High yield exam facts Flashcards

1
Q

rules for estimating electron PDD characteristics:

A

R50 = Energy/2.33

1) Surface dose = 73+Energy
e. g 6MeV SD =79%

2) “4,3,2 divide rule”: Dmax = Dose/4, R90 = D/3, R10 = Dose/2.

E.g 6/4 = 1.5cm = Dmax, 6/3 = 2cm = D90, 6/2 =3cm = R10 (therefor D50 = 2.5cm)

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2
Q

alpha/beta ratios for acute, and late responding tissues:

Define standard fractionation

A

Acute = 10Gy
Late = 3Gy
(Don’t forget has units of Gy)

Standard fractionation: 1.8-2Gy/fraction, daily fractions, five days a week.

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3
Q

When does the brachiocephalic vein become the subclavian?

A

In the root of the neck, the internal jugular (IJV) and subclavian veins unite to form the brachiocephalic veins posterior to the medial ends of the clavicles.

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4
Q

Define monitor unit

A

1) SSD
MU = dose (cGy)/
CalibrationFactor(PDD.WF.OF)

2) SAD
MU = dose (cGy)/
CalibrationFactor(TPR.WF.OF)

SSD - The source surface distance (if different to reference conditions)
OF - The field size (usually referred to as the output factor or total scatter factor)
PDD - The percent depth dose of the point in question
WF (wedge factor) The presence of any beam modifying devices in the beam (such as a wedge)
CF - The calibration factor (only important if 1 MU is not equal to 1 cGy under reference conditions)

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5
Q

Define Housfeild unit

A
u = linear attenuation
ux = linear attenuation of beam

HU = ((ux - uwater)/(uwater- uair)) X 1000

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6
Q

Define physical half life

A

The time it takes for 1/2 the atoms of a radioactive material to decay to half their number.

Defined by a decay constant, such that Thalf = ln(2)/decayconstant

Where
decay constant it the basic term in a decaying exponential.

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7
Q

Define effective half life

A

The time taken for a concentration of a radioactive to material to be reduced by half in a body, either by decay or clearance.

Teff = ln(2)/Effective decay constant

where

Effective decay constant is the sum of physical and biological decay constants

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8
Q

Define radioactive equilibrium:

A

The state where a radioactive nuclide is decaying at the same rate it is being produced. The key condition is that the parent nuclide has a longer half-life than its descendants.

decayconstan1 x NumberAtoms 1 = decayconstant2 x NumberAtoms 2

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9
Q

Types of radioactive equilibrium (and examples):

A
1) Half-life of parent nucleus is longer than a half-life of the daughter nucleus, but the concentration of parent nuclei significantly decreases in time. In this case, the parent and daughter nuclide decay at essentially the same rate, but both concentrations of nuclides decreases as the concentration of parent nuclei decreases. Contrary to secular equilibrium, the half-life of the daughter nuclei is not negligible compared to parent’s half-life.
E.g the cow: Moly 89 (67hrs) -> Technicium 99 (6hrs)
2) Secular equilibrium: Where parent half life is many orders of magnitude greater than daughter, and concentration of parent essentially doesn't change.
radium 226 (1600 years) -> Radon 222 (3.6 days)
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10
Q

What defines the inferior border of the superior mediastinum?

Some critical shit that happens there

A

Plane of Ludwig/Transthoracic plane/sternal plane

Plane from angle of Louis (sternal angle) to inferior border endplate T4.

Bifurcation of pulmonary trunk
Bifurcation of trachea

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11
Q

Factors that effect the therapeutic ratio can be broken into:

A

1) Physical: Fractionation pattern, radiation quality, total dose, treatment time, temperature
2) Biological: Tumour factors (radiosenitivity, size, location), host factors, tissue factors (e.g. organisation)
3) Chemical: Concurrent therapies, oxygenation, protectors, sensitizers
4) Technical: system accuracy, conformity, geographic miss, presence of hotspots.

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12
Q

Steps in angiogenesis:

A

1) Angiogenic switch in favour of angiogenesis:
pro-angio>anti-angio
E.g pro: VEGF, TNF alpha, TGF beta
E.g anti: Angiostatin, endostatin, interferon
2) Endothelial cell proliferation
3) Neoangiogenesis
4) Resolution/maturation phase - often missing in tumour angiogenesis leading to shitty leaky, collapsing vessels.

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13
Q

Define effective energy:

A

The theoretical mono energetic beam that has the same HVL as a polyenergetic beam under study. Practically difficult due to beam hardening requiring progressively greater HVLs…

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14
Q

1mm Al filters out energies up to? This is roughly equivalent to?

A

filters up to 10Kev

Roughly equivalent to inherent filtration (i.e your inherent filtration curve should start at 10Kev).

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15
Q

G2/M check point proteins

A

Cyclin B - CDK1
(Cyclin B promoted by Cyclin A - CDK1)
CHK1/CHK2 (ATR/ATM) - p53 - p21
CDC25a

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16
Q

Compare pulmonary arteries to veins

What do the main pulmonary veins drain?

A

Pulmonary arteries follow bronchial tree to alveoli.
Pulmonary veins follow intersegmental septa and exit hilum inferior to arteries.

Right:
Superior drains upper and middle lobe
Inferior drains LL

Left:
Superior drains UL + LIngular
Inferior drains LL

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17
Q

Lymphatic drainage of the breast should always been with:

Inferior border of breast? and ribs cover

After the apical nodes what happens?

How much of the lymphatic drainage of the breast is through the axillary nodes

With obstruction of usual lymphatics what can happen?

A

“Deep and superficial (Sappey’s) plexi merge”

Inframammary fold, breast covers ribs 2-6

Subclavian trunk -> right or left thoracic ducts

Axillary nodes drain 75%

Lymphatics may cross to contralateral side through superficial (dermal channel), deep (internal mammmary interconnections) or to the retro-pectoral nodes.

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18
Q

Roots of:
Sacral plexus
Sciatic nerve
Pudendal nerve

A

Sacral plexus
L4-S4

Sciatic nerve
L4-S3

Pudendal nerve
S2-S4

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19
Q

Roots of the sacral plexus:

Divided into what rami?

A

L4-S4.

Anterior Rami (s1-s4): Pelvic splanchnic, pudendal, perineal (S4)
Anterior division of anterior rami (L4, S3) - gives off tibial sciatic branch.
Posterior rami (L4, s2) - Given of common peroneal sciatic branch
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20
Q

Methods/systems/equipment to avoid or detect dose delivery errors?

A

● Record and Verify System

● Select and Confirm

● Interlocks

● Imaging

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21
Q

What is the Record and Verify System?

What does it include?

A

Record and Verify System
○ Ensures that the planned treatment is delivered in a similar manner every day, consistent with plan, and records in real time. Measured variables are compared against tolerance and system alerts if outside.

○	Includes daily measurements of:
■	MU (recorded in real time)
■	beam energy
■	beam mode (photons/electrons)
■	jaw positions
■	collimator, gantry and couch angles
■	wedging
■	SSD
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22
Q

What is the Select and Confirm System?

What does it include?

A

○ Ensures correct treatment parameters
○ When a setting is selected, mechanical changes are checked to have occurred before treatment continues.
○ System also checks that the field correlates with the mechanical positions of the field, collim

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23
Q

What 2 types of error impact treatment accuracy?

A

● Systematic errors
○ constantly inconsistent error that is reproducible
○ inherent accuracy of treatment or positioning
○ eg. errors in patient setup, incorrect collimation, treatment plan transcription errors, incorrect calibration of measurement tools

● Random errors
○ errors due to unpredictable variations in measurements, fluctuate around a mean value.
○ Can be minimized with more precise measurements and improved patient immobilization
○ eg. patient movement, organ motion, inconsistent interpretation of skin marks and positioning.

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24
Q

Radiation worker dose limit:

Chest XR dose

Abdo CT dose

A

20msv/year averaged over 5 years, not more than 30mSv in any one year

CXR 0.02 - 0.1

CT Abdo: 10-20 mSv (depending on study - e.g tripple phase)

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25
Q

The primary cellular target of ionising radiation is DNA.

i. List the four (4) main types of DNA lesions caused by therapeutic ionising radiation.

A

1) ds-DNA break
2) ss - DNA break
3) Base modifications
4) Interstrand crosslinks

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26
Q

Describe the processes of non-homologous end joining (NHEJ)

A

1) Detection: DSBs detected by Ku70 and Ku80 proteins which bind to site (also protect ends)
2) Recruit: DNA-PKcs recruited - autophosphorylates and phosphorylates other proteins.
3) Artemis (protein complex) recruited to DNA break, forms complex with DNA-PKcs and is activated by phosphorylation.
4) Processing: Artemis endonuclease activity processes the DNA ends ready for ligation.
If non-blunt end of DNA i.e. a 3’ or 5’ overhang, then the absent DNA can be generated accurately by polymerases.
5) DNA ends ligated

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27
Q

Describe the processes of homologous end joining

A

Homologous Recombination uses sister DNA with the same sequence as a template for repair. After activation as above:
1) Single stranded filaments made around DSB
2) Filaments coated with RPA
3) RAD51 displaces RPA and SEARCHES and INVADES sister chromatid
4) HELICASES UNWIND DNA and hold open SEPARATION FORK and polymerases SYNTHESISE 5’-3’ along separation fork.
5) Finally crossover points are CUT by RESOLVASES, and ligated
Detection→Recruitment/activation→Processing→Ligation

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28
Q

Why are lower photon energies used in lung plans?

A

Remember the graph of 6Mv
- pre interface less scatter, but then due to less attenuation of beam, dose is higher. Higher dose causes increased range scattered electron = wider penumbra.

Therefore:

1) Energies >6Mv will cause increased dose to lung due increased electron range
2) Higher energy/less attenuated beams will have a build up region within the more solid tumour leading to less even coverage of the tumour.

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29
Q

Difference between LET and stopping power

A

While mean stopping power refers to the energy lost by the particle beam traversing the surrounding media, linear energy transfer (LET) refers to the energy absorbed by the media per unit of distance travelled by the ionizing radiation.

LET does not include radiative energy (i.e it leaves the area - um).

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30
Q

Why does a 6Mv beam deposit less dose in a bone inhomegeniety?
Why is the beam attenuated after?

A

Less electrons/gram = less compton attenuation

But more attenuation of the primary beam (electrons per cm) leads to decreased dose behind inhomogeneity.

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31
Q

Job of each HPV oncogene:

A

E5 = EGF ,E6 = p53, E7 = Rb

E5
Activates EGF signalling pathway (i.e RAS-Raf-Mek-Erk, and PI3K-AKT-mTOR) ->Cell growth and proliferation

E6
Binds p53 induces its degradation

E7
Binds Rb releasing E2F: Cyclin E increases, Cylcin A-CDK2 stimulated, cell goes into S Phase.
Inactivates CIP/KIP (p21, p27)

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32
Q

Name some tumour suppressor

A

TP53
Rb1
PTEN
INK4a locus

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33
Q

Hallmarks of Cancer - 6+2?

A

6 Hallmarks + 2 enabling characteristics

1) Sustained proliferative signaling (e.g. autocrine, increased TKR or GFs)
2) Evading Growth Suppressors
3) Resisting Cell Death
4) Angiogenesis
5) Activating invasion and/or metastasis
6) Replicative immortality

Enablers:
Genome Instability
Tumour-promoting inflammation

Emerging hallmarks:
Evading immune destruction
Deregulating cellular energetics

34
Q

What is the lymphatic drainage of:

1) Body of pancreas
2) Tail of pancreas

A

Pancreosplenic nodes - follow splenic to coeliac nodes.

35
Q

What does the pudendal artery and nerve pass through to ext the ol pelv? what other thing goes through there?

A

The lesser sciatic foramen, also the tendon of internal obturator

36
Q

Describe illiopsoas at the level of the symphysis:

A

Lateral and most bulky part is illiacus.

37
Q

Where do these nodes drain:
Apical axillary
Sacral/pre sacral

A

Apical -> subclavian trunk - >thoracic duct

Pre sacral:
Drain to any of
1) Common iliac
2) Lumbar trunks
3) Inferior mesenteric
38
Q

How long is the male urethra?

Name the parts

A

18-22cm

Prostatic, membranous, bolbous, spongy, and navicular fossa, external urethral orifice.

39
Q

How many segments of the liver are there? Give the 1 st 4 with land marks

A

There are 8.
The 1st is the caudate lobe
2 and 3 are left lobe (2 sup, 3 inf)
4 is high and runs the right side of falciform, laterally bounded by Cantillie’s line.
The rest circle clock wise from inferior so that 5 is superior to 8 and 6 (inferior) and 7(superior) form the borders.

40
Q

Hepatic lobule components

A

6 portal triads (portal venue, arteriole, bile duct) at the points of a hexagram surrounding a central vein (to hepatic vein) connected by sinusoids and surrounded by hepatocytes.

41
Q

Basic mechanisms of combining therapies:

A

1) Spatial co-operation
2) Cytotoxic enhancement
- Independent - give full doses sequentially
- Additive - if concurrent consider reduced dose
- Synergistic - give concurrently and reduce dose

Described by the dose modifying factor (ratio of iso effective dose without/ied with)

3) Biological co-operation - Hypoxic cell cytoxins (tirapazamine), and hypoxic cell radiosensitizers (misonidazole, nimorazole)
4) Temporal modulation - EGFR receptor blockers

42
Q

MOAs:

1) Tirapazamine:
2) The nitromidazoles (the modern form is called?)

A

Tirapazamine:
Pro drug, activated in hypoxic cells (via reductases) to form free radicals.

Nitromidazoles (currently nimorazole - the least neurotoxic):
Able to diffuse to hypoxic cells where replaces the role of O2 in damage fixation.

43
Q

What cell has the CTLA-4 protein (targeting drug)?

What cell has the PD-1?

A

CTLA-4 is on the APC and targeted by Ipilumimab

PD-1 is on the T Cell and is targeted by pembro

44
Q

Contents of middle mediastinum:

A
pericardium
heart
great vessels joining the heart
ascending aorta
pulmonary trunk
right pulmonary artery
left pulmonary artery
  the lower half of the superior vena cava
tracheal bifurcation and both main bronchi
phrenic nerves
cardiac plexus
tracheobronchial lymph nodes
45
Q

Limitations of the LQ model:

A

● Based on in vitro data (Clongenic assay) – For example does not reflect fundamental in vivo processes like radiation induced T-cell response and revascularisation ect
● At very low doses per fraction <1 Gy, the LQ model could underestimate the biological effect of a given dose, due to the low-dose hyper-radiosensitivity phenomenon.
● At very high doses per fraction >6 Gy, the LQ model underestimates the biological effect due to factors such as vascular and stromal damage not being taken into account.
● Difficult to relate to underlying radiobiological mechanisms
● The LQ formula does not include a time factor and assumes sufficient time between fractions for repair of sublethal damage
● It does not take into account tissue/tumour repopulation over time
● It has not been validated with concurrent chemotherapy.

46
Q

The principal mechanism of action of the taxane class of drugs is the:

A

The principal mechanism of action of the taxane class of drugs is the disruption of microtubule function. Microtubules are essential to cell division, and taxanes stabilize GDP-bound tubulin in the microtubule, thereby inhibiting the process of cell division as depolymerization is prevented.

47
Q

Some mechanisms of synergistic enhancement from systemic therapy:

A

Think about the Rs

1) Re-oxygenation due to CTx debulking of tumour
2) Redistribution - cells trapped in sensitive phase (e.g taxanes prevent mitosis)
3) Impaired DNA repair
4) Decreased repopulation - e.g taxanes prevent microtubule formation/mitosis

48
Q

Define: Tumour suppressor gene

A

Genes that check and regulate cell growth and repair, preventing proliferation of mutated or damaged cells.

49
Q

Examples of tumour suppressor genes:

A

BRCA1/BRCA2 (ds-DNA break repair)
PTEN - Inhibits AKT
Tp53
Rb1

50
Q

sub sites of the oropharynx:

A

1) base of tongue,
2) tonsil and pillars, and
3) uvula, soft palate, and (4 is often included in 3)
4) posterior pharyngeal wall.

51
Q

Lymphatic drainage of the subsides of oropharynx:

A

Tonsils:
Channels drain unilaterally (WELL LATERALISED TONSILS) through the reteropharynx/peripharyngeal space to jugulodiagstric/deep cervical nodes.

BOT:
Midline drains bilaterally to jugulodigastrics. and more laterally, drains unilaterally to those.

Soft palate, uvula (sometimes posterior wall included):

(1) medially to the middle third of the jugular chain,
(2) laterally to the retropharyngeal (RP) lymphatics, and
(3) anteriorly to the hard palate and subsequently into the submental and submandibular nodal group

Posterior pharyngeal wall (the epiglottis, the borders of the tonsillar complexes, and the lateral aspects of the piriform sinuses inferiorly): Drains bilaterally Predominately to IIA, also to middle deep Cx nodes (occasionally to posterior triangle).

52
Q

things in the nasopharynx:

A
Torus Tubaris
Tubal tonsils
Opening of eustachian tubes
Salpingopharygeal recess
Pharyngeal recess
53
Q

Drainage of the nasopharynx

A

Laterally (predominant pathway) through superior constrictors to drain into uppermost deep cervical drains (can also drain to level Va).
Posterior (roof and posterior wall): drain to upper retropharygeal nodes.

54
Q

Formula for BED:

A

BED = n x d (1 + d/α/β)

where n = number of fractions, d=dose/#

55
Q

Formula for EQD2:

A

EQD= D((d+α/β)/(2+α/β))

56
Q

Describe the sublingual gland

A

Paired almond shaped and sized salivary gland (the smallest of the 3 paired man salivary glands) in the anterior floor of mouth. Lobes either side of midline/frenulum of tongue. Covered superiorly by floor of mouth mucosa.
Produces mucinous saliva.
Excreted though 5-8 lateral ducts (of Rivinus) and large/main anterior duct (Bartholen’s) which empties via the caruncles on each side of the frenulum.

57
Q

Describe the submandibular gland

A

1 of three paired salivary glands
Ovoid in shape and roughly thumb sized.
Produces a mix of serous and mucous saliva.
Lies along the body of the mandible, both partly deep and partly superficial to the mylohyoid
muscle.

58
Q

Describe the parotid

A

Paired/bilateral structure. Largest of the 3 paired salivary glands. The superficial surface is approximately triangular, 5cm high, 4cm deep, 3cm wide.
Lobulated irregular shaped, it can be divided into deep and superficial lobes, separated by the facial nerve.
Along with the masseter lies within a depression known as the parotid region (this region has SCM as posterior border, zygomatic arch superior, masseter anteriorly, inferior border of mandible inferiorly)
Produces serous saliva.

59
Q

The hypogastric nerve arises from

And supplies?

Injury results in?

A

The hypogastric nerve arises from the ventral nerve roots of T12 to L3 and supplies sympathetic nerve innervation. The hypogastric nerve may be associated with the visceral fascia of the mesorectum.
Injury to the hypogastric plexus results in increased bladder tone, impaired ejaculation, and dyspareunia.

60
Q

Modes of Cell Death:

A
Mitotic catastrophe
Necrosis
Apoptosis (Type 1 Death)
Autophagy (Type 2 Death)
“Senescence” = Reproductive Death
61
Q

Morphological appearance of Apoptosis:

A
Cell shrinkage 
Membrane blabbing (forming the next thing)
Apoptotic bodies
Condensed chromatin
Nuclear fragmentation
DNA laddering
62
Q

Morphological appearance of Necrosis:

A
Cell swelling
Mitochondrial swelling
Membrane rupture
Uncondensed chromatin
Clumping of DNA
63
Q

What do you always forget to draw when drawing the stomach?

A

Angular incisure, also point out the cardia

64
Q

Which adductor muscle makes up the posterior wall of the adductor canal?

What forms the roof and lateral?

Contents?

A

Adductor longus

Sartorial forms roof

Initially rectus femurs forms wall, then more inferiorly it rectus medius.

femoral artery and vein, branches of femoral nerve, sub sartorial nerve.

65
Q

Define Integral Dose:

Why may it be more relevant for understanding carcinogenesis (second malignancy) after XRT?

A

Integral Dose = Volume x density x average Dose to that volume.

Whole body exposure events (e.g. A-Bomb survivors) often provide the data for predicting risk associated with radiation exposure, however relating ID to second malignancy data may be more relevant for radiotherapy exposures.

66
Q

CHARACTERISTICS of stochastic effects:

A

1) No threshold
2) Probability increases with dose
3) Severity of malignancy not related to dose

Typically used to describe malignancy risk following exposure.

Described in terms of effective dose (i.e tissue weight applied to equivalent dose).

67
Q

CHARACTERISTICS of deterministic effects:

A

Are dependent on prior events
1) Require a threshold to occur
2) Severity is associated with dose
Used to describe specific toxicities (e.g. cataracts require a threshold level of injury)

68
Q

An effective dose of 1 Sv has a risk of?

A

An effective dose of 1 Sv has a risk of 5.5% chance of developing malignancy.

69
Q

Limitations to the linear no threshold model:

A

Incomplete data available for the entire range of exposure (limiting any model)

Does not capture some data for risk at low doses (i.e protective hormesis, and threshold), this in turn may have made people overly fearful of very low doses of radiation.

70
Q

For I-131:
Type radiation
Half life
Form

A

90% Beta, 10% gamma
8 days
Liquid

71
Q

Half life of samarium-153?

What is good about that

A

2 days, effective half-life is only 2 hours

Good if the person wants to be cremated.

72
Q
For I-131:
Type radiation
Half life
Form
Specific activity
Decays to?
A
90% Beta, 10% gamma
8 days
Liquid
4600 TBq/gram
Xenon 131
73
Q

Half life of samarium-153?

What is good about that

Another benefit?

A

2 days, effective half-life is only 2 hours

Good if the person wants to be cremated.

TBq/g = 1620

74
Q

Common patterns to all the liquid isotope species

A

All are beta emitters,
The most powerful I-131 and Samarium-153 are have beta 10, and 30% respectively
and TBq/grams
4600 and 1602

75
Q

What is internal conversion?

A

A shaky nuclei bumps out an inner shell electron as it moves to a more stable state (w/o change in Z)

76
Q

What is electron capture?

A

inner shell electron stolen to make a neutron, with emission of CR +/ auger.

77
Q

Another name for positron decay?

A

Beta minus - ie. proton become a neutron by loosing an e

78
Q

Scatter power applies to?

What is it

A

The scattering angle of a CHARGED particle per unit path length within an absorber.
UNITS = rad.sqr/cm

79
Q

Stopping power

A

Energy lost due to collisional interactions by a charged particle per unit path length as it traverses matter.

MeV/cm

80
Q

What do Joiner and van de Kogel define as late and early tissue

A

early > 6 Gy

Late <5 Gy

81
Q

Classic tumour antigens

A

CEA

Ca-125