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Medicine 1 > Anatomy - Atrial Fibrillation > Flashcards

Anatomy - Atrial Fibrillation Flashcards

1
Q

What are the locations of the spontaneously firing cells in the heart?

A
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2
Q

What are the spontaneous discharge rates in the heart?

A

SA node = 70-80 action potentials/min

AV node = 40-60 action potentials/min

Purkinje = 20-40 action potentials/min

Fastest drive heart, hence SA node

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3
Q

What does the action potential graph of a pacemaker cell look like?

A
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4
Q

What is the route of excitation spread through conducting tissue?

A
  • SA node (pacemaker)
  • Rapidly through the atria (~ 1m/sec)
  • AV node (slow conducting ~ 0.05m/sec - delay)
  • Rapidly through bundle of His & down the bundle branches & Purkinje fibres (~ 1-4m/sec)
  • Through ventricular muscle cells
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5
Q

What aids the rapid spread of excitation in heart?

A

Intercalated discs between fibres

Gap junctions, providing low resistance pathways

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6
Q

How is the spread of excitation coordinated in atria and ventricles?

A

Atrial excitation and contraction are complete before ventricular contraction –> enables efficient emptying of blood from atria to ventricles

Ventricular excitation occurs synchronously –> enables ventricles to contract as coordinated units, expelling blood effectively

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7
Q

What does the action potential graph of ventricular cell look like?

A
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8
Q

What does excitation-contraction coupling require?

What are the order of events?

A

Calcium

  • 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 & 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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9
Q

What is the function of the plateau phase during heart contraction?

A

Protects heart from tetanus

Provides long refractory period

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10
Q

What is the direction of ventricular excitation?

A

Endocardium to epicardium

Apex to base

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11
Q

What does activation of sympathetic nerves do to the heart?

What does the graph look like?

A

Increases heart rate by activating ‘beta’1-adrenoceptors in sino-atrial node

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12
Q

What does activation of parasympathetic nerves do to the heart?

What does the graph look like?

A

Decrease heart rate by activating M2 muscarinic receptors in sino-atrial node

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13
Q

What 5 things does an ECG provide?

A
  • Timing and direction of cardiac events –> atrial and ventricular depolarisation, ventricular repolarisation
  • Rate/rhythm disturbances –> tachycardia/bradycardia, sinus rhythm, arrythmia
  • Conduction abnormalities –> A-V conduction time
  • Mass of active myocardium –> ischaemic areas
  • Nothing about mechanical force, only electrical conduction
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14
Q

What is the difference between indifferent (negative) and unipolar (positive) electrodes?

A
  • = measure average

+ = measure from cells closest

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15
Q

What does depolarisation do to the polarity of a cell?

What happens with depolarisation towards and away from positive electrode?

A

Inside = positive

Outside = negative

Towards = upward deflection on ECG trace

Away = downward deflection on ECG trace

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16
Q

What happens when electrode is perpendicular to depolarisation?

What happens during depolarisation towards and away from negative electrode?

A

No change on ECG trace

Towards = downward deflection on ECG trace

Away = upward deflection on ECG trace

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17
Q

What is the relationship between electrodes on an ECG trace?

What is a bipolar potential?

A

Focally positioned negative electrode = records same as diametrically opposite positive electrode

Both positive and negative

Composite of what + and - electrodes measure

Longer line on ECG trace

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18
Q

What does repolarisation do to a cells polarity?

What are the principles of repolarisation?

A

Inside = negative

Outside = positive

Reverse principle of depolarisation

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19
Q

What is the recorded potential difference?

A

Mean vector of different wavefronts

Excitation = depolarisation moves in different directions

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20
Q

What are the 3 main events of the cardiac cycle?

A
  • Atrial depolarisation
  • Ventricular depolarisation
  • Ventricular repolarisation
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21
Q

What happens during the P wave?

A

Atrial depolarisation

At bottom of peak, all cells are repolarised

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22
Q

What happens during P-Q?

A

Septum depolarisation

Small negative

Generally away from electrode

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23
Q

What happens during QRS?

A

Main ventricular depolarisation

Large positive

Towards electrode

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24
Q

What happens during S-T?

A

Base of ventricle depolarisation

Small negative

Away from electrode

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25
Q

What happens during T wave?

A

Ventricular repolarisation

Positive

Away from electrode

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26
Q

Where do the unipolar limb leads measure?

A
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27
Q

Where do the unipolar chest leads go?

A

4th intercostal space at right sternal margin

5th intercostal space at mid-axillary line

V1-V6

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28
Q

Where are bipolar limb leads placed and how do you get the actual measurement?

A

Left = positive electrode

Right = negative electrode

Actual measurement = between 2 positive electrodes

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29
Q

What are the 2 different ways an ECG can present?

A
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30
Q

What are the 6 rules to remmeber about ECG traces?

A
  • The first wave, irrespective of its polarity, is always called a P wave
  • The final wave is called a T wave (unless U waves (rare) are present
  • The first positive wave after a P wave is called an R wave
  • Any negative wave after a P wave but before an R wave is called a Q wave
  • Any negative wave after an R wave is called an S wave
  • Any positive wave after an S wave is called R’
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31
Q

What are the durations of all of the different ECG waves?

A
  • P duration = 0.08s
  • P-R interval = <0.2s
  • QRS = 0.1s
  • ST length = ejection
  • T-P interval = filling
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32
Q

What does it mean when QRS complex has left or right axis deviation?

A
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33
Q

What are the different types of heart block?

A
  • 1st degree = long P-R
  • 2nd degree = some P with no QRS
  • 3rd degree = complete block = no A-V conduction
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34
Q

What is tachycardia and what does it look like on ECG?

A

Atrial or ventricular

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35
Q

What does atrial fibrillation look like on ECG?

A

Ventricular = requires defibrillation or death

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36
Q

What are the different types of anaemia?

A

–Iron deficiency anaemia

–Megaloblastic anaemia

–Haemolytic anaemia

–Aplastic anaemia

–Sickle cell

–Thalassaemias

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37
Q

What are the symptoms of anaemia?

A
  • Reduced Hb levels
  • Shortness of breath
  • Weakness/lethargy
  • Tachycardia
  • Pale nail bed and conjunctiva
  • Severe elderly may cause angina
  • Glossitis (painful red tongue)
  • Angular cheilitis (fissures at corner of mouth)
  • RBC DPG elevated
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38
Q

What are the causes of anaemia?

A
  • Reduced input –> poor diet, stomach removal
  • Increased output –> menstruation, GI bleeding ulcers, colon cancer
  • Increased demand –> pregnancy
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39
Q

What are the treatment options for anaemia?

A
  • Find and treat underlying cause
  • Oral iron
  • Prophylaxis in pregnancy
  • Transfusion
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40
Q

What are the properties of renal anaemia?

A
  • Complicates CRF
  • Leads to normocytic anaemia
  • Treat with Fe and EPO
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41
Q

What are the properties megaloblastic anaemia?

A
  • Abnormal RBC maturation from defective DNA synthesis (bone marrow contains megaloblasts)
  • Macrocytic
  • Due to vitamin B12 or folate deficiency
  • Jaundice
  • B12 = required for cell division –> from animal products
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42
Q

What are the properties of folic acid?

A
  • Folate = essential for thymidylate synthesis (rate limiting step in DNA synthesis)
  • Found in most foods (greens, liver, yest, marmite)
  • Used in pregnancy
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43
Q

What is the function of methotrexate?

A

Inhibits dihydrofolate reductase

Impaired folate regeneration

Treated with folinic acid

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44
Q

What is pernicious anaemia?

A

Lack of intrinsic factor for B12 absorption due to autoimmune disease

Treat with hydroxocobalamin

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45
Q

What is Chron’s disease?

A

Malabsorption of B12, folate or iron

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46
Q

What are the properties of haemolytic anaemias?

A
  • Increased rate of RBC destruction
  • Spherocytosis - genetic - abnormal reduction in RBC membrane protein (spectrin) - cells fragile
  • Acquired - haemolytic transfusion reaction, malaria, drug-induced
  • Jaundice (?) and enlarged spleen - folate deficiency may occur due to increased erythropoiesis
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47
Q

What are the properties of sickle cell anaemia?

A

•Genetic

  • SNP: Single Nuleotide Polymorphism

•Amino-acid substitution

  • Valine for glutamic acid
  • Abnormal Hb - insoluble forms crystals at low O2 - RBC form sickle shapes and may block microcirculation.
  • Causes haemolytic anaemia
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48
Q

What are the properties of thalassaemias?

A
  • Genetic
  • Reduced rate of ‘alpha’ or ‘beta’ globin units production many variations
  • Deletion of both a-genes leads to death in uterus as Hb (‘gamma’4) produced
  • One ‘alpha’-gene deletion reduced RBC volume and haematocrit
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49
Q

What are the properties of aplastic anaemia?

A
  • Insufficient production of RBCs, WBCs and platelets (pancytopenia) - although may just be RBCs (pure red cell aplasia)
  • Deceased resistance to infections, increased bleeding, increased tiredness
  • Mostly acquired : viral, radiation or drugs
  • Cytotoxic (anticancer) agents
  • Chloramphenicol
  • Sulphonamides
  • Insecticides
50
Q

How do you treat aplastic anaemia?

A
  • Bone marrow transplant - with tissue match
  • Immunosuppressants - to prevent immune destruction of stem cells
  • Colony-stimulating factors - increase WBC count
51
Q

What is polycystaemia and what is it caused by?

A
  • Increased Hb content and haematocrit (>55 in males and >47 in females)
  • Increased blood viscosity - poor tissue perfusion
  • Primary: Changes in bone marrow, stem cell defect
  • Secondary: Increased erythropoietin - altitude, smoking, renal carcinoma
52
Q

What are the signs and symptoms of polycythaemia?

A

–Ruddy appearance

–Cyanosis: sluggish blood flow leads to greater deoxygenation

–Headaches

–Blurred vision

–Hypertension

53
Q

How do you treat primary polycythaemia?

A
  • Venesection (bleeding)
  • Radioactive Phosphorus - myelosuppression
  • Cytotoxic agents - myelosuppression
54
Q

What are all these parts?

A
55
Q

What are the stages of heart development?

A
  • Linear heart tube formation
  • Formation of cardiac loop
  • Heart septation
  • Cavitation of ventricle
  • Formation of valves and great vessels
  • 4-chambered heart
56
Q

What are each of these parts?

A
57
Q

What are each of these parts?

A
58
Q

How does the cardiac loop form?

A
59
Q

What are the benefits of X-rays?

A
  • Quick and inexpensive examination
  • Good for initial examination for assessing lungs and bones
  • Low radiation dose
60
Q

What are the drawbacks of X-rays?

A
  • Uses ionising radiation
  • Limited spatial information
  • Poor examination for soft tissue pathology
61
Q

What are the benefits of CT?

A
  • 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
62
Q

What are the drawbacks of CT?

A
  • Can involve large doses of ionising radiation
  • Risk of allergy to iodine-based contrast
  • Particularly poor at assessing the spinal cord and reproductive organs
63
Q

What are the benefits of fluoroscopy?

A
  • Dynamic real time anatomical assessment
  • Commonly used for interventional procedures
  • Low radiation dose
64
Q

What are the drawbacks of fluoroscopy?

A
  • Doses for complex IR procedures can be large
  • Always requires use of contrast agents
  • Poor soft tissue assessment and overlapping anatomy
65
Q

What are the benefits of MRI?

A
  • Does not use ionising radiation
  • Excellent anatomical detail
  • Multiple phases enable some functional assessment of tissues
66
Q

What are the drawbacks of MRI?

A
  • Time consuming and expensive
  • Safety issues regarding metallic implants
  • Claustrophobic
67
Q

What are the benefits of ultrasound?

A
  • Dynamic study allowing real time assessment
  • Does not involve ionising radiation
  • Modality of choice for paediatric and antenatal imaging
68
Q

What are the drawbacks of ultrasound?

A
  • Poor assessment of air-filled structures and bone
  • More heavily operator/patient dependent
  • Attenuation of sound waves limits scan depth
69
Q

What are the benefits of nuclear medicine?

A
  • Large number of tracers available to assess different tissues
  • Provides anatomical and functional information
  • Usually allows more definitive assessment of pathology identified on other modalities
70
Q

What are the drawbacks of nuclear medicine?

A
  • Scan acquisition is time consuming
  • Poor resolution compared to alternative cross-sectional imaging
  • Radiation exposure continues after termination of examination
71
Q

What is the radiation law?

A
  • Ionising Radiation Regulations (IRR)
    • Protection of employees against exposure to ionising radiation as a result of work activities
  • Ionising Radiation Medical Exposure Regulations (IRMER)
    • Intended to protect patients from the hazards associated with ionising radiation
  • ALARP Principle
72
Q

What are the 2 coagulation pathways and what causes them to occur?

A

Intrinsic coagulation pathway –> occurs due to exposure to collagen from injured blood vessel wall or test tube

Extrinsic coagulation pathway –> occurs due to damaged tissue releasing thromboplastin

73
Q

What are the properties of platelets?

A
  • Non-nuclear cellular fragments
  • Form mechanical plugs during blood vessel injury
74
Q

What happens during adhesion and aggregation reactions with platelets?

A
  • 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
  • Leads to platelet mass to plug area of endothelial damage - promotes coagulation reaction: -vely charged phospholipids on activated platelets which have adhered to site of damage localize fibrin formation
  • Coagulation involved in: Haemostasis - stopping blood loss through damaged vessels
75
Q

What are the 3 laboratory tests for platelet and coagulation and how are they carried out?

A

Bleeding time

  • Incisions to forearm with venous cuff
  • Increased in platelet dysfunction/thrombocytopenia

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

Activated partial thromboplastin time (APTT)

  • Examines ‘intrinsic pathway’
  • Altered by changes in Factors XII, XI, IX, VIII, X, V, II or I
76
Q

What are 3 clotting and bleeding disorders?

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
77
Q

What is atrial fibrillation, associated risks and treatment?

A

Random electrical impulese leading to irregular atrial contraction

Lack or coordinated heartbeat

Risk = cardioembolic stroke

Treatment = anti-coagulants

78
Q

What are the properties of arterial thombosis?

A
  • Form at atherosclerotic sites
  • Lead to arterial blockage
  • MI and stroke
79
Q

What is the difference between venous and arterial thrombosis?

A

Venous = more of a coagulation factor event, i.e. DVT

Arterial = more of a platelet event, i.e. stroke, MI

80
Q

What is the atherosclerosis timeline?

A
81
Q

What is haemophilia A and how do you treat it?

A
  • Genetic - carried on X-chromosome, so males (XY) most affected and females (XX) carriers
  • Low or lacking Factor VIII of the clotting cascade
  • Haemorrhage and prolonged bleeding (e.g. after tooth extraction)
  • Treat with Factor VIII from blood donors or analogue of vasopressin (ADH) which increases patients Factor VIII release
82
Q

What is haemophilia B and how do you treat it?

A
  • Deficiency of Factor IX
  • Treated with prophylactic Factor IX
83
Q

What is emicizumab used for and how is it administered?

A
  • For Haemophilia A
  • Monthly sc injections as opposed to daily infusions of Factor VIII
  • Bispecific MAB: binds to activated Factor IX and X
  • Very effective at reducing bleeds
    • 30% of pts with Haemophilia A treated with Factor VIII develop resistance due to inhibitory factors produced
84
Q

What is Von Willebrand’s 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
85
Q

What happens in liver disease in relation to coagulation etc.?

A
  • Reduced synthesis of clotting factors leads to increased bleeding
    • Increased Prothrombin time
86
Q

What is thrombocytopenia and what is it caused by?

A
  • Reduced platelet number
  • Spontaneous skin bleeding (purpura)
  • Causes:
    • Idiopathic
    • Viral
    • Drug-induced –> treat with steroids if unresponsive splenectomy
    • Toxins
87
Q

What is disseminated intravascular coagulation and how is it treated?

A
  • Large amounts 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
88
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
89
Q

What is an ischaemic stroke and the different types?

A
  • Caused by blockage of blood flow to brain - 85% of all strokes
  • Thrombotic and embolic
  • Small vessel disease = lacunar stroke (20%)
  • Large artery atherosclerosis (20%)
  • Cardioembolic stroke = caused by atrial fibrillation (25%)
  • Cryptogenic stroke = no known causes (35%)
90
Q

What is a mini stroke?

A
  • Transient ischaemic attack
  • No permanent disability
  • Lasts up to 24 hours
91
Q

WWhat is a haemorrhagic stroke and the types?

A
  • Caused by artery in ,or to, brain rupturing
  • Intracerebral haemorrhage = 85%
  • Subarachnoid haemorrhage = 15%
92
Q

What are the 4 types of atrial fibrillation and their properties?

A
  • Paroxysmal AF
    • Episodes come and go and usually stop within 48 h without any treatment
  • Persistent AF
    • Each episode lasts for longer than seven days (or less when it’s treated)
  • Long-standing persistent AF
    • Continuous AF for a year or longer
  • Permanent AF
    • AF is present all the time
93
Q

What are causes of atrial fibrillation?

A
  • Hypertension
  • Atherosclerosis
  • Congenital heart disease
  • Cardiomyopathy
94
Q

What are treatments for atrial fibrillation?

A
  • Medicines to reduce the risk of a stroke
  • Medicines to control AF (beta-blockers, anti-arrythmics)
  • Cardioversion (electric shock treatment)
  • Catheter ablation (electrocardiology)
  • Having a pacemaker fitted
95
Q

How do you diagnose a stroke?

A
  • Physical examination – medical history
  • Neurological examination
  • Radiological examination (imaging via CT or MRI)
  • Check BP, HR and cholesterol
  • Right cerebral hemisphere à visual awareness, spatial awareness, proprioception, memory, recognition
  • Left hemisphere à language, analytical thinking, mathematical skills
96
Q

How do you determine stroke prognosis?

A
  • Location of the brain damage
  • Size of the brain damage
  • The presence of other medical conditions
  • Possibility of stroke recurring
97
Q

What are the treatments for ischaemic stroke?

A
  • Recombinant tissue plasminogen activator (rt-PA) – short therapeutic window (4.5 h of stroke onset)
  • Mechanical thrombectomy (physical removal of blood clot from the larger arteries)
  • Carotid endarterectomy – surgery to remove carotid plaque
98
Q

What are the treatments for haemorrhagic stroke?

A
  • No medical therapy - treat hypertension
  • Surgery to stop or prevent bleeding
99
Q

What are alternative stroke treatments?

A
  • Hypothermia –> intravascular cooling, surface cooling
  • Cellular treatment –> stem cells, endothelial progenitor cells
100
Q

What is warfarin and how does it work?

A
  • Oral anticoagulant
  • Vitamin K antagonist
  • Vitamin K essential for production of prothrombin and Factors VII, IX and X (Vitamin K important for post-ribosomal carboxylation of glutamic acid residues of these proteins)
  • Warfarin blocks Vitamin K reductase, needed for Vit K to act as a cofactor (Vitamin K Epoxide Reductase Complex, VKORC)
  • Prevents thrombosis
101
Q

Who takes warfarin and what can increased drug action lead to?

A
  • Patients with replaced valves, atrial fibrillation, PE, DVT
  • Takes several days to act
  • Dose = determined by international normalised ratio (INR)
  • Has many drug interactions
  • Increased actions = gastric bleeding, cerebral bleeding, haemoptysis, blood in faeces, blood in urine and easy bruising
102
Q

What is heparin and how does it work?

A
  • Injectable anticoagulant
  • Activates antithrombin lll
  • Antithrombin = complexes with serine protease of factors to inactivate some clotting factors and thrombin
  • Immediate action
  • Prevents thrombosis
  • Used while warfarin takes effect
  • Unfractionated heparins monitored vie APTT
103
Q

What are DOACs?

A
  • Direct oral anticoagulants
  • Dabigatran = oral thrombin inhibitor
  • Prevents thromboembolism –> less bleeding than warfarin, fewer drug interactions, no monitoring required
104
Q

What is prostacyclin and how does it work?

A
  • Endothelial-derived vasodilator
  • PGI2
  • Prevents platelet aggregation by acting on platelets to increase cAMP
  • Thromboxane = TXA2 = promotes aggregation, decreases cAMP
105
Q

What is nitric oxide and how does it work?

A
  • Endothelial-derived vasodilator
  • L-arginine + O2 –> NO + citrulline by nitric oxide synthase
  • Nitric oxide - prevents both platelet adhesion and aggregation by increasing platelet cGMP
106
Q

What is aspirin, who is it for and how does it work?

A
  • Antiplatelet drug
  • Low dose aspirin (75mg)
  • Prevents MI in patients who have previously had an MI
  • Not recommended for primary prevention
  • Reduces stroke incidence
  • Inhibits cyclo-oxygenase (irreversible)
  • Favours PGI2 production over TXA2 –> platelets have no nuclei, no COX produced, no TXA2 until new platelets synthesised –> endothelial cells have nuclei, produce COX, PGI2 produced
107
Q

What is dipyridamole and how does it work?

A
  • Antiplatelet drug
  • Phosphodiesterase inhibitor - prevents cAMP and cGMP breakdown - cAMP to AMP
  • Prevents thrombosis
  • Inhibits adenosine uptake
  • Used in conjunction with aspirin
108
Q

What is the role of GP llb/llla?

A

Binds to fibrinogen, leading to cross-linking of platelets

109
Q

What is clopidogrel?

A
  • Inhibits ADP-induced expression of GP
  • For those who can’t take aspirin
  • Same effectiveness as aspirin
110
Q

What is abciximab?

A
  • Monoclonal antibody against GP llb/llla
  • Given to those undergoing angioplasty
  • Only used once
111
Q

What is fibrinolysis and how does it work?

A
  • i.e. alteplase
  • Endogenous system to dissolve clots
  • Activated parallel to clotting system
  • Plasminogen –> plasmin
  • Plasmin = digests fibrin of clot
  • Fibrinolytic agents = activate plasminogen to plasmin conversion
112
Q

What are thrombolytics and when are they used?

A
  • Given immediately after MI à dissolve thrombus causing MI
  • Used for PE too
  • Best with aspirin (can cause bleeding) –> not used after surgery, haem stroke, ulcers
  • Used in thromboembolic stroke
113
Q

What are the properties of drug interactions and what affects them?

A
    • toxicity or reduced activity
  • Problem for drugs with small therapeutic window
  • Increased by conditions, i.e. renal impairment
  • May be beneficial or adverse
  • Food can have impact
114
Q

What strategies can you use to combat drug interactions?

A
  • Avoid
  • Alternatives
  • Reduce dose
  • Monitor patient
115
Q

What is the process of drug interaction absorption?

A
  • 2 drugs interact and alter rate of uptake
  • ATP binding cassette / multiple drug resistance transporter
  • Drugs can induce or inhibit it
  • Digoxin is substrate and induction of MDR1 reduces bioavailability
116
Q

What is drug displacement?

A
    • drugs protein bound, only act in free form
  • A result of drugs competing for binding sites
117
Q

What are the 2 CYP450-mediated metabolism processes?

A

Inhibition or induction

+ drugs metabolised by multiple CYPs

118
Q

What are the properties of CYP enzyme inhibition?

A
  • Antifungals, macrolide
  • Rapid 1-2day onset
  • Reverse quickly when stopped
119
Q

What happens when warfarin INR increases?

A

+ bleeding risk

120
Q

What happens when NSAIDs and warfarin interact?

A
    • interactions
  • Aspirin = antiplatelet, so + bleeding effects
  • NSAIDs associated with gastric bleeding, + with warfarin
121
Q

What are the 4 main drug interactions to remember?

A

Warfarin and NSAIDs = leading to enhanced bleeding

Warfarin and antibiotics (esp erythromycin and ciprofloxacin) = leading to enhanced bleeding

Simvastatin and macrolides = avoid

Simvastatin and amlodipine = caution dose

122
Q

What are the causes of different patient responses to therapy?

A
  • Metabolism
  • Renal function
  • Interactions
  • Resistance
  • Pharmacogenetics
    • Genetic differences in pharmacokinetics
    • Genetic differences in pharmacodynamics
    • Ethnicity

Medicine 1 (28 decks)

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