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Stage 2 > Case 4 > Flashcards

Case 4 Flashcards

1
Q

What are the roles of the cardiovascular system?

A
  • Blood flow to tissues and organs (supply and demand)
  • Homeostasis
    Transport of hormones and signalling molecules
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2
Q

Is there a direct connection between the two sides of the heart?

A

There is no direct connection with in adults (usually)

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3
Q

Where does the heart pump blood to?

A
  • Left side pumps into the aorta (systemic)
  • Right side pumps to the pulmonary artery
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4
Q

Which side of the heart is more prone to problems?

A

The left side (especially due to pressure)

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5
Q

How does uidrectional blood flow in the heart occur?

A
  • The valves prevent the back flow of blood
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6
Q

Why does pressure drop in the circulation?

A
  • Difference in pressure between aorta (highest) and vena cava (lowest)
  • Energy is lost from the blood to the vessel wall resistance
  • Blood flow through each circulation is proportional to pressure gradient
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7
Q

What happens if you increase resistance to blood flow?

A

Make sit more difficult for the heart to pump blood to the peripheries

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8
Q

What determines resistance (R) to blood flow?

A

The radius (r) of the arterioles

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9
Q

What is stroke volume?

A
  • Volume of blood pumped by one ventricle
  • ~75mls
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10
Q

What is cardiac output (CO)?

A
  • Volume pumped per ventricle per minute
  • 5L/min
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11
Q

What is venous return (VR)?

A
  • Volume of blood returning to the heart
  • VR should equal CO
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12
Q

What are intercalated disc?

A
  • Junction between adjacent cells
  • Packed filled with proteins that form gap junctions (allows electricity to move quickly)
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13
Q

What is the SAN?

A
  • a small group of cells
  • one of few cells in the body that can spontaneously produce electricity- intrinsic property
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14
Q

How is electrical energy spread in the heart?

A
  • spontaneous depolarisation of the san (don’t see on ecg)
  • comes out of san and spreads through the atria
  • atria contracts (atria systole)
  • av node depolarises and passes electricity down the ventricles - av node delay - allows atria muscle to contract to push more blood into the ventricles
  • av node passes depolarisation down the interventricular septum
  • then ventricular depolarisation occurs and then a wave of contraction follows it pushing the blood up and out of the heart
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15
Q

What is the role of the annulus fibrosis?

A
  • Non-conducting layer between atria and ventricles
  • Electrically insulated the chambers from each other
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16
Q

What is the P wave?

A

Atrial depolarisation

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17
Q

What is the PR(Q) interval?

A

Interval between beginning of excitability of atria and ventricles (~0.16s)

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18
Q

What is the QRS complex?

A

Ventricular depolarisation
Atrial repolarisation occurs but is obscured

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19
Q

What is the Q-T interval?

A

Contraction occurring (~0.35s) but also includes ventricular repolarisation

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20
Q

What is the S-T segment?

A

All ventricular tissue depolarised, contraction occurring

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21
Q

What is the T wave?

A

Ventricular repolarisation

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22
Q

How to calculate cardiac output?

A

HR X SV

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23
Q

What helps venous return?

A
  • Skeletal muscle pump/ contractions
  • Respiratory pump
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24
Q

What are the neurotransmitters that affect the SAN?

A
  • sympathetic system - noradrenaline/ adrenaline
  • parasympathetic- acetylcholine/ muscarinic receptors
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25
Q

How do sympathetic nerves affect heart rate?

A
  • activation causes release of noradrenaline - binds to B1 adrenoceotors on the cardiac pacemaker and myocyte cell membrane
  • increases opening of HCN channels in pacemaker cells - increase Na+ influx
  • opens Ca2+ channels
  • increase in slip of prepotential (phase 4)
  • heart rate increases
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26
Q

What are HCN channels?

A

Channels that control the release of sodium into the cell and when activated allows depolarisation to occur quicker

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27
Q

How do parasympathetic nerves affect the heart rate?

A
  • activation causes release of acetylcholine - binds to muscarinic cholinergic receptors
  • decrease opening of HCN channels - decrease Na+ influx
  • slows opening of Ca2+ channels
  • opens additional K+ channels (ligand gated)
  • hyperpolarises membrane and reduces slope of prepotential
  • heart rate decreases
  • the parasympathetic nerves constantly affect the SAN and is a very quick response
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28
Q

What are the sequence of mechanical events in the cardiac cycle?

A
  1. Ventricular filling
  2. Atrial contraction
  3. Isovolumetric ventricular contraction
  4. Ventricular ejection
  5. Isovolumetric ventricular relaxation
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29
Q

What controls stroke volume?

A
  • contractility
  • preload (degree of stretch)
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30
Q

What is contractility?

A

Symapthetic nerves and calcium can change contractility (effected by mechanisms extrinsic to the heart)
It is changes in SV w/out changes in resting ventricular muscle fibre length

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31
Q

What is preload?

A
  • Degree is stretch in the ventricles due to end diastolic pressure - dependent on end diastolic volume
  • Changes in stroke volume dependant on resting ventricular muscle fibre length
  • Mechanism intrinsic to the heart
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32
Q

What is cardiac workload?

A

Mechanisms regulating force of contraction and workload may be: heterometric (intrinsic) or homeometric (extrinsic)

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33
Q

What is starlings law of the heart?

A

Force of contraction is proportional to the initial fibre length in diastole
Almost empty chamber (low preload) -actin and myosin overlap is not optimal/ reduces ability to contract
Full ventricle (high preload) - some stretching of ventricular muscles/ optimum cross bridges available/ increased affinity of troponin C to Ca2+/ maximal force produced
Over full heart (heart failure) - actin and myosin are physically separated therefor preventing interaction so a reduced force is generated

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34
Q

What is the level of stretch of the heart determined by?

A

Venous return and the filling of the ventricle

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35
Q

Effects of sympathetic nerve stimulation on the heart:

A
  • increased in stroke volume without a change in initial fibre length
  • increased contractility - positive inotropic effect
    Anything that is a beta1 agonist will increase contractility
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36
Q

What controls Mean Arterial Pressure (MAP)?

A
  1. Blood volume
  2. Effectiveness of the heart as a pump (CO)!! - determined by heart rate and stroke volume
  3. Resistance of the system to blood flow!! - determined by diameter of arterioles
  4. Relative distribution of blood between arterial and venous blood vessels
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37
Q

How do you calculate MAP?

A

MAP = CO X TPR (total peripheral resistance)

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38
Q

What do baroreceptors do?

A

Detect changes in blood pressure and makes sure they’re kept within the appropriate range

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39
Q

When would you offer ambulatory blood pressure monitoring (ABPM)?

A

Offer it if the clinical BP is between 140:90 mmHg and 180/120mmHg to confirm the diagnosis of hypertension

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40
Q

What is the blood pressure measurement that confirms hypertension?

A
  • Clinic blood pressure of 140/90 mmHg or higher (150/90 mmHg for adults ages 80 and over)
  • ABPM daytime average or HBPM average of 135/85 mmHg or higher (145/85 mmHg for adults aged 80 and over)
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41
Q

What is stage 1 hypertension?

A

Clinic blood pressure ranging from 140/90 mmHg to 159/99 mmHg and subsequent ABPM daytime average or HBPM average BP ranging from 135/85 mmHg to 149/94 mmHg

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42
Q

What is stage 2 hypertension?

A

Clinic BP of 160/100 mmHg or higher but less than 180/120 mmHg and subsequent ABPM daytime average or HBPM average BP of 150/95 mmHg or higher

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43
Q

Which type of hypertension usually has no identifiable cause and develops gradually over years?

A

Essential hypertension

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44
Q

What are some recognised links (causes) to secondary hypertension?

A
  1. Diabetes
  2. Kidney disease
  3. Thyroid disease
  4. Sleep apnoea (secondary cause)
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45
Q

Which type of hypertension doesn’t have a genetic link?

A

Secondary hypertension

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46
Q

What mechanisms should prevent elevations in arterial BP?

A

Baroreceptors should detect the change and increase nerve activity to activate the parasympathetic system to decrease the blood pressure
Nerve activity however reduces with sustained high blood pressure

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47
Q

What is atherosclerosis?

A

The build up of fatty plaques in the arteries

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48
Q

What is the mechanism of action of calcium channel blockers?

A
  • They inhibit the influx of calcium ions
  • They act on: myocardial muscles (inhibit contractility); myocardial conducting system (inhibit formation and propagation of depolarisation); vascular smooth muscle (coronary or systematic vascular tone reduced/ vascodilation)
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49
Q

What is the pharmacokinetics of calcium channel blockers?

A
  • oral route: bioavailability 60%
  • Half-life of amlodopine 30-50hrs
  • Steady-state plasma concentrations - 7-8 days of daily dosing
  • Liver CYP450 - slowly metabolised
  • Renal elimination but poor renal function does not significantly reduce elimination
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50
Q

What is the mechanism of action if ACE inhibitors?

A

Inhibits the angiotensin-converting enzyme in the renin-angiotensin system

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51
Q

What is the pharmacokinetics of lisinopril?

A
  • Oral administration: 25% bioavailability
  • Peak plasma conc: 4-8h - half life 12h
  • Water soluble - not metabolised in the liver and undergoes renal excretion unchanged
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52
Q

What is the first line treatment of hypertension for those over 55?

A

Calcium channel blockers - for those of Afro Caribbean decent too

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53
Q

What is the first line treatment of hypertension for those under 55?

A

ACE inhibitors

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54
Q

What is the mechanism of action of ARBs?

A

Selective competitive blockers of angiotensin II at the AT1 receptor

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55
Q

What are the advantages of ARBs?

A

No dry cough

56
Q

What is the pharmacokinetics of losartan?

A
  • Oral administration: 32% bioavailability
  • First-pass metabolism 14% to active metabolite which is more potent, non-competitive and longer acting
  • Cytochrome P450 metabolism - half-life of 2h and 3-9h for metabolite
  • Extensive plasma protein binding
  • Excreted in urine and bile
57
Q

What is the mechanism of action of thiazide-like diuretics (e.g. indapamide)?

A
  • Inhibition of Na+ and Cl- réabsorption from the DCT by blocking the Na+-Cl- symporter
  • At lower doses vasodilation is more prominent than diuresis
58
Q

What is the pharmacokinetics of thiazide-like diuretics?

A
  • Oral administration
  • 75% plasma protein bound
59
Q

What are B-blockers competitive inhibitors of?

A

Catecholamines

60
Q

What are the two types of adrenoreceptors?

A
  • Alpha: 1- IP3/DG (increase); 2-cAMP (decrease)
  • Beta: 1- cAMP; 2- cAMP; 3- cAMP (all increase)
61
Q

What is epichlorohydrin?

A

A special epoxide for providing a 1,2,3-substituted compound

62
Q

What were the side effects caused by first generation beta blockers (pindolol/timolol)?

A
  • Crossed the BBB - dizziness/ sedation
  • Bronchoconstriction in asthmatics
  • Lower cardiac output
63
Q

What was the issue with propranolol?

A
  • Has a high logP = 3.66 therefore highly lipophilic
  • Possible CNS side effects due to BBB penetration
64
Q

How was propranolol altered/ modified?

A
  • Reduce logP, take out one aromatic ring, use a logP lowering group like acetamide and sulphonamide
65
Q

How were 2nd gen beta blockers made to be less lipophilic (eg practolol)?

A
  • made less potent than propranolol
  • more selective so fewer CNS side effects (more polar, logP 0.79)
  • B1 selective over B2 (cardio selective over vascular and bronchial)
  • contain extended para subsitute
66
Q

What are the symptoms of high BP?

A
  • Asymptomatic
  • Headaches
  • Eye issues (very red eyes); problems with the retina and blood vessels burst
  • primary - no know cause
  • secondary - know cause
  • tumour on adrenal glands can elevate Bp
  • Meds (NSAIDS)
67
Q

What to do when diagnosing hypertension?

A
  • measure both arms
  • irregular pulse - has to be measure manually
  • 140/90mmHg or higher then take another measurement and still high then take another
  • record the lower of the last two measurements as the clinic BP
68
Q

What is stage 1 hypertension?

A

Clinical blood pressure is greater than 140/90 mmHg and subsequent ambulatory BP monitoring average or home BP monitoring is greater than 135/85mmHg

69
Q

What is stage 2 hypertension?

A

Clinic BP is greater than 160/100 mmHg and subsequent ABPM average is greater than 150/95 mmHg

70
Q

What is stage 3 hypertension?

A

Clinic systole BP is greater than 180 mmHg or diastolic BP is greater than 110 mmHg

71
Q

What sort of lifestyle advice would you give to those with hypertension?

A
  • lose weight is over weight
  • exercise
  • fresh fruit and veg
  • reduce salt and smoking and alcohol
72
Q

What is the first line treatment for hypertension?

A
  • <55 - ACE inhibitors or A2RBs
  • > 55 or black people of African/ Caribbean family origin of any age - calcium channel blocker
  • if CCB is unsuitable/ not tolerated offer a thiazide-like diuretic
73
Q

How do ACE inhibitors work and what to consider when prescribing?

A
  • target the conversions of angiotensin 1 to angiotensin 2 (a vasoconstrictor) so therefore it prevents the creation of a vasoconstrictor - can make you dizzy (postural hypotension- systolic drops by 20 and diastolic drops by 10) as they allow vasodilation
  • start low and go slow
  • check U&Es - can affect kidney function (can cause hyperkalamia)
  • care with ADRs (a dry cough)
  • drug interactions (especially those that cause hyperkalamia)
  • angioedema - allergic to ACE inhibitors and more likely to occur in certain ethnic groups
74
Q

How to A2RBs work and points to consider when prescribing?

A
  • stop the activity of angiotensin 2 (do not stop the conversion)
  • don’t cause a cough
  • more expensive than ACE inhibitors
75
Q

How do dihydropyridine CCBs work and points to consider when prescribing?

A
  • Caution in heart failure
  • ADRs - oedema (particularly in the legs), (don’t want to give to those with heart failure)
  • Drug interactions - beta-blockers (can cause bad bradycardia)
  • Food interactions- may also interact with grapefruit juice (CYP450 inhibitors)
76
Q

What are the three types of CCBs?

A
  1. Benzodiazepines
  2. Diphenhydramine
  3. Dihydropyridines (interested in these for hypertension)
77
Q

How do thiazide-like diuretics work and points to consider when prescribing?

A
  • Indapamide and chlortalidone now replace bendroflimethiazide
  • Give the dose early in the morning
  • Higher dose cause more side effects with little effect on BP
  • Cab disturb electrolytes (which can be clinically significant) - can increase glucose and uric acid (cause gout?)
  • Loop diuretics (e.g. furosemide) are NOT used to treat hypertension
78
Q

What is the second line treatment for hypertension?

A
  • CCB in combination with either an ACE inhibitor or an ARB
  • If a CCB is not suitable or tolerate offer a thiazide-like diuretic
  • For black people of African or Caribbean descent, consider an ARB in preference to an ACE inhibitor, in combination with a CCB
79
Q

What is the third line treatment for hypertension?

A
  • Before progressing to step 3, ensure that treatment doses at step 2 are optimal
  • We should then look at the combination of ACE inhibition (or A2RB), CCB and thiazide-like diuretic
80
Q

What is the fourth line treatment for hypertension?

A
  • If BP remains a over 140/90 mmHg after ACE inhibitor (or A2RB), a CCB and a diuretic, it is known as resistant hypertension
  • Treatment options include: additional diuretics (potassium sparing diuretic (spirolactone)) ; using higher dose thiazide-like diuretic; using alpha or beta-blocker
81
Q

How do alpha blockers treat hypertension and things to consider when prescribing?

A
  • Includes: Doxazosin, Prazosin, Terazosin
  • Also used to treat benign prostatic hypertrophy
  • Side effects: postural hypotension; urinary incontinence
82
Q

How do beta blockers work and things to consider when prescribing?

A
  • Less common nowadays - end in olol
  • Target beta receptors in the heart (beta1) - makes patients tired
  • Selectivity re B1 + B2 receptors and bronchspasm?
  • ADRs: coldness of the extremities; sleep disturbances; caution when stopping (rebound tachycardia - Sympathetic nervous system may increase)
83
Q

What is ACS?

A
  • Acute coronary syndrome
  • An umbrella term that encompasses three things: unstable angina; myocardial infarction (STEMI- ST segment elevation myocardial infarction and NSTEMI- Non-ST segment elevation myocardial infarction)
84
Q

What is MI?

A
  • Myocardial ischaemia - reduced blood flow to the cardiac tissue- less O2 to perfusé the cardiac cells
  • Myocardial infarction- death of cardiac cells
85
Q

What are causes of ACS?

A
  • Due to sub total (UA+NSTEMI) or total (STEMI) coronary artery occlusion
  • Occurs as a complication of advanced atherosclerosis/ atherosclerosis CAD
  • Triggered by an athermatous plaque disruption (rupture or erosion) -> coronary thrombosis-> formation of thrombi (either total occlusion or sub-total occlusion)
86
Q

What is unstable angina (UA) characterised by?

A
  • Typically diagnosed with SA first
  • Acceleration in frequesn or severity of chest pain
  • New onset angina pain
  • Angina chest pain that abruptly occurs at rest
  • No enzymatic evidence (biochemistry) of myocardial necrosis
  • Presence of an active pro-thrombotic surface at the site of plaque rupture —> increased risk of MI
87
Q

What is NSTEMI characterised by?

A
  • Unstable plaque rupture + thrombosis-> partial occlusion of artery
  • Postive enzymatic evidence (biochemistry) of myocardial necrosis
  • Presence of persistent pro-thrombotic surface at site of plaque rupture—> increased roak of recurrent ischaemic episodes
88
Q

What is STEMI characteristed by?

A
  • Unstable plaque rupture + thrombosis—> complete occlusion of artery
  • Positive enzymatic evidence (biochemistry) of myocardial necrosis
  • Ishaemia-induced electro instability —> increased risk of sudden cardiac death
89
Q

What is the difference in ECG of STEMI and NSTEMI?

A
  • STEMI - ST elevations
  • NSTEMI - ST depressions
    -UA - no change
90
Q

What is acute myocardial infarction?

A
  • Death of heart muscle
  • Ultimate result of sustained myocardial ischaemia
  • High mortality rate
  • Necrosis of myocardial tissue within 20-40 minutes of occlusion
  • Significant necrosis at 2-3 hrs
91
Q

Major clinical features of MI

A
  • Pain - be specific - sharp heavy pain in the chest that starts centrally and radiates to the left hand side (may include the shoulder blade)
  • Lasting >20 minutes
  • Often associated with nausea, sweating, dyspnoea, palpitations
  • May present without chest pain (CP) = ‘silent infarct’ (e.g. in elderly/ DM)
  • Can also experience: hypotension, dizziness, syncope (fainting)
  • ECG changes: T wave inversion; ST segment elevation; Q wave development
  • Enzymatic changes (biochemistry): troponin enzymes released by heart tissue
92
Q

What are the ECG changes in MI?

A
  • T wave inversion
  • ST segment elevation
  • Q wave development
93
Q

What are the enzymatic changes (biochemistry) of an MI?

A
  • cardiac troponin (T and I) levels are the most established and specific markers of myocardial necrosis
  • serum levels increase within 3-12h from the onset of chest pain, peak at 24-48h and reduce to baseline over 5-14 days
  • Troponin T: can be relaxed from cardiac muscle or skeletal muscle (less specific)
  • Troponin I: extremely specific for cardiac muscle = ideal marker for cardiac injury
  • Emerging bio markers; heart fatty acid-binding protein; B-type natriuretic peptide —> newest focus; ischaemia-modified albumin; co-peptin
94
Q

Diagnosing criteria for MI

A
  • rise and/or fall of serum cardiac biomarkers
  • plus at least one of the following: symptoms of ischaemia; ECG changes (new ST/T wave changes); development of Q waves; loss of myocardium on imaging
95
Q

Risk factors of MI

A
  • Non-modifiable: age; male gender; family history of IHD; certain ethnic groups
  • Modifiable: smoking; hypertension; DM; hyperlipidaemia; obesity; sedentary lifestyle
96
Q

Clinical management principles of MI

A
  • Relieve pain
  • Recognise (working diagnosis to definite diagnosis)
  • Treat
  • Prevent complications
  • Myocardial salvage (pharmacological and/ or non-pharmacological): reduce myocardial oxygen demand (B2 cardio selective B-blockers and nitrates); restore myocardial blood supply through reperfusion (either thrombolytic ‘clot busters’; anticoagulant + antiplatelet combination; PCA/stent)
  • Improve survival (pharmacological and/ or non-pharmacological): secondary prevention
97
Q

How do you improve survival of an MI?

A
  • termed secondary prevention
  • combination of pharmacological and non pharmacological
  • will be overlap between salvaging and improving survival - often life long meds post MI
  • SAAB+GTN: statin (atorvastatin-gold standard); ACEi; dual antiplatelet (2 for 12 months then move to one); beta blocker; GTN
  • Non pharmacological- cardiac rehabilitation
98
Q

What is ischaemic heart disease?

A
  • Deprivation of supply to cardiac tissue causing cell death (irreversible)
  • Angina symptoms
  • Heart attack
99
Q

What is cardiac failure?

A
  • Inability of heart to distribute blood
  • Heart failure
100
Q

What is cardiac dysrhythimia?

A
  • Disruption of contraction control
  • Cardiac arrest
101
Q

How does adaptation to O2 demand change in the heart?

A
  • Mainly by changes of n vascular resistance
  • O2 demand = blood flow X arteriovenous O2 concentration difference
  • O2 demand increases (hypertension….
    INCOMPLETE
102
Q

What are metabolic autoregulatory factors of the heart?

A
103
Q

What are endothelium-mediated auto regulatory factors relating to the heart?

A
  • Bradykinin, histamine and Ach are vasodilators
  • Act indirectly by releasing nitric oxide (NO), which diffuses into vascular muscle
  • Raises cGMP, activates protein kinase G - causing vascular relaxation
104
Q

What are neurohumoral autoregulatory factors relating to the heart?

A
105
Q

Causes of ischaemic heart disease (coronary heart disease)

A
  • Atherosclerosis (most cases)
  • Arteritis
  • Embolism and endocarditis
  • Coronary artery wall thickening: amylodosis
  • Coronary spasm (eg cocaine induced spasm)
  • Congenital artery disease: arteriovenous fistula
106
Q

Modifiable fish factors for ischaemic heart disease

A
  • Hypertension
  • Hypercholestérolémia
  • Smoking
  • Diabetes mellitus
  • Sedentary life style
  • Obesity
107
Q

Non modifiable risk factors of Ischaemic heart disease

A
  • Age
  • Male gender
  • Family history
108
Q

What is angina?

A

-Chest pains - not a disease itself
-Primary symptom associated with ischaemic heart disease
-Caused by transient episodes of myocardial cardiac ischaemia
-Pain from myocardium after switching to anaerobic metabolism (low O2 supply)

109
Q

What are the three types of angina pectoris?

A
  1. Stable
  2. Unstable
  3. Varient
110
Q

What is stable angina?

A
111
Q

What is unstable angina?

A
112
Q

What is varient angina?

A
  • Focal/ diffuse coronary vasospasm
  • Pain resulting from lack of O2 …
113
Q

Consequences of myocardial ATP deficiency

A
  1. Impairment of ventricular systolic pumping action
  2. Decreased compliance of myocardium during diastole
  3. Pulmonary congestion and dyspnea
114
Q

Learn the nitrates oathway

A
115
Q

Give two examples of nitrates

A

GTN and isosoribide mononitrate

116
Q

Wat are the two actions of nicotandil?

A
  1. 2.
117
Q

What is the mechanism of beta blockers?

A
118
Q

What are causes of atherosclerosis?

A

Hyperlipidemia
Smoking
Primary inherited disorders
Secondary lipid disorders

119
Q

What are the consequences of atherosclerosis?

A
  • Narrowing of the lumen leading to IHD
  • Stiffening of the vessel wall (calcification)
  • Thrombus obstructing residual lumen and causing peripheral embolism (eg cerebral infarction, stroke)
    …
120
Q

Prophylactic intervention got atherosclerosis

A
  • Dietary changes to reduce cholesterol and lipids
  • Cessation of smoking
  • Control of BP
  • Control of diabetes
  • Regular, moderate exercise
  • Drugs to reduce plasma cholesterol
121
Q

Pharmacological interventions for lowering lipid levels

A
122
Q

What is the mechanism of action for statins?

A
123
Q

What are the side effects of statins?

A
124
Q

What drug is used to prevent cholesterol absorption?

A

Resins eg …

125
Q

What are side effects of resins?

A
126
Q

What is a mechanism of action of resins?

A
127
Q

Which drug is used to reduce VLDL secretion?

A

Niacin (nicotine acide/ vitamin B3)

128
Q

Which drug is used to increase the synthesis of lipoprotein lipase?

A

Fibrates (eg gemfibrozol, fenofibrate)

129
Q

What are radioisotopes?

A

Radioactive isotopes that are produced as a result of natural decay

130
Q

What is diagnostic imaging?

A

Exploiting the tissue penetration of gamma rays derived from nuclear decay or positron annihilation

131
Q

What is targeted therapy?

A

Exploiting the cellular toxicity of non-penetrating alpha and beta particles and secondary electrons

132
Q

What is a cyclotron?

A
  • A particle accelerator
  • An electrically powered machine producing a beam of charged particles
133
Q

What is PET?

A

Positron emission tomography

134
Q

What is PET?

A

Positron emission tomography

135
Q

What is SPECT?

A

Single photon emission computed tomography

Stage 2 (5 decks)

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