taste disturbances
  • corneal mircodeposits
  • liver dysfunction
  • thyroid dysfunction
  • pulmonary toxicity
91
Q

What are the side effects of Digoxin?

A
  • N&V
  • blurred vision
  • anorexia
  • bradycardia
92
Q

What interaction occurs between Amiodarone and Digoxin, and what action should be taken?

A
  • Amiodarone increases the levels of Digoxin.
  • Reduce dose of Digoxin by 50% if continued use.
93
Q

What is a transient ischaemic attack?

A

The acute loss of focal, cerebral or ocular function with symptoms lasting less than 24 hours.

94
Q

What are the two different types of haemorrhagic stroke, and how they present?

A
  • intracerebral haemorrhage - blood vessel bleeding into the deep cerebral tissue of the brain
  • subarachnoid haemorrhage - blood vessel near the surface of the brain bleeding into the subarachnoid space
95
Q

What are ischaemic strokes caused by?

A
  • Arterial thrombosis - clot forms in one of the arteries in the brain, caused by the rupture of athersclerotic plaques.
  • Arterial embolism - clot or debris forms/accumulates at a site away from the brain. This may be dislodged and move to the brain causing a clot.
96
Q

What is the ischaemic penumbra?

A

The areas peripheral to the infarct where there is reduced perfusion. This tissue can remain viable for several hours.

97
Q

What is the immediate management of a TIA with no AF (within 24 hours)?

A
  • Aspirin 300mg STAT, unless C/I
98
Q

What is the immediate management of a suspected minor stroke and TIA with no AF (within 24 hours)?

A

Refer to specialist. Repeat is very likely!

99
Q

What is the immediate management of a confirmed minor stroke and TIA with no AF (within 24 hours)?

A
  • Dual anti-platelet therapy + PPI
  • Clopidogrel 300mg STAT, then 75mg OD (continue 75mg long term as monotherapy)
  • Aspirin 300mg STAT then 75mg for 21 days
  • The same management can be done with Ticagrelor substituted for Clopidogrel
100
Q

What secondary prevention management is required after a minor stroke?

A
  • Anti-thombotic (anti-platelet)
  • Hypertension control (if needed)
  • High intensity statin (Atorvastatin 80mg)
101
Q

What is the immediate management of a confirmed minor stroke and TIA with AF (within 24 hours)?

A
  • rapid onset anti-coagulant, unless C/I
102
Q
A

Y3 (6 decks)

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