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Medicine 2 > RCM Week 4 ( Atrial Fibrillation) > Flashcards

RCM Week 4 ( Atrial Fibrillation) Flashcards

1
Q

Where are spontaneously firing cells located and what are their spontaneous discharge rates

A

1) SA node (right atrial wall near opening of superior vena cava) 70-80 action potentials / min
2) AV node (base of right atrium near septum, just above A-V junction) 40-60 action potentials / min
3) bundle of His, bundle branches, purkinje fibres 20-40 action potentials / min

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2
Q

What is the order that excitation spreads in a coordinated manner through the specialised conducting tissue

A
  1. SA node (pacemaker)
  2. Rapidly through atria (1m/sec)
  3. AV node (0.05 m/sec)
  4. Rapidly through bundle of His and down the bundle branches and purkinje fibres (1-4 m/sec)
  5. Through the ventricular muscle cells
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3
Q

What facilitates the rapid spread of excitation through the heart

A

Intercalated discs between the fibres

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4
Q

What is the role of gap junctions

A

Provide low resistance pathways and therefore cardiac muscle functions as a syncitium (single unit)

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5
Q

How is efficient emptying of blood from atria to ventricles enabled

A

Co-ordination of the spread of excitation means that atrial excitation and contraction are complete before ventricular contraction (due to AV delay)

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6
Q

Describe the role of calcium is excitation-contraction coupling

A
  • Influx of Ca2+ during action potential
  • triggers release of further Ca2+ from sarcoplasmic reticulum
  • free Ca2+ activates contraction of myocardial fibres (systole)
  • amount of Ca2+ determines cross bridge cycling and force of contraction
  • uptake of Ca2+ by sarcoplasmic reticulum and extrusion of Ca2+ by Na+ / Ca2+ exchange and outward Ca2+ pump
  • lowers free Ca2+ allowing relaxation (diastole)
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7
Q

Which direction does ventricular excitation / contraction occur from

A
  • endocardium to epicardium and

- apex to base

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8
Q

What does an electrocardiogram measure

A

Electrical activity of the heart (depolarisation and repolarisation) recorded from electrodes positioned on the surface of the body (the electrocardiograph is the recorder)

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9
Q

What does an ECG provide information about

A

1) timing and direction of cardiac events: atrial and ventricular depolarisation, ventricular repolarisation
2) rate/ rhythm disturbances : tachycardia / bradycardia ; sinus rhythm; arrhythmia

3) conduction abnormalities : A-V conduction time

4) mass of active myocardium :
Ischaemic areas

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10
Q

Rules of interpreting an electrocardiogram

A

1) depolarisation moving towards a positive electrode gives an upward deflection
2) depolarisation moving away from a positive electrode gives a downward deflection
3) amplitude is maximal when the positive electrode is not the vector and minimal / biphasic when perpendicular
4) depolarisation moving towards a negative electrode gives a downward deflection
5) depolarisation moving away from a negative electrode gives an upward deflection ie a vocally positioned negative electrode records the same thing as a diametrically opposite positive electrode

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11
Q

What are the 3 essential parts of the electrocardiograph

A

1) an amplifier - magnifies the small potential differences produced by the electrical activity of the heart and manifest at the surface of the body
2) recording system - gives a visual display and / or permanent record of these potential changes
3) selector- allows records to be taken from various combinations of electrodes

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12
Q

What does an ECG do

A

Examines the coordination of excitation within the heart by the changes in electrical potential at the body surface caused by the electrical activity of the heart

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13
Q

What is on the x and y axis of the ECG trace

A

Y axis: amplitude
X axis: time

This allows us to measure the interval between ECG waves (using the R waves) and hence calculate heart rate

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14
Q

Where are the ECG electrodes placed and what colour corresponds with each position

A

Right arm = white
Left arm = black
Right leg = green
Left leg = red

Can be placed on the ankles and wrists or the legs and shoulders and will give the same signal as any activity reaching the wrists / ankles must also pass through the shoulders / legs

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15
Q

What is a 12 lead ECG and where are the additional 6 electrodes placed

A

It is much more common for patients to undergo a 12 lead ECG, where an additional 6 unipolar recording electrodes are positioned on the chest.
Placed as follows:
V1- fourth intercostal space at the right margin of the sternum
V2- fourth intercostal space at left margin of sternum
V3- midway between position 2 and 4
V4- fifth intercostal space at junction of midclavicular line
V5- at horizontal level of position 4 at left anterior axillary line
V6- at horizontal level of position 4 at mid-axillary line

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16
Q

What does atrial fibrillation look like on an ECG

A

Absence of p waves and irregularly irregular QRS complex.
Absence of p waves shows abnormal atrial depolarisation and an irregular QRS complex is caused by abnormal depolarisation of ventricles

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17
Q

What is fibrinolysis

A

The breakdown of a clot

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18
Q

What is warfarin

A

An oral anticoagulant
Prevents unwanted thrombosis
Vitamin K antagonist

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19
Q

Why is warfarin a vitamin k antagonist

A

Vitamin k is essential for production of prothrombin and for post ribosomal carboxylation of glutamic acid residues for these proteins

Warfarin blocks vit K reductase needed for vit K to act as a cofactor

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20
Q

Why do patients with replaced heart valves need warfarin

A

To prevent clot formation

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21
Q

Why is warfarin difficult to use

A

If conc is slightly too high can lead to bleeding so must be monitored by monitoring the INR with a specific target value and adjust the dose
- do this by regularly blood testing the patient

Can cause cerebral, gastric bleeding, coughing up blood, blood in urine or faeces or easy bruising

  • also has lots of drug interactions
    Macrolides prevent the breakdown of warfarin- patient is more likely to bleed
  • may be reduced by enzyme inducers
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22
Q

Examples of injectable anticoagulants

A

Unfractionated heparin or LMWHs (eg enoxaparin, tinzaparin- much easy to use and don’t need monitoring as closely as heparins)

  • activate antithrombin III (natural protein)
  • antithrombin - inactivated some clotting factors and thrombin by complexing with serine protease of the factors
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23
Q

What can you do if patient is given too much warfarin

A

Vit K injection which quickly reverses the effects

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24
Q

What is heparin

A

Acts almost immediately (unlike warfarin which takes a few days)

  • used to prevent thrombosis (venous unstable angina) and used to prevent blood clotting on collection
  • used while warfarin takes effect
  • unfractionated heparin monitored by APTT
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25
Q

What are direct oral anticoagulants (DOACs)

A

Dabigatran: an oral thrombin inhibitor

  • prevents thromboembolism:
  • less bleeding than warfarin
  • fewer drug interactions
  • does not require monitoring
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26
Q

What is prostacyclin

A

A prostaglandin produced by platelets both endothelial cells that line blood vessels - derived vasodilators

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27
Q

What does PGI2 and thromboxane do

A

PGI2- prevents platelet aggregation- acts on platelets to increase cAMP

Thromboxane - promotes aggregation, decreases cAMP

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28
Q

What does nitric oxide do

A

Prevents both platelet adhesion and aggregation by increasing platelet cGMP

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29
Q

How does low dose aspirin work as an anti platelet drug

A

75mg

  • used to prevent MI in patients who have previously had an MI
  • recommended for secondary but not primary prevents
  • reduces incidence of stroke
  • inhibits cycle-oxygenase (irreversible)
  • rarely used as a painkiller nowadays due to the stomach effects
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30
Q

Why does aspirin favour PGI2 over TXA2

A

Because platelets have no nuclei - cant produce any more cycle-oxygenase (COX) - no more TXA2 until new platelets are synthesised (7 days)
- endothelial cells have nuclei and can produce more COX

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31
Q

What is dipyridamole

A

Antiplatelet drug
- phosphodiesterase inhibitor - prevents breakdown of cAMP and cGMP (which are broken down by phosphodiesterases)

  • used to prevent thrombosis
  • also inhibits adenosine uptake
  • used in conjunction with aspirin

Study found dipyridamole plus aspirin is more effective than aspirin alone in prevention of cerebral ischaemia of arterial origin

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32
Q

What is glycoproteins IIb / IIIa

A

ADP from aggregating platelets leads to expression of glycoproteins IIb/ IIIa

GP IIb / IIIa - binds fibrinogen which leads to cross linking of platelets

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33
Q

What is clopidogrel

A

Inhibits ADP- induced expression of glycoprotein. For patients who cant take aspirin - similarity effective / safe

  • recent CURE trial indicated that clopidogrel plus aspirin greatly reduced MIs in patients at risk
  • is used in combination with aspirin
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34
Q

What is abciximab (antiplatelet)

A

Monoclonal antibody against GP IIb / IIa
- given to patients undergoing angioplasty (only use once)
Cannula inserted into radial artery - open coronary artery with balloon and insert stent

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35
Q

What are thrombolytics

A

Used in thromboembolic stroke to dissolve clots with reperfusion

  • alteplase licensed for ischaemic stroke
    Give immediately after an MI- dissolve thrombus that has caused blockage of coronary arteries and the MI (emergency angioplasty is now the primary treatment)
    Also used for pulmonary embolism
  • best given with aspirin but can cause bleeding
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36
Q

What is reperfusion

A

Restoring blood flow after a heart attack or stroke

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37
Q

What is haemostasis

A

The stopping of the flow of blood by coagulation and platelet processes

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38
Q

What are clotting mechanisms

A

Intrinsic - exposed collagen from injured blood vessel wall

Extrinsic - damaged tissue releases thromboplastin

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39
Q

What are platelets

A

Non nuclear cellular fragments
Form mechanical plugs during blood vessel injury
- adhesion and aggregation reactions :
- adhesion: to subendothelial surface on damage / disease- due to binding to Von WIllebrand’s factor
- adhesion causes release reaction: ADP and thromboxane which promote platelet aggregation

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40
Q

What do aggregation and adhesion reactions of platelets lead to

A

Leads to platelet mass to plug area of endothelial damage

Promotes coagulation reaction: -ve charged phospholipids non activated platelets which have adhered to site of damage localise fibrin formation

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41
Q

How can you assess if there is any dysfunction to clotting

A

1) bleeding time
- incisions to forearm with venous cuff
- increased in platelet dysfunction / thrombocytopenia

2) prothrombin time (international normalised ratio INR)
- time for coagulation following addition of thromboplastin
- prolonged by abnormalities of factors VII, X, V, II or I, liver disease or warfarin

3) activated partial thromboplastin time (APTT)
- examines intrinsic pathway
- altered by changes in factors XII, XI, IX, VIII, X, V, II or I

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42
Q

What happens to INR in someone with liver disease

A

They produce less coagulation factors and so INR rises

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43
Q

Disorders of clotting and bleeding

A

Thrombosis- unwanted blood clots

Venous- clots (thrombi) form in veins (DVT) due to stasis of blood, may travel to lungs - pulmonary embolism 
‘Economy class syndrome’

Atrial fibrillation- risk of TIA (transient ischaemic attack) or stroke)

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44
Q

What happens to the heart in atrial fibrillation

A

The atria are diseased, stretched, fibrosed and this stops the SAN from being the pacemaker of the heart and instead you get multiple pacemakers meaning there is no coordinated contraction and this means clots can from in the atria.

In the left atria this can break off and lead to a cardiembolic stroke and in the right atria this would lead to a pulmonary embolism

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45
Q

What is arterial thrombosis

A

Arterial: form at atherosclerotic sites and lead to arterial blockage:

  • heart attack
  • cerebral vessels (stroke)

Biggest killer in the western world at the moment

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46
Q

Describe the atherosclerosis timeline

A
  1. Foam cells
  2. Fatty streak
  3. Intermediate lesion
  4. Atheroma
  5. Fibrous plaque
  6. Complicated lesion / rupture
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47
Q

What is haemophilia A

A

Genetic condition - carried on X chromosome, so males (XY) are most affected and females (XX) are carriers

  • low or lacking factor VIII of the clotting cascade
  • haemorrhage and prolonged bleeding (eg after tooth extraction)
  • treat with factor VIII from blood donors or analogue of vasopressin (ADH) which increases patients factor VIII release
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48
Q

What is emicizumab

A

A monthly subcutaneous injection for patients with haemophilia A instead of daily infusions of factor VIII

  • bispecific MAB: binds to activated factor IX and X
  • very effective at reducing bleeds
    30% of patients with haemophilia A treated with factor VIII develop resistance due to the inhibitory factors produced
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49
Q

What is haemophilia B

A

Deficiency of factor IX

Treated with prophylactic factor IX

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50
Q

What is Von willebrands disease

A

Hereditary lack or defect in vWF
- leads to increased bruising, nose bleeds, mucosal bleeding

Rx: analogue of vasopressin (ADH), factor VIII or vWF

51
Q

What is liver disease

A

Reduced synthesis of clotting factors leads to increased bleeding

  • increased prothrombin time
52
Q

What is thrombocytopenia

A 
Reduced platelet number 
- spontaneous skin bleeding (purpura) 
Causes: 
Idiopathic 
Viral 
Drug induced 
Toxins
53
Q

What is DIC (disseminated intra vascular coagulation)

A

Large amount of fibrin generated by procoagulant material such as amniotic fluid

  • vast consumption of clotting factors and platelets
  • widespread haemorrhage but may also be thrombosis
  • give platelets and fresh frozen plasma
54
Q

What is factor V Leiden mutation

A

Abnormal factor V

  • single nucleotide polymorphism
  • less susceptible to deactivation
  • increases risk of venous (but not arterial) thrombosis
  • esp with oral contraceptives / pregnancy
55
Q

What is anaemia

A

A common clinical condition define by having reduced levels of Hb

  • symptoms include: shortness of breath, weakness / lethargy, tachycardia.
  • skin colour is not a reliable sign as this is determined by blood flow. Nail bed and conjunctiva may be pale
  • may cause angina in elderly patients
  • glossitis (painful red tongue) and angular cheillitis (fissures at corner of mouth)
  • DPG may be elevated in RBCs so O2 more readily given up to tissues
56
Q

What is the difference between acute and chronic bleeding

A

Acute- rapid blood loss as in haemorrhage

  • severe loss of blood
  • BP falls
  • over time there is haemodilution

Chronic - long term bleeding as in gastric bleeding / excessive menstruation

57
Q

What is megaloblastic anaemia

A

Abnormal RBC maturation due to defective DNA synthesis, out of step with cytoplasmic development: bone marrow contains megaloblasts

  • macrocytic due to vit B12 or folate deficiency
  • jaundice due to breakdown of Hb due to increased ineffective erythropoiesis (many are symptomless and diagnosed on blood test)
58
Q

What is folic acid

A

Essential for thymidylate synthesis (a rate limiting step in DNA synthesis as theymidine is a pyrimidine base)
- found in most foods esp liver, greens, yeast and marmite.

59
Q

What is methotrexate

A

A drug that inhibits dihydrofolate reductase (therefore folate regeneration is impaired)

60
Q

What is pernicious anaemia

A

Lack of intrinsic factor for absorption of B12 due to autoimmune disease - treat with hydroxocobalamin

61
Q

What are haemolytic anaemias

A

Increased rate of RBC destruction

  • spherocytosis: genetic, abnormal reduction in RBC membrane protein (spectrin)
  • acquired: haemolytic transfusion reaction, malaria, drug-induced
62
Q

What is sickle cell anaemia

A

Genetic condition : single nucleotide polymorphism

  • AA substitution (valine for glutamic acid)
  • abnormal Hb - insoluble forms crystals at low O2- RBC form sickle shapes and may block microcirculation
  • causes haemolytic anaemia
63
Q

What are the thalassaemias

A

A spectrum of anaemias

  • genetic
  • reduced rate of a or B globin units production many variations
  • deletion of both a genes leads to death in uterus as Hb (y4) produced
  • one a-gene deletion reduced RBC volume and haematocrit
64
Q

What is aplastic anaemia

A

Insufficient production of RBCs, WBCs and platelets (pancytopenia)- although may just be RBCs (pure red cell aphasia)
- decreased resistance to infections, increased bleeding, increased tiredness

  • mostly acquired: viral, radiation or drugs:
    Cytotoxic anti cancer agents, chloramphenicol, sulphonamides, insecticides.

Treat with: bone marrow transplant with tissue match immunosuppressants to prevent immune destruction of stem cells and colony stimulating factors can increase WBC count

65
Q

What is polycythaemia

A

Increased Hb content and haematocrit (>55 in males and >47 in females)
Increased blood viscosity - poor tissue perfusion
S&S:
- ruddy appearance
- cyanosis : sluggish blood flow leads to greater deoxygenation
- headaches
- blurred vision
- hypertension

Caused by:
Primary: changes in bone marrow, stem cell defect
Secondary: increased erythropoietin - altitude, smoking, renal carcinoma

66
Q

What are the stages of heart development

A

1) linear heart tube formation
2) formation of the cardiac loop
3) heart septation
4) cavitation of ventricle
5) formation of valves and great vessels

67
Q

How does the cardiac loop form

A

As the ventricles and bulbus cordis of the heart grow faster than other regions, the heart bends in a rightward direction. This leads to the atrium and sinus venosus which were initially caudal to the ventricle, moving cranially and dorsally

68
Q

What are endocardial cushions

A

Localised swellings in the OFT and AV canal full of extracellular matrix
They grow and protrude more into the lumen

69
Q

What are the stages of septation of the primordial atrium

A

1) perforations form in septum primum, the developing foramen secundum (4 weeks)
2) foramen secundum formed, foramen primum closes and septum secundum is initiated (5-6 weeks)
3) valve of foramen ovale forms from septum primum
4) valve of foramen closes the foramen ovale

70
Q

How are the semilunar valves formed

A

When division of the trancus arteriosus is nearly complete, swellings begin to form near the entrance to the newly formed aorta and pulmonary trunk (outflow region of the heart), from endocardial cushions. These swellings are the primordial aortic and pulmonary valves and will ultimately form the mature semilunar valves

71
Q

Describe postnatal circulation of the heart

A
  • 3 shunts close
  • lungs expand
  • decreasing resistance to blood flow
  • pressure in RA
72
Q

Benefits and drawbacks of plain x ray

A

Benefits:

  • quick and inexpensive examination
  • good for initial examination for assessing lungs and bones
  • low radiation dose

Drawbacks:

  • uses ionising radiation
  • limited spatial information
  • poor examination for soft tissue pathology
73
Q

Benefits and drawbacks of CT

A

Benefits:

  • relatively quick scanning time of large areas of the body
  • provides very good anatomical information in multiple planes
  • appropriate to assess for most acute clinical problems

Drawbacks:

  • can involve large doses of ionising radiation
  • risk of allergy die to iodine based contrast
  • particularly poor at assessing the spinal cord and reproductive organs
74
Q

Benefits and drawbacks of fluoroscopy

A

Benefits:

  • dynamic real time anatomical assessment
  • commonly used for interventional procedures
  • low radiation dose

Drawbacks:

  • doses for complex IR procedures can be large
  • always requires use of contrast agents
  • poor soft tissue assessment and overlapping anatomy
75
Q

Benefits and drawbacks of MRI

A

Benefits:

  • does not sue ionising radiation
  • excellent anatomical detail
  • multiple phases enable some functional assessment of tissues

Drawbacks:

  • time consuming and expensive
  • safety issues regarding metallic implants
  • Claustrophobic
76
Q

Benefits and drawbacks of nuclear medicine

A

Benefits:

  • large numbers of tracers available to assess different tissues
  • provides anatomical and functional information
  • usually allows more definitive assessment of pathology identified on other modalities

Drawbacks:

  • scan acquisition is time consuming
  • poor resolution compared to alternative cross-sectional imaging
  • radiation exposure continues after termination of examination
77
Q

Risks associated with ionising radiation

A
  • damage to tissue can occur directly from radiation exposure or indirectly due to formation of free radicals
  • effects include cataracts and hair loss to more severe malignancy and hereditary effects
78
Q

Define drug interaction

A

An interaction is said to occur when the effects of one drug are changed by the presence of another drug, food, drink or an environmental chemical agent

79
Q

Describe the different pharmacokinetic mechanisms

A

Absorption: 2 drugs may interact to alter rate of uptake eg tetracycline + Fe2+ salts of Ca2+ (milk_

PH: passive absorption of drugs best in unchanged form, governed by pKa value:

  • rises in pH (antacids, H2 antagonists, PPIs) may influence absorption of other drugs
  • separate by several hours
80
Q

What is digoxin

A

Digoxin is used in treating heart failure and arrhythmias and is a substrate for P-glycoprotein

81
Q

What is rifampicin

A

Rifampicin is an antibiotic that is an inducer of P-glycoprotein

82
Q

What is MDR1

A

Multiple drug resistance transporter aka P-glycoprotein / ATP binding cassette

  • may be induced (rifampicin)
  • may be inhibited (verapamil)
83
Q

Describe the drug interaction: displacement

A

Many drugs are protein bound but only act in free form
- drugs may compete for binding sites, resulting in displacement, transient increases in toxicity but then increased elimination

84
Q

What is cytochrome P450- mediated metabolism

A
  • many drugs are metabolised by multiple CYPs
  • some drugs are metabolised by single CYPs and these are the most likely to be involved in clinically- relevant interactions as there is only one pathway in which they are broken down
85
Q

What is P450

A

A family of enzymes in the liver and they start phase 1 metabolism of drugs

86
Q

Describe the interactions of simvastatin

A

Is contraindicated with macrolides (severe) : increases side effects
- interaction with amlodipine, verapamil, diltizaem

  • for amlodipine + statin :
  • use 10mg atorvastatin
  • pravastatin does not interact
  • use 20mg simvastatin as maximum dose
87
Q

What is the induction type of drug interaction

A

Enzyme induction: when an interactions increases the activity of metabolising enzymes eg rifampicin and carbamazepine

  • reduces plasma conc of warfarin
  • monitor INR and increase dose
  • may take a week or 2 for effect
  • effect may persist on stopping inducer
88
Q

What are the risks of NSAIDs and warfarin

A

Significant interactions:

  • aspirin is antiplatelet - enhanced bleeding effects
  • NSAIDs are associated with gastric bleeding which is enhanced by warfarin
  • avoid NSAIDs and warfarin
  • ensure patients on warfarin don’t medicate with NSAIDs
89
Q

What are the risks of warfarin with diet

A

Vit K rich foods may reduce activity of warfarin eg greens such as Brussels sprouts

  • diet may alter anticoagulant control
  • avoid significant changes in diet

Cranberry juice has been shown to potentiate warfarin leading to fatalities

90
Q

What are the effects of grapefruit juice and simvastatin.

A

Grapefruit juice interacts with simvastatin and some Ca antagonists
- psoralen in grapefruit juice may interfere with Cyt P450- dependent metabolism (CYP3A4) and increase levels of simvastatin

  • psoralen may also inhibit P-glycoprotein transport
91
Q

Describe the interactions of clopidogrel and PPIs

A

Omeprazole makes clopidogrel less effective: avoid omeprazole or esomeprazole

  • due to both being biotransformed by the same Cyt P450
  • clopidogrel is no longer converted to active metabolite
92
Q

What are the 4 key interactions

A

Warfarin and NSAIDs: lead to enhanced bleeding
Warfarin and antibiotics (esp erythromycin and ciprofloxacin): lead to enhanced bleeding

Simvastatin and macrolides: avoid
Simvastatin and amlodipine : caution dose

93
Q

Describe clopidogrel resistance

A

Polymorphism of the P2Y 12 receptor may also contribute towards clopidogrel resistance

94
Q

What is the role of the OATP1B1 transporter

A

It is encoded by SLCO1B1 and effluxes simvastatin to remove it from circulation

Some patients have a variant (SLCO1B1*5 which has loss of function so plasma [simvastatin] rises and increases risk of toxicity

95
Q

Describe the warfarin anticoagulant

A 
Dose is individual to patient because there there are lots of competing pathways to the plasma concentration of warfarin (difficult drug to use) 
CYP2C9 polymorphism ( dependent on ancestory) 
- genetic variation in metabolism of S enantiomer 
Reduced clearance, lower doses required
96
Q

Define stroke

A

A sudden focal / global cerebral deficit of vascular origin lasting >24 hours

97
Q

What is an ischaemic stroke

A

85% of all strokes are ischaemic
Occur because of an occlusion of an artery leading to the brain or within the brain itself so the tissue cannot be supplied with sufficient quantities of blood - becomes starved of oxygen and nutrients so tissue starts to die within 30 seconds

98
Q

What are the 2 types of ischaemic stroke

A

Thrombotic - most common type, occur when a blood clot or thrombus actually blocks the blood to the part of the brain (night or early morning) generally preceded by a mini stroke

Embolic- piece of blood clot travels to the brain where it is too tight or narrow to let it pass so it closes the artery (caused by AF)

99
Q

What is a haemorrhagic stroke

A

Caused by rupture of an artery in or on the brain

Intracerebral haemorrhage - 85%
Subarachnoid haemorrhage -15%

Symptoms: headache, nausea, vomiting, reduced consciousness, weakness in one part of the body
High mortality

100
Q

Modifiable risk factors of strokes

A
  • hypertension
  • diabetes mellitus
  • hyperlipidaemia - lipoprotein a
  • CVD : CHD, LVH, asymptomatic carotid stenosis
  • haematological issues: factor VIII, sickle cell disease, fibrinogen
  • inflammatory issues: CRP, WBC count, vWF
  • others: oxidative stress, waist to hip ratio (not BMI), smoking, alcohol, HRT, oral contraceptive use
101
Q

What is sinus rhythm

A

The hearts normal rhythm. It’s rate is between 60 and 100 bpm at rest

102
Q

When does AF occur

A

When abnormal electrical impulses suddenly start firing in the atria which override the hearts natural pacemaker which can no longer control the rhythm of the heart

  • is a condition in which the upper chambers of the heart (atria) beat (quiver) irregularly instead of beating effectively to move the blood into ventricles
103
Q

How does AF cause strokes

A

AF allows blood to slow down or pool thereby increasing the risk of stokes

104
Q

What are the 4 types of AF

A

Paroxysmal AF: episodes come and go and usually stop within 48h without any treatment

Persistent AF: each episode lasts for longer than 7 days (or less when it is treated)

Long standing persistent AF: continuous AF for a year or longer

Permanent AF: AF is present all the time

105
Q

Causes of AF

A 
High blood pressure (hypertension) 
Hardening of arteries (atherosclerosis) 
Congenital heart disease 
Cardiomyopathy 
Heart valve disease 
Asthma, pneumonia, COPD, lung cancer, diabetes
Overactive thyroid gland
106
Q

How is AF treated

A

Treatment options include medications to control heart rate and reduce the risk of stroke and procedures eg cardioversion to restore normal heart rhythm
If there is no underlying cause then treatment options are:
1) medicines to reduce the risk of a stroke (anticoagulants)
2) medicines to control AF (beta blockers, anti- arryhtmics)
3) cardioversion - electric shock treatment
4) catheter ablation (electrocardiology)
5) having a pacemaker fitted

107
Q

Symptoms of strokes

A
  • sudden weakness / numbness in the face, arm or leg - on one side of the body
  • sudden confusion and difficulty speaking or understanding speech
  • sudden vision problems in one or both eyes, uncontrolled eye movements / eyelid dropping
  • sudden loss of balance and coordination
  • sudden difficulty with swallowing or drooling
  • loss of memory
  • personality changes and mood changes
108
Q

How are strokes diagnosed

A

Physical examination n- medical history
BP, HR and cholesterol checks
- neurological examination : monitor for signs and symptoms- location / size of the damage
- the right cerebral hemisphere: difficulties with attention, perception, memory, learning, recognition, visual awareness, spatial awareness, proprioception
- the left hemisphere: language and logical functions, analytical thinking and mathematic skills

109
Q

What is the outcome of a stroke dictated by

A
  • location of the brain damage
  • size of brain damage
  • presence of other medical conditions
  • possibility of stroke returning
110
Q

How are ischaemic strokes treated

A
  • recombinant tissue plasminogen activator - short therapeutic window
  • mechanical thrombectomy (physical removal of blood clot from the larger arteries
  • carotid endarterectomy - surgery to remove carotid plaque
111
Q

How are haemorrhagic strokes treated

A

No medical therapy - treat hypertension or surgery to stop or prevent bleeding

112
Q

How is hypothermia treated

A

Intravascular or surface cooling

113
Q

What are cellular treatment options for strokes

A

Stem cells, endothelial progenitor cells

114
Q

How can you prevent strokes

A

Control high blood pressure (eg ACE inhibitors and ARBs)

  • lower cholesterol (statins)
  • control diabetes
  • quit smoking
  • maintain healthy weight
  • manage stress
115
Q

Causes of dizziness

A
  • postural hypotension
  • hypotension
    -syncope
  • AF
  • vertigo
    (Inner ear infection)
116
Q

How does AF cause dizziness

A

Heart loses the ability to relax properly so atria cannot fill properly so there is resistance at tricuspid or mitral valve. This reduces cardiac output so blood pressure falls

117
Q

3 basic components of the circulatory system

A

1) heart- pump that provides the pressure gradient needed for blood to flow
2) blood vessels - passageways through which blood is distributed to different parts of the body
3) blood- transport medium for delivery of gases, nutrients and hormones

118
Q

What can cause changes in heart rhythm

A

Problems with conduction eg between atria and ventricles (heart block)

Atrial fibrillation (affects 10% of people over 75)

Ventricular fibrillation (this will kill unless attended to very quickly)

119
Q

What is tachycardia and bradycardia

A

Tachycardia - fast heart rate

Bradycardia - slow heart rate

120
Q

What are the symptoms of atherosclerosis in different areas

A

Coronary arteries: angina (chest pain) complete blockage or release of thrombus can cause a heart attack

Carotid artery- slurred speech, muscle weakness, most severely a stroke

Renal artery- hypertension (renal stenosis)

Arms / legs - muscular pain on exercise

121
Q

What does NICE define hypertension as

A

Diastolic BP> 90mmHg

Systolic >140mmHg

122
Q

What are vein-artery-vein triplets

A

In our extremities, muscular arteries are often accompanied by veins on either side so that the pulsation slightly compress the veins, driving the blood towards the heart due tot he valves

123
Q

Where are spontaneously firing cells located

A

1) sino-atrial node (right atrial wall near opening of superior vena cava)
2) atrio- ventricular node (base of right atrium near septum, just above A-V junction)
3) bundle of his, bundle branches, purkinje fibres

Medicine 2 (16 decks)

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