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INT > NON MODIFIABLE AND MODIFIABLE RISK FACTORS FOR CANCER > Flashcards

NON MODIFIABLE AND MODIFIABLE RISK FACTORS FOR CANCER Flashcards

1
Q

ABSOLUTE RISK

A

THE CHANCE THAT A PERSON WILL DEVELOP A DISEASE DURING A GIVEN TIME; IDENTIFIES HOW MANY PEOPLE ARE AT RISK FOR DISEASE IN THE GENERAL POPULATION (NOT SPECIFIC TO A CERTAIN GROUP OR INDIVIDUAL, E.G. 1/8 WOMEN WILL GET BREAST CANCER IN THEIR LIFETIME)

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2
Q

RELATIVE RISK

A

COMPARES THE RISK OF DISEASE BETWEEN 2 GROUPS OF PEOPLE (COMPARES ONE GROUP WITH A CERTAIN RISK FACTOR FOR A DISEASE TO ANOTHER GROUP’S RISK) (E.G. SMOKERS ARE X TIMES MORE LIKELY TO DEVELOP LUNG CANCER THAN NON-MOKERS)

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3
Q

INCIDIENCE IS USUALLY CALCULATED FOR a time period of?

A

1 YEAR

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4
Q

RESEARCH REPORTS OFTEN GIVE INCIDENCE AS AN INCIDENCE RATE, WHICH IS:

A

THE ESTIMATED NUMBER OF PEOPLE WHO WILL DEVELOP A DISEASE OUT OF EVERY 100,000 PEOPLE

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5
Q

INCIDENCE RATE FOR CANCER IS OFTEN ADJUSTED FOR:

A

AGE
(OLDER AGE IS A RISK FACTOR FOR MANY CANCERS, SO SOMETIMES INCIDANCE RATE COULD APPEAR HIGH JUST BECAUSE A POPULATION IS PREDOMINANTELY OLD, SO ADJUSTING FOR AGE IS COMMON)

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6
Q

SOME FACTORS INCIDENCE STATISTICS MAY LOOK AT:

A
  • SEVERAL CANCERS COMBINED
  • SPECIFIC AGE RANGES
  • SPECIFIC TYPES OF CANCER
  • SPECIFIC STAGES OF A TYPE OF CANCER
  • SPECIFIC CANCER RISK FACTORS
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7
Q

INCIDANCE RATE THAT FOR EXAMPLE COVERS JUST A CERTAIN ETHNICITY WOULD BE CALLED:

A

SPECIFIC INCIDENCE RATE

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8
Q

THE PREVALENCE NUMBER FOR CANCER INCLUDES:

A
  • THOSE NEWLY DIAGNOSED (THIS IS INCIDENCE)
  • THOSE RECEIVING TREATMENT
  • THOSE WHO HAD CANCER TREATMENT IN THE PAST
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9
Q

HOW IS PREVALENCE EXPRESSED?

A
  • AS A NUMBER OR A PRECENTAGE

- PER 100,000 PEOPLE

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10
Q

MORTALITY RATE

A

THE NUMBER OF DEATHS FROM A DISEASE PER 100,000 PEOPLE DURING A TIME PERIOD (USUALLY 1 YEAR)
(CAN BE AGE ADJUSTED IN SOME CASES, E.G. CANCER)

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11
Q

CATEGORIES OF CANCER RISK FACTORS (3)

A

UNMODIFIABLE INTRINSIC RISK FACTORS (UNAVOIDABLE SPONTANEOUS MUTATIONS THAT ARISE AS A RESULT OF RANDOM ERRORS IN DNA REPLICATION; OCCUR IN DIFFERENT ORGANISMS AT DIFFERENT RATES —> RANDOM REPLICATION ERROR RATE)

NON INTRINSIC RISK FACTOR
A) ENDOGENOUS RISK FACTORS (PARTIALLY MODIFIABLE, RELATED TO INDIVIDUAL CHARACTERISTICS LIKE HORMONE LEVELS, IMMUNE SYSTEM, METABOLISM, DNA DAMAGE RESPONSE…)
B) EXOGENOUS RISK FACTORS (MODIFIABLE, E.G. CARCINOGENS, VIRUSES, RADIATION, LIFESTYLE CHOICES…)

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12
Q

HOW MANY PEOPLE WILL DEVELOP CANCER IN THEIR LIFETIME? WHY?

A

1/2

ONE OF THE MAIN REASONS IS PEOPLE LIVING LONGER

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13
Q

HALF OF ALL CANCERS ARE IN PEOPLE OLDER THAN?

A

70

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14
Q

% OF CANCERS LINKED TO INHERITED FAULTY GENES?

A

5%

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15
Q

HOW MANY PEOPLE HAVE FAULTY BRCA1 OR BRCA2 GENE (BREAST CANCER GENE)

A

CCA 1 IN 400 (RARE)

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16
Q

HOW COMMON ARE BRCA MUTATIONS IN GEN POP COMPARED TO PEOPLE WITH BREATS CANCER?

A

LESS THAN 1% OF GEN POP (CCA 1 IN 400 PEOPLE)
10% OF WOMEN WITH BREAST CANCER
20% OF MEN WITH BREAST CANCER

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17
Q

MUTATIONS IN BRCA GENES ARE ASSOCIATED WITH INCREASED RISK OF WHICH CANCERS?

A
  • BREAST
  • OVARIAN
  • PROSTATE
  • PANCREATIC
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18
Q

% OF WOMEN VS MEN WHO ARE EXPECTED TO DEVELOP BREAST CANCER BY THE AGE OF 80 IF THEY HAVE A BRCA1 OR BRCA2 MUTATION?

A

70% OF WOMEN (BRCA1 OR 2)

10% OF MEN (WITH BRCA 2 MUTATION SPECIFICALLY)

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19
Q

ASSOCIATION OF BRCA GENES WITH OVARIAN CANCER?

A

ALMOST 45% OF PEOPLE WITH A FAULTY BRCA1 GENE WILL DEVELOP OVARIAN CANCER BY THE AGE OF 80

ALMOST 20% OF PEOPLE WITH A FAULTY BRCA2 GENE WILL DEVELOP OVARIAN CANCER BY THE AGE OF 80

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20
Q

LYNCH SYNDROME OTHER NAME:

A

HEREDITARY NON POLYPOSIS COLON CANCER (HNPCC)

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21
Q

MUTATIONS IN WHICH GENES ARE ASSOCIATED WITH LYNCH SYNDROME?

A

MLH1, MSH2, MSH6. PMS2

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22
Q

RISK OF BOWEL CANCER FOR PEOPLE WITH LYNCH SYNDROME?

A
  • UP TO 70% OF PEOPLE WILL DEVELOP BOWEL CANCER, USUALLY BEFORE THEY TURN 50
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23
Q

APART FROM BOWEL CANCER, LYNCH SYNDROME IS ASSOCIATED WITH AN INCRASED RISK FOR WHICH CANCERS?

A
  • WOMB
  • OVARIAN
  • STOMACH
  • GALLBLADDER
  • PROSTATE
  • URINARY TRACT (E.G. BLADDER)
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24
Q

LI-FRAUMENI SYNDROME (LFS)

A
  • CAUSED BY A MUTATION IN TP53 GENE (TSG, INVOLVED IN CELL DIVISION) TP53 is the genetic blueprint for a protein called p53.
  • INCREASED RISK FOR BREAST CANCER, BON CANCER, ACUTE MYELOID LEUKAEMIA, SOFT TISSUE SARCOMA, BRAIN TUMOURS, ADRENAL GLAND CANCER
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25
Q

PTEN HAMARTOMA TUMOUR SYNDROME

A
  • INCLUDES COWDEN SYNDROME
  • MUTATION IN PTEN GENE
  • INCRESES RISK OF DEVELOPING BENIGN TUMOURS AND DIFFERENT TYPES OF CANCERS (BREAST CANCER, THYROID CANCER, WOMB, BOWEL, KIDNEY, SKIN CANCER)
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26
Q

FAMILIAL ADENOMATOUS POLYPOSIS (FAP)

A
  • MUTATION IN THE APC GENE (CAN CAUSE 100s OF BENIGN GROWTHS (POLYPS) TO DEVELOP- IN THE BOWEL AT A YOUNG AGE)
  • RARE, LINKED TO CCA 1% OF BOWEL CANCERS
  • IF UNREATED, PEOPLE WILL ALMOST CERTAINLY DEVELOP BOWEL CANCER BY THE TIME THEY ARE 40
    + INCREASED RISK OF STOMACH CANCER, PANCREATIC CANCER, LIVER CANCER
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27
Q

MUTYH ASSOCIATED POLYPOSIS (MAP)

A
  • MUTATIONS IN THE MUTYH GENE, A PERSON MUST INHERIT 2 MUTATED COPIES
  • PEOPLE WITH MAP DEVELOP POLYPS AND ARE LIKELY TO DEVELOP BOWEL CANCER UNDER THE AGE OF 60
    (+ SMALL INCREASE OF RISK FOR OVARIAN, BLADDER, BREATS AND WOMB CANCER)
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28
Q

PEUTZ JEGHERS SYNDROME (PJS)

A
  • MUTATION IN STK11 GENE
  • SOME SIGNS CAN APPEAR DURING CHILDHOOD
  • INCLUDES DARKER SKIN AROUND THE MOUTH, LIPS, FIGERS AND TOES
  • ICREASED RISK FOR BREAST, BOWEL, PANCREATIC, STOMACH AND OVARIN CANCER
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29
Q

JUVENILE POLYPOSIS SYNDROME (JPS)

A
  • LINKED TO THE BMPR1A AND SMAD4 GENES
  • CAN CAUSE POLYPS IN THE STOMACH AND SMALL BOWEL
  • JUVENILE IS THE NAME OF THE TYPE OF POLYP AND NOT RELATED TO THE AGE AT WHICH THEY DEVELOP
  • INCREASED RISK OF STOMACH AND BOWEL CANCER
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30
Q

PALB2 GENE MUTATION AND CANCER RISK

A
  • CAN INCREASE BREATS CANCER RISK

- UP TO 50% OF WOMEN WITH A FAULTY PALB2 WILL DEVELOP BREAST CANCER BY THE AGE OF 70

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31
Q

VON HIPPEL LINDAU SYNDROME (VHL)

A
  • RARE
  • MUTATION IN THE VON HIPPEL-LINDAU GEN
  • INCREASED RISK OF DEVELOPING PANCREATIC NEUROENDOCRINE TUMORS (pNETs) & RENAL CELL CARCINOMA (TYPE OF KIDNEY CANCER)
32
Q

TUBEROUS SCLEROSIS (TS)

A
  • MUTATIONS IN TSC1 AND TSC2 GENES
  • SKIN, BRAIN HEART AND KIDNEY RPOBLEMS
  • INCREASED RIKS OF RENAL CELL CARCINOMA
33
Q

BIRT-HOGG-DUBE SYNDROME (BHDS)

A

CAUSED BY FAULTS IN THE FLCN GENE
- OFTEN LEADS TO DEVELOPMENT OF MULTIPLE BENIGN SKIN TUMOURS (FIBROFOLLICULOMAS) ON THE FACE, NECK AND UPPER BODY
+ INCREASED RISK OF KIDNEY CANCER

34
Q

MULTIPLE ENDOCRIE NEOPLASIA (MEN) TYPE 1 AND 2

A

MEN1: TUMOURS USUALLY IN PANCREAS, PARATHYROID GLAND AND PITUATIARY GLAND (+BOWEL, STOMACH, ADRENAL GALNDS)

MEN2: MUTATION IN THE RET GENE, CAN CAUSE TYPE OF THYORID CANCER CALLED MEDULLARY THYROID CANCER (+INCREASED RISK OF ADRENAL GLAND TUMOURS)

35
Q

WHO DOES RETINOBLASTOMA MOST COMMONLY AFFECT?

A

CHILDREN YOUNGER THAN 5

36
Q

RB1 GENE MUTATIONS CAN INCREASE RISK OF;

A

RETINOBLASTOMA

37
Q

FAMILIAL ATYPICAL MULTIPLE MOLE MELANOMA SYNDROME (FAMMM)

A
  • INCREASES RISK OF MELANOMA
  • PEOPLE TEND TO HAVE A LARGE NUMBER OF MOLES OR UNUSUAL MOLES
  • USUALLY AT LEAST ONE CLOSE RELATIVE WITH MELANOMA DIAGNOSIS (PARENT, SIBLING OR A CHILD)
  • POSSIBLY DUE TO A MUTTION IN CDKN2A GENE
38
Q

HEREDITARY PAPILLARY CANCER

A
  • LINKED WITH HIGH RISK OF DEVELOPING KIDNEY CANCER (HEREDITARY PAPILLARY RENAL CELL CARCINOMA, HPRCC, MUTATION IN THE MET GENE, USUALLY CAUSES MORE THAN 1 TUMOUR IN BOTH KIDNEY, & HEREDITARY LEIOMYOMATOSIS AND RENAL CELL CANCER, HLRCC, CAUSED BY MUTATIONS IN THE FH GENE, CAUSES BENIGN SKIN TUMOURS CALLED CUTANEOUS LEIOMYOMATA. FIBRIOIDS IN THE WOMB OR UTERINE LEIOMYOMATA AND KIDNEY CANCER)
39
Q

WHICH SEX IS SLIGHTLY MORE SUSCEPTIBLE TO NON-SEX-SPECIFIC CANCERS?

A

MALES

40
Q

WHICH CANCER TYPE CAUSES MOST CANCER DEATHS IN BOTH SEXES?

A

LUNG AND BRONCHUS

41
Q

TOP 3 MOT COMMON CANCERS IN MEN VS WOMEN:

A

M:

  • PROSTATE
  • LUNG AND BRONCHUS
  • COLON AND RECTUM

W:

  • BREAST
  • LUNG AND BRONCHUS
  • COLON AND RECTUM
42
Q

5 key modifiable risk factors associated with the risk of developing cancer and other chronic diseases

A
  • TOBACCO USE
  • ALCOHOL CONSUMPTION
  • EXCESS BODY WEIGHT
  • PHYSICAL INACTIVITY
  • HEALTHY EATING
43
Q

% OF PREVENTABLE CANCER CASES

A

CCA 50%

44
Q

RISK FACTORS FOR CANCER RANKING

A

1) SMOKING (19% OF CANCER CASES AND 29% OF CANCER DEATHS)
2) EXCESS BODY WEIGHT
3) ALCOHOL
4) UV RADIATION
5) PHYSICAL INACTIVITY

45
Q

EXAMPLES OF CANCERS HIGHLY AND BARELY DEPENDANT ON LIFESTYLE FACTORS

A
  • 100% OF CASES OF CERVICAL CANCER AND KAPOSI SARCOMA ARE LINKED TO LIFESTYLE FACTORS
  • 4.3% OF CASES OF OVARIAN CANCER ARE LINKED TO LIFESTYLE
46
Q

CANCERS THAT ARE LINKED TO MODIFIABLE RISKS RESPONSIBLE FOR MOST DEATHS

A

1) LUNG CANCER (BOTH MEN AND WOMEN)
2) COLORECTAL CANCER (BOTH MEN AND WOMEN)
3) LIVER CANCER (MEN) AND BREAST CANCER (WOMEN)

47
Q

%OF LUNG CANCERS ASSOCIATED WITH SMOKING?

A

81.7%

48
Q

ALL CERVICAL CANCERS ARE ASSOCIATED WITH:

A

HPV INFECTION

49
Q

% OF MELANOMAS ASSOCIATED WITH UV RADIATION

A

96% FOR MEN

93.7% FOR WOMEN

50
Q

EXAMPLES OF THE LEAST PREVENTABLE CANCERS (<25% PREVENTABLE)

A
  • OVARY
  • PROSTATE (0%)
  • BRAIN (0%)
  • LEUKAEMIA
  • NHL
51
Q

EXAMPLES OF CANCERS THAT ARE THE MOST PREVENTABLE (>75%)

A
  • CERVIX UTERI (100%)
  • LUNG
  • ORAL CAVITY
  • OESOPHAGUS
  • MELANOMA
  • STOMACH
52
Q

DIFFERENCE IN LIFE EXPECANTCY FOR SMOKERS VS NON SMOKERS

A

ON AVERAGE, NON SMOKERS LIVE 10 YEARS LONGER

53
Q

TOBACCO ACCOUNTS FOR 1 IN HOW MANY DEATHS IN THE UK?

A

1/5

54
Q

DO ALL FORMS OF TOBACCO CAUSE CANCER?

A

YES, AND THE GREATEST RISK COMES FROM COMBUSTIBLE FORMS (TOBACCO SMOKE), SINCE MOST CANCER CAUSING SUBSTANCES ARE RELEASED DURING THE BURNING PROCESS (THERE IS NO SAFE FORM OF TOBACCO SMOKE)

55
Q

ASSOCIATION OF EXCESS BODY WEIGHT TO CANCER?

A
  • RESPONSIBLE FOR ABOUT 11% OF CANCERS IN WOMEN AND 5% IN MEN
  • RESPONSIBLE FOR CCA 7% OF CANCER DEATHS
56
Q

EXCESS BODY WEIGHT IS THOUGHT TO BE A FACTOR IN WHAT % OF ENDOMETRIAL CANCERS?

A

MORE THAM 50%

57
Q

HOW DOES BODY WEIGHT AFFECT CANCER RISK?

A
  • INFLAMMATION IN THE BODY
  • CELL AND BLOOD VESSEL GROWTH
  • CELLS’ ABILITY TO LIVE LONGER THAN THEY NOMALLY WOULD
  • LEVELS OF CERTAIN HORMONES, LIKE INSULIN AND ESTROGEN
  • INSULIN LIKE GROWTH FACTOR 1 (IGF-1)
  • THE ABILITY OF CANCERS TO METASTASIZE
58
Q

ALCOHOL AND CANCER CASES/DEATHS

A

ACCOUNTS FOR 6% OF CASES AND 4% OF DEATHS

59
Q

HOW DOES ALCOHOL RAISE CANCER RISK?

A
  • CAN ACT AS AN IRRITANT, ESP IN THE MOUTH AND THROAT
  • CAN BE CONVERTED TO ACETALDEHYDE IN THE BODY, WHICH CAN DAMAGE DNA IN THE CELLS
  • CAN LEAD TO OXIDATIVE STRESS
  • CAN DAMAGE THE LIVER, CAUSING INFLAMMATION AND SCARRING
  • MAY HELP OTHER HARMFUL CHEMICALS (LIKE THOSE IN TOBACCO SMOKE) ENTER THE CELLS LINING OF THE UPPER DIGESTIVE TRACT MORE EASILY
  • MAY SLOW THE BODILY ABILITY TO BREAK DOWN AND GET RID OF HARMFUL CHEMICALS
  • AFFECTS ABSORPTION OF SOME NUTRIENTS, SUCH AS FOLATE
  • CAN ADD EXTRA CALORIES TO THE DIET, CONTRIBUTING TO WEIGHT GAIN
60
Q

HOW MUCH PURE ALCOHOL IS THERE IN A STANDARD DRINK?

A

10-12 g

61
Q

UV RADIATION; 3 MAIN GROUPS?

A

UVA RAYS (HAVE THE LEAST ENERGY, CAUSE SKIN AGEING, WRINKLES, SOME INDIRECT DAMAGE TO DNA AND PLAY A ROLE IN SOME SKIN CANCERS)

UVB RAYS (HAVE SLIGHTLY MORE ENERGY, CAN DAMAGE DNA IN CELLS DIRECTLY, MAIN RAYS THAT CAUSE SUNBURNS, THOUGHT TO CAUSE MOST SKIN CANCERS)

UVC RAYS (MORE ENERGY THAN THE OTHER RAYS SO THEY REACT WITH OZONE HIGH IN THE ATMOSPHERE AND DON’T REACH THE GROUND, BUT COME FROM SOME MAN MADE SOURCES LIKE ARCH WELDING TORCHES, MERCURY LAMPS, UV SANITIZING BULBS ETC)

62
Q

WHICH TYPE OF UV RAYS IS ASSOCIATED WITH MOST SKIN CANCERS?

A

UVB

63
Q

WHICH TYPE OF UV RAYS IS PRESENT IN SOME MAN MADE SOURCES, LIKE MERCURY LAMPS, ARC WELDING TORCHES AND UV SANITIZING LAMPS?

A

UVC

64
Q

WHICH UV RAYS REACH THE GROUND?

A

95% OF THEM ARE UVA RAYS, AND REMAINING 5% UVB RAYS

65
Q

WHEN ARE THE UV RAYS THE STRONGEST?

A

BETWEEN 10am AND 4pm

66
Q

STRENGHT OF UV RAYS REACHING THE GROUND FROM THE SUN (THE MAIN SOURCE OF UV RAYS) DEPENDS ON:

A
  • TIME OF THE DAY
  • SEASON OF THE YEAR
  • DISTANCE FROM THE EQUATOR (LATITUDE)
  • ALTITUDE
  • CLOUDS
  • REFLECTION OFF SURFACES (BOUNCE OFF OF RAYS)
  • CONTENTS OF THE AIR (E.G. OZONE IN THE AIR FILTERS OUT SOME UV RADIATION)
67
Q

TYPES OF SKIN CANCER

A

BASAL CELL CANCER

SQUAMOUS CELL CANCER

MELANOMA (THE RAREST, A BIT LESS RELATED TO THE SUN EXPOSURE THAN OTHER 2)

68
Q

MAN MADE SOURCES OF UV LAMPS

A
  • SUNLAMPS AND SUNBEDS
  • PHOTOTHERAPY (UV THERAPY)
  • BLACK-LIGHT LAMPS (USED TO VIEW FLUORESCENT MATERIAL)
  • MERCURY VAPOR LAMPS (CAN BE USED TO LIGHT LARGE PUBLIC AREAS SUCH AS STREETS OR GYMS (2 BULBS, ONE EMITTING LIGHT AND THE OTHER FILTERING OUT UV RAYS, IF WORKING PROPERLY THEY DO NOT EXPOSE PEOPLE TO UV RAYS)
  • HIGH PRESSURE XENON AND XENON-MERCURY ARC LAMPS, PLASMA TORCHES AND WELDING ARCS (MANY ARE MAINLY OF CONCERN IN TERMS OF WORKPLACE UV EXPOSURE)
69
Q

MELANOMA IS ALSO CALLED:

A

‘BLACK SKIN CANCER’

70
Q

SQUAMOUS CELL CARCINOMA IS ALSO KNOWN AS

A

‘WHITE SKIN CANCER’

71
Q

MOST COMMON FORM OF SKIN CANCER IN FAIR-SKINNED POPULATIONS WORLDWIDE?

A

BASAL CELL CARCINOMA

72
Q

REASONS EXPLAINING INCREASE IN OCCURENCE OF SKIN CANCERS

A
  • REVEALING FASHION TRENDS
  • SHIFT IN LIFESTYLES, MOVING TOWARDS MORE OUTDOOR ACTIVITY
  • SUN SEEKING BEHAVIOUR
  • DESIRE FOR TANNED SKIN, USE OF SUNBEDS
73
Q

UP TO WHICH AGE IS IT RECOMMENDED FOR CHILDREN TO AVOID ALL DIRECT EXPOSURE TO SUNLIGHT?

A

1 Y.O.

74
Q

BEING PHYSICALLY ACTIVE REDUCES THE LIKELIHOOD OF WHICH CANCERS?

A
  • COLORECTUM

- BREAST AND ENDOMETRIUM (WOMEN)

75
Q

RECOMMENDED AMOUNT OF PHYSICAL ACTIVITY PER WEEK

A

150 MINUTES OF MODERATE PA PER WEEK
OR
75 MINUTES OF VIGOROUS PA PER WEEK (OR AN EQUIVALENT COMBINATION OF BOTH)

FOR CHILDREN AND YOUNF PEOPLE; AT LEAST 60MINS PER DAYS (MODERATE TO VIGOROUS)

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