Indigenous Health Flashcards

1
Q

How are scabies transmitted?

A

From person to person by skin-to-skin contact-the more parasites on a person, the greater the chance for spread-can also spread from clothing and bed linen but scabies do not survive for long once they are off the skin

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2
Q

What is a classic symptom for scabies infection?-what are the main areas on the body infested by scabies?

A

Extreme pruritis, especially at night-main areas: web spaces between fingers, flexor aspect of wrists and elbows, axillae, male genitalia and women’s breasts-infants and children can have atypical lesions that are generally distributed but are still usually concentrated on hands, feet, and body folds

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3
Q

How do you make a definitive diagnosis of scabies?

A

Skin scrapings from burrows or other lesions and examine under a low power microscope-look for mites, feces or eggs

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4
Q

What factors place the Aboriginal population in all countries (both rural and urban) at risk of scabies infections? (8)

A
  1. Crowded housing, shared beds and crowded schools/day cares2. Failure to recognize infestation3. Limited access to medical care4. High peds population5. Faulty application of treatment regimens6. Failure to treat close contacts7. Failure to eradicate scabies from clothing and bed linen8. Lack of running water
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5
Q

What is the treatment of scabies?

A
  1. 5% permethrin cream (needs to be 5%!!!! Cannot use the 1% used for treating head lice)-apply to skin and wash off after 8-14 hrs (8 for 6 yo)-repeat application 1-2 weeks later if live mites are still seen-one dose is curative usually-take a bath or shower, dry off, then apply to entire body ESPECIALLY to skin folds, fingernails, toenails, behind the ears and groin, face and scalp-contraindicated in infants
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6
Q

What are possible medications used for treating scabies in infants?

A
  1. Permethrin (1st line, preferred) - do not use in infants under 3 months 1. Sulfur in Petrolum Jelly
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7
Q

What is the incubation period of scabies?

A

3 weeks…so if you come into contact with scabies, you may not start showing symptoms until then!

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8
Q

What is the evidence on Ivermectin for treatment of scabies?

A

Needs only single oral dose but only acts at certain stages of the life cycle of the parasite (whereas permethrin acts at all stages)-so far, it is not licensed in Canada and is not recommended currently over permethrin

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9
Q

What is the most common complication of scabies infection?

A

Secondary bacterial skin infection

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10
Q

What are the 3 categories of inhalants in inhalant abuse?

A
  1. halogenated hydrocarbons (ie. hairsprays, varnish, cooking sprays, etc.) (moon gas, poor man’s pot, hippie crack, whiteout)2. nitrous oxide (whipping cream aerosols, balloon tanks) (ie. whippets, shoot the breeze)3. volatile alkyl nitrites (angina medications, room odourizers, etc.) (ie. poppers, thrust, climax)
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11
Q

The majority of inhalant related deaths are caused by which inhalants?

A
  1. gasoline2. air fresheners3. propane/butane
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12
Q

What are the effects of inhaling volatile alkyl nitrites (ie. poppers, climax, thrust)?

A

Vasodilatory effects = hypotension and syncope, sensations of warmth and flushing, sphincter relaxation and penile engorgement in young men for anal sex

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13
Q

What is the leading cause of death among inhalant abusers?-mechanism of death?

A

“Sudden sniffing death syndrome” = cardiac arrhythmia caused by:1. disrupted myocardial electrical propagation caused by the inhalant which is worsened by hypoxia2. inhalants also sensitize the heart ao adrenaline so when a user is startled during inhalation (such as being caught), a burst of adrenaline can cause them to have cardiac arrest

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14
Q

What are long term effects of chronic abuse of inhalants? (6)

A
  1. Irreversible neurological effects: damage of myeline and neuronal membranes by lipophilic chemicals-cortical atrophy, brainstem dysfunction with irritability, tremor, ataxia, nystagmus, slurred speech, deafness2. Cardiomyopathy3. Distal renal tubular acidosis4. Hepatitis5. Bone marrow toxicity (from hydrocarbons)6. Pulmonary toxicity (emphysema, wheezing)
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15
Q

What is the CRAFFT screening tool?

A

Screens for abuse of alcohol and drugs-C (car): Have you ever ridden ina car by someone including yourself who was high or drunk?-R (relax): do you ever use alcohol or drugs to relax, feel better about yourself or fit in?-A (alone): do you ever use alcohol or drugs while you are by yourself or alone?-F (forget): do you ever forget things you did while using alcohol or drugs?-F (family): do your family members or friends ever tell you you should cut down on your drinking or drug use?-T (trouble): have you ever gotten into trouble while you were using alcohol or drugs?**2 or more yes answers indicates potential substance abuse problem

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16
Q

What is the rate of smoking among first nations people in Canada compared to the general Canadian population?

A

First nations: 59% compared to general Canadian population of 20% (3x higher)-in 15-17 yo First nations teens, rate is again 3x higher (more common in girls than boys)

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17
Q

What are the main complications of smoking? (4)

A
  1. Myocardial & vascular disease 2. Chronic lung disease (COPD, lung cancer)3. Development of T2DM with faster progression of complications in diabetics who smoke4. Increased risk of fires
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18
Q

What are the complications of postnatal exposure to second hand smoke? (5)

A
  1. Increased LRTI2. Increased acute otitis media3. Increased asthma4. decreased lung growth5. increased risk of SIDS
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19
Q

What are the complications of perinatal exposure to smoking during pregnancy? (6)

A
  1. Increased number of perinatal deaths2. Increased preterm deliveries3. Placental insufficiency4. Congenital abnormalities5. Increased risk of learning disabilities/ADHD6. Increased risk of nicotine dependence in adolescence for child
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20
Q

In what age group is the highest prevalence of tobacco use?

A

Youth 15-24 yo

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21
Q

What are the current anti-smoking strategies put in place by provinces? (6)

A
  1. Smoke free public and workplaces2. Health warnings on tobacco products3. Hiding tobacco products at stores (shower curtain law)4. Banning tobacco advertising and displays5. Taxing tobacco at high level to deter regular smoking among adolescents6. Efforts to standardize legal age limits and penalties for selling to minors
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22
Q

What are the 5 steps to quitting smoking?

A
  1. Get ready2. Get support3. Learn new skills and behaviours4. Get medication and use it correctly5. Be prepared for relapse or difficult situations
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23
Q

What are the 5 As in the role of the health care professional in smoking control?

A
  1. Ask about tobacco use2. Advise urge to quit3. Assess willingness to attempt quitting4. Assist counselling and pharmacological therapy (nicotine patch or bupropion)5. Arrange follow up
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24
Q

What is the main difference between community acquired MRSA vs. healthcare associated MRSA?

A

CA-MRSA:1. generally more suspectible to antimicrobials (with exception of beta lactams)2. Can produce cytotoxins capable of inducing tissue necrosis

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25
Q

What are the common risk factors for community acquired MRSA? (7)

A
  1. Overcrowding2. Frequent skin to skin contact between people3. Participation in activities that result in abraded or compromised skin surfaces4. Sharing of potentially contaminated personal items5. Challenges in maintaining personal clealiness and hygiene (ie. due to water shortages or lack of clean water)6. Limited access to health care7. Exposure to antibiotics
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26
Q

What is the medical management of infected scratches/furuncles/impetigo with MRSA?-what about abscesses secondary to MRSA?

A

Infected scratches/furuncles/impetigo: 1. Wet warm compresses2. Washing with warm soap and water3. Consider topical antibiotics depending on local sensitivity patterns or for more severe infections, use oral antibioticsAbscesses:1. Incision and drainage +/- antibiotics

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27
Q

True or false: decreasing microbial carriage by decolonization reduces the recurrence of community-acquired MRSA-what are methods of decolonization?

A

FALSE! -methods of decolonization: nasal mupirocin, antiseptic baths with dilute bleach baths or chlorhexidine, oral rifampin-overtime, CA-MRSA in some communities has shown resistance to mupirocin and there is concern that using rifampin could increase drug-resistant TB in high risk communities-studies re: bleach baths’ effectiveness and safety are on the way

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28
Q

What is ONE vaccine that can help prevent severe MRSA infections?

A

Seasonal influenza vaccine!! Encourage this for all children since in MRSA-endemic communities, there is a risk for severe MRSA pneumonia following an influenza infection

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29
Q

What recommendations can you make to patients and families about how to manage MRSA skin and soft tissue infections to prevent spread?

A
  1. Keep wounds covered with clean, dry bandages. If you can’t cover, then exclude from contact sports or child care until wound drainage stops or wounds are healed2. Dispose of used dressings in a plastic-lined garbage container with sealed lid immediately after they are removed3. Hand hygiene before and after changing dressings4. Bathe regularly and change clothes and bedding often5. Avoid sharing personal items like towels, bedding, clothing and bar soap6. Seek medical attention if fever or other signs of illnes develop or if a lesion doesn’t improve within 48 hrs of starting treatment7. Regular cleaning of contact surfaces in the home with household cleaner or detergent
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30
Q

True or false:When a patient has been diagnosed with CA-MRSA, we should test everyone else in the household to determine carriage rate.

A

FALSE! This is not helpful.

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31
Q

What is the leading cause of death in Canadian indigenous children and youth?-what about leading cause of death in Canadian children in general?

A

Unintentional injuries = occurs at rates 3-4x national average-leading cause of death in canadian children: still unintentional injuries!

32
Q

What are the two most common causes of death due to injury in children

A

Children

33
Q

What are potential long term consequences of severe injuries?

A
  1. Disability2. Interference with education3. Interference with growth and development4. Impact on future employability5. Increased risk of depression and substance abuse
34
Q

Why is there a disproportionate risk of injury among Indigenous children compared to non-indigenous children?

A
  1. Lower incomes, less education and higher unemployment2. More likely to live in unsafe, substandard housing3. More likely to have minimal access to health care personnel and resources (including post discharge rehab care)4. Historical inequities, cultural alienation and loss of connectedness with the environment have contributed to depression, alcohol and substance abuse and risk taking behaviours and inadequate parenting skills for some5. Lack of culturally appropriate or targeted injury prevention programs (CPR training, swimming lessons, etc.)
35
Q

What type of mechanism causes the most injuries and deaths in First Nations children and youth?-what are contributing factors to this higher risk in indigenous populations?

A

MVCs-increased risk since communities are isolated, health care facilities are harder to get to, road conditions are poor, more use of ATVs and snow mobiles, underuse of seatbelts, inadequate enforcement of restraint laws, lack of helmet use, substance abuse

36
Q

What are factors contributing to a higher risk of death from fire in indigenous communities? (5)

A
  1. Higher proportion of smokers at home2. Wood-framed, substandard housing3. Underuse of working smoke detectors4. Longer travel times for fire rescue personnel and equipment5. Shortage of trained firefighters
37
Q

What are the 6 Es of successful injury prevention?

A
  1. Education: identify community champions to disseminate safety messages, use anticipatory guidance about seat belts/helmets/personal flotation devices, develop IP programs like first aid/swimming lessons/fire prevention, etc.2. Empowerment: incorporate indigenous culture, language and beliefs into IP planning3. Enabling: provide easier access and affordability to IP education and devices through community purchasing4. Engineering: design safer products and environments (well lit roads, etc.)5. Enforcement6. Employment
38
Q

Use the six E’s of injury prevention to teach about MVCs.

A
  1. Education: avoid alcohol while driving, use seat belts2. Empowerment: community plan for safety education and promotion for alcohol reduction and use of seat belts3. Enabling: car pooling, designated drivers, affordable child restraints4. Engineering: improved road and lighting conditions, separation of pediatrian and motor vehicles, restraining livestock5. Enforcement: max speed limits, child restraints, alcohlol usage6. Employment: local enforcement and education, first response team
39
Q

What medical conditions has vitamin D deficiency been linked to? (9)

A
  1. Osteoporosis2. Asthma3. Rheumatoid arthritis4. MS5. Inflammatory bowel disease6. Diabetes7. Disturbed muscle function8. TB resistance9. Specific types of cancers
40
Q

What is the pathway of vitamin D metabolism?

A

Vitamin D3 is produced in the skin of animals from exposure to ultraviolet rays (and vitamin D2 is from plants)-this is then first metabolized in the liver by 25-hydroxylation to 25(OH)D2 and D3 = inactive but stable forms (THIS is what we measure in the lab to define vitamin D status)-then the 25(OH)D2 and D3 undergo 1-hydroxylation in the kidney to 1,25(OH)2D2 and D3 = active but unstable forms

41
Q

What is the definition of OPTIMAL plasma 25(OH)D levels?

A

Optimal = level at which PTH production and calcium reabsorprtion from bone are minimized and intestinal calcium absorption is stabilized-optimal range is anywhere from 30 ng/mL to 90 ng/mL (or 75-150 nmol/L)

42
Q

What level of 25(OH)D is considered potentially toxic?

A

> 200 ng/mL = associated with hypercalcemia and calcium deposition in tissues-> 500 ng/mL is considered for sure toxic

43
Q

What factors influence the amount of exposure to sunlight?

A
  1. Skin pigmentation2. Latitude3. Clothing choices4. Use of sunscreen
44
Q

Fill in the blank: as your BMI increases, your plasma 25(OH)D _____.

A

Decreases!-plasma 25(OH)D varies inversely with BMI-thus overweight and obese children are at higher risk for vitamin D deficiency and may need higher intake

45
Q

When do maternal vitamin D stores get depleted in pregnancy?

A

3rd trimester: this is when rapid development of the fetus increases incorporation of calcium into the skeleton

46
Q

Maternal deficiency in vitamin D can be associated with what issues in the newborn? (4)

A
  1. Hypocalcemia2. Rickets3. SGA4. Dental malformationsthe fetus and the newborn are entirely dependent on the mother for their supply of vitamin DThus, moms need enough vitamin D to meet their own needs and their infant’s needs
47
Q

What is the recommended vitamin D intake for breastfeeding, healthy term infants?-what about babies from northern Native communities during the winter months?

A

-400 IU daily for breastfed, healthy term infants-800 IU daily for infants in northern latitudes (ie. north of the 55th parallel aka north of Edmonton) during the winter months (Oct to April)

48
Q

What level of vitamin D supplementation in the mother during pregnancy is effective in assuring adequate vitamin D in breast milk for newborns?

A

Start with 2000 IU/d but can go up to 4000 IU/d as needed-can periodically check 25(OH)D and calcium levels

49
Q

What is the vitamin D requirement in adults?

A

Some say anyway from 200 IU/d up to 4000 IU/day. Different studies say different things but needs increase as you get older

50
Q

What is thought to be the tolerable upper intake level for Vitamin D in infants

A

1000 IU/day - try not to exceed this

51
Q

What is the recommended daily vitamin D intake for premature babies?

A

200 IU/kg/day to max of 400 IU/day

52
Q

How much sun exposure should infants and children get to take advantage of vitamin D production in skin but minimize skin damage?

A

How much sun exposure should infants and children get to take advantage of vitamin D production in skin but minimize skin damage?

53
Q

What are known risk factors for type 2 diabetes?

A
  1. Genetic markers ie. family history2. Maternal gestional diabetes3. Obesity4. Physical inactivity
54
Q

What are the components of metabolic syndrome? (6)

A
  1. Acanthosis nigricans2. PCOS3. Hypertension4. Dyslipidemia5. Steatohepatitis6. Insulin resistance
55
Q

What are the criteria for screening for type 2 diabetes?-what are the screening methods?-what levels are diagnostic for type 2 DM?

A

Obtain a blood sugar level (random glucose or fasting blood glucose) in all chidlren who have the following risk factors:Need all of the following:1. At risk ethnic group: Aboriginal/asian/hispanic/african american/pacific islander descent2. BMI > 85th percentile3. Age 10 or older-AND-One of the following:1. Sedentary lifestyle2. Mom with gestational diabetes3. 1st or 2nd degree relative with type 2 DM4. Acanthosis nigricans5. Dyslipidemia6. Hypertension7. PCOS***Random glucose > 11.1 or fasting glucose > 7.0 is diagnostic

56
Q

How much physical activity should be incorporated into daily routine for schools/daycares/programs?-what else can schools do to decrease obesity/type 2 DM?

A

at least 30 minutes of high energy physical activity-encourage healthy eating and healthy active living into school curriculum-schools should be discouraged from selling candy or other sweets for fundraising purposes-cafeterias should provide healthy foods

57
Q

What are diagnostic criteria for FAS? (4)-what is it called if a patient doesn’t meet all 4 criteria?

A

Require history of prenatal alcohol consumption by mom and the following triad of features:1. Poor growth prenatally and postnatally2. Characteristic facial features3. Neurological abnormalities: ADHD, poor abstract thinking, lack of foresight, inability to make choices, inappropriate behaviour, developmental delay, lack of inhibitions, difficulty with transitions, academic difficulties, excessively friendly even to strangers and lack ability to discriminate between friends/family/strangers-if doesn’t meet all 4 criteria: atypical FAS

58
Q

What brain changes can be caused by fetal exposure to alcohol?

A

Microcephaly with cerebral dysgenesis, holoprosencephaly (characteristic of FAS), corpus callosum agenesis, brainstem and cerebellum maldevelopment, many many more-overall: variability of brain lesions can be seen depending on how much alcohol is ingested, pattern and time of drinking, mom’s genetic ability to metabolize alcohol

59
Q

What facial features are characteristic of FAS?

A
  1. Short palpebral fissues2. Hypertelorism3. Flattened face4. Short nose5. Absent or hypoplastic filtrum6. Thin upper lip and bowing of the mouth downwards
60
Q

What is the most consistent physical finding in newborns with FAS (apart from characteristic facial appearance which might be difficult to appreciate)?

A

Growth retardation, especially microcephaly!!-can also be jittery, irritable, hypotonic

61
Q

True or false: Low alcohol consumption levels can cause FAS, just as binge drinking does.

A

FALSE!-Some studies show that low alcohol consumption levels are unlikely to cause FAS-effects are more likely related to high blood alcohol levels and the number of drinks consumed at a time is more important than the average alcohol consumption-ie. less than 5 drinks, less than once per week had no measurable effect

62
Q

What are the definitions are the following:-abstainers-low-risk drinkers-at-risk drinkers-problem drinkers

A

-Abstainers: consume no alcohol-low-risk drinkers; consume 1-2 drinks per day, 3x/wk or less. They do not use alcohol while driving/pregnant/breastfeeding-at-risk drinkers: consume 7-21 standard drinks per week, consume more than 3-4 standard drinks per occasion, drink in high-risk situations-problem drinkers: consume > 21 standard drinks per week and may experience negative consequences from drinking (behavioural/family/medical/mental health/employment/legal issues)

63
Q

What is the T-ACE approach to alcohol risk assessment?

A

-Tolerance: how much alcohol do you drink before you feel its effects?-Annoyed: has anyone annoyed you by saying you should cut down on your drinking?-Cut down: have you ever thought you should cut down?-Eye opener: have you ever had a drink to get going in the morning?-if the tolerance question is answered with 2 or more drinks, the score is 2. A positive response to the other questions gives a score of 1 for each question. A total score of 2 or more indicates an AT RISK drinker

64
Q

What are characteristics of newborns with exposure to alcohol in utero?

A
  1. Poor sleeping2. Hypersensitive to touch/light/sound3. Irritable4. Difficulty establishing routines5. Poor feeding
65
Q

What is the 4 digit diagnostic scale for the diagnosis of FAS?

A

Four criteria are assessed, quantified and assigned a rating of 1-4 for each criteria, depending on the degree of abnormality:1. Impaired growth2. Facial abnormalities3. Abnormal brain function4. Degree of maternal drinking4 digit diagnostic code: 1111 (normal) to 4444 (unequivocal FAS) depending on findings in these 4 areas-results in 22 code combinations leading to different diagnostic possibilities-can have FAS, alcohol exposed; FAS, alcohol exposure unknown; or atypical FAS, alcohol exposed***Rating for abnormal brain function: Rating of 4: definite brain dysfunction = defines a situation of static encephalopathy and depends on definite findings of brain damage (microcephaly, abnormalities of brain imaging, persistent neuro findings of prenatal origin, or IQ of 60 or lower)Rating of 3: probably brain dysfunction = static encephalopathy as well, abnormalities in 3 of 4 areas of brain functioning (cognition, achievement, adaptation, language)Rating of 2: possible brain dysfunction = neurobehavioural disorder only suggesting possibility of brain damageRating of 1 = no brain problems demonstrated

66
Q

What are the consequences of delaying intervention for children with FAS?

A
  1. Risk of abuse (excessively friendly children, irritable babies)2. Risk of trouble with the law (lack sense of consequence)3. Learning disabilities/school failure/loss of self esteem***If early intervention takes placed, a lot of these can be prevented or at least modified-do NOT wait for a definitive diagnosis, start making referrals right away
67
Q

What are the 4 key objectives of early childhood intervention and education in children with FAS?-what are strategies for dealing with difficult behaviours?

A
  1. Establish and maintain sense of self worth2. Establish acceptable interpersonal behaviour3. Foster independence4. Teach children how to make acceptable decisionsRemember that difficult behaviours might be due to attempts at communication or frustration with transitions/difficulty understanding/etc.1. Keep tasks simple2. Use concrete examples3. Keep instructions simple and give them one at a time4. Concentrate on life skills
68
Q

What are methods of primary prevention of FAS?

A
  1. School based educational programs2. Early recognition3. Treatment of at-risk women4. Community-sponsored, culturally centered support programs5. Physicians should ask all women about their drinking habits
69
Q

What is the definition of early childhood caries? -most common causative organism?

A

Presence of tooth decay involving any primary tooth in a child

70
Q

What is the causative triad for caries?

A
  1. Presence of cariogenic bacteria2. Exposure to fermentable carbs in diet3. Host susceptibility (integrity of tooth enamel)
71
Q

What is the most prevalent pediatric infectious disease?

A

Early childhood caries

72
Q

What are potential consequences of early childhood caries?

A
  1. Pain = altered chewing, eating, sleeping = potential growth restriction2. Early tooth loss = speech difficulties and decreased self esteem3. Increased risk of decay in permanent dentition as well with possible malalignment and crowding of permanent teeth4. Requires extensive treatment under general anesthesia
73
Q

What is the biggest risk factor for early childhood caries?-why??

A

Poverty: household crowding, family size, nutrition, health behaviours, parenting practices (ie. prolonged bottle use with juice, sugary snacks, smoking), etc.

74
Q

What are prenatal strategies that can prevent or delay early childhood caries?

A

There is evidence for vertical transmission of cariogenic bacteria!-should involve pregnant women in oral health screening/dental treatment/education on oral health hygiene, improve nutrition, encourage use of fluoride toothpaste

75
Q

What is the evidence on fluoride supplementation through diet as opposed to water/fluoride varnish/toothpaste?-what is the evidence on the use of sealants to prevent caries?

A

No evidence to support using this!-sealants: protect pits and fissures on tooth from caries = evidence that populations at high risk of dental caries should get sealants on both primary and permanent molars

76
Q

At what age should children start going to the dentist?

A

Within 6 months of first tooth eruption OR by 12 months of age

77
Q

True or false: all indigenous children should have access to the evidence-based schedule for fluoride varnish and assessment to determine need for sealant placement on teeth

A

True!!-fluoride varnish should be provided as part of a regular child health clinic program