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FOO > MALNUTRITION AND REPRODUCTION > Flashcards

MALNUTRITION AND REPRODUCTION Flashcards

1
Q

HOW MANY WOMEN WORLDWIDE ARE AFFECTED BY INFERTILITY?

A

80 MILLION

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2
Q

WHAT PERCENTAGE OF ALL INFERTILITY CASES ARE MALE?

A

50%

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3
Q

COMMON CAUSES OF INFERTILITY?

A

AGE, TOBACCO, NUTRITION AND BODY WEIGHT, DRUG OR OTHER SUBSTANCE ABUSE, PHYSICAL ACTIVITY..

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4
Q

WHICH ASPECTS OF FEMALE FERTILITY HAVE BEEN ASSOCIATED WITH UNDER OR OVER NUTRITION?

A

OVULATION, OOCYTE MATURATION, EMBRYO QUALITY AND THEIR EFFICIENCY TO IMPLANT

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5
Q

WHICH BMI CAN MAKE IT TAKE LONGER FOR WOMEN TO CONCEIVE?

A

MORE THAN 25 AND LESS THAN 19

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6
Q

HIGH BMI ASSOCIATED WITH ADVERSE PREGNANCY OUTCOMES SUCH AS:

A

GASTROINTESTINAL DIABETES, HYPERTENSION AND PREMATURE BIRTH

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7
Q

WHICH NUTRITION RELATED ISSUES CAN AFFECT MALE FERTILITY AND HOW?

A

DEFICIENCIES IN VITAMINS AND MINERALS HAVE AN IMPACT ON SPERM MOTILITY
DIETS HIGH IN CARBS AND FATS CAN CLOG ARTERIES, BLOCK THE BLOOD SUPPLY TO GENITAL AREAS
VIT D DEFICIENCY IMPAIRS SEMEN QUALITY, TAIL MOTILITY AND LEADS TO LOWER SPERM COUNTS

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8
Q

VIT D DEFICIENCY IMPACT ON MAIL FERTILITY?

A

IMPAIRS SEMEN QUALITY, TAIL MOTILITY AND LEADS TO LOWER SPERM COUNTS

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9
Q

DEFICIENCY IN WHICH VITAMIN, WHICH IS IMPORTANT IN FETAL DEVELOPMENT, IS ONE OF THE MOST COMMON IN THE DEVELOPED COUNTRIES?

A

VITAMIN B9/FOLIC ACID

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10
Q

CASES OF NTDs HAVE BEEN REDUCED BY HOW MUCH WITH THE INTRODUCTION OF FOLATE SUPPLEMENTATION?

A

70%

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11
Q

WOMEN OF REPRODUCTIVE AGE SHOULD TAKE HOW MUCH FOLATE PER DAY?

A

400 micrograms

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12
Q

CONSEQUENCES OF FOLATE DEFICIENCY DURING PREGNANCY?

A
  • IMPAIRED PRODUCTION OF ERYTHROCYTES IN MOTHER’S BONE MARROW; RESULTS IN CELLS THAT ARE NOT MATURE OR FUNCTIONAL AND ARE ENLARGED, CALLED MEGALOBLASTS; LEADS TO MEGALOBLASTIC ANEMIA
  • NEURAL TUBE DEFECTS, BECAUSE FOLIC ACID IS NECESSARY FOR THE NEURAL TUBE TO CLOSE (SPINA BIFIDA, ONE OF THE MOST COMMON EXAMPLES)
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13
Q

WHAT ARE MEGALOBLASTS?

A
  • ENLARGED, NOT MATURE OR FUNCTIONAL ERYTHROCYTES (RESULT OF FOLATE DEFICIENCY), CAN LEAD TO MEGALOBLASTIC ANEMIA
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14
Q

NORMAL WEIGHT GAIN DURING PREGNANCY?

A

11-15KG

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15
Q

WHAT CONTRIBUTES TO THE WEIGHT GAINED DURING PREGNANCY?

A

WEIGHT OF THE FETUS ITSELF, PLACENTA, UTERUS, AMNIOTIC FLUID, INCREASED BLOOD VOLUME, BREAST TISSUE INCREASE, EXTRA FAT AND PROTEIN STORAGE

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16
Q

MAJORITY OF WEIGHT GAIN IN PREGNANCY HAPPENS IN WHICH TRIMESTER?

A

3rd

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17
Q

CHANGE IN ENERGY REQUIREMENTS PER TRIMESTER?

A

NO CHANGE IN 1ST TRIMESTER, INCREASE BY 350KCAL/DAY IN THE 2ND TRIMESTER AND A BIT LESS THAN 500KCAL/DAY IN THE 3RD TRIMESTER

18
Q

NUTRIENT REQUIREMENTS IN PREGNANCY:

A
  • INCREASE PROTEIN INTAKE BY 25g A DAY IN THE 2ND AND 3RD TRIMESTER
  • INCREASE CARBOHYDRATES BY 45g A DAY DURING PREGNANCY
  • FAT INTAKE TO REMAIN THE SAME AS PRE PREGNANCY
19
Q

HOW DOES THE NEED FOR IRON CHANGE DURING PREGNANCY?

A

50% INCREASED

20
Q

WHY DOESN’T THE INTAKE OF CALCIUM DURING PREGNANCY NEED TO BE INCREASED ALTHOUGH THE FETUS WILL BE TAKING 1/3 OF MOTHER’S DAILY NEEDS IN LATER STAGES OF PREGNANCY?

A

BECAUSE CALCIUM ABSORPTION DOUBLES DURING EARLY PREGNANCY AND THE CALCIUM IS STORED IN MOTHER’S BONES

21
Q

HOW MUCH CALCIUM DOES THE FETUS USE DAILY IN LATER STAGES OF PREGNANCY?

A

300 milligrams

22
Q

WHY SHOULD ZINC INTAKE BE INCREASED DURING PREGNANCY AND WHY SHOULD THE SUPPLEMENTATION BE DONE CAREFULLY (NOT EXCESSIVE)?

A

ZINC HELPS WITH DNA AND RNA SYNTHESIS

ZINC AND IRON COMPETE FOR ABSORPTION IN THE INTESTINE AND CAN INHIBIT EACH OTHER

23
Q

RISK FACTORS FOR POOR NUTRITION DURING PREGNANCY + EXPLANATIONS:

A
  • MULTIPLE BIRTHS; E.G. TWINS OR TRIPLETS, MOTHER HAS INCREASED NUTRITIONAL REQUIREMENTS THAT AREN’T ALWAYS MET
  • SMOKING; NICOTINE IMPAIRS NUTRIENT ABSORPTION IN THE INTESTINE AND IT ALSO SUPPRESSES APPETITE AND INHIBITS AgRP/NPY NEURONS
  • AGE (TEENAGERS OR 35+ Y.O.); HIGHER PREVALENCE OF FEEDING BEHAVIOURAL ISSUES
  • ALCOHOL USE; CAN CAUSE FETAL ALCOHOL SYNDROME
  • HAVING AN EATING DISORDER; ANOREXIA, BULIMIA, PICA
  • PHYSIOLOGICAL RISKS; GI DISORDERS, CANCERS
  • PRE PREGNANCY BMI
  • POVERTY AND FOOD INSECURITY; EDUCATION, SES, ACCESS TO FOOD AND FOOD QUALITY
24
Q

FETAL ALCOHOL SYNDROME MANIFESTATIONS:

A
  • IMPAIRED FACIAL FEATURES (LOW NOSE BRIDGE, VERY THIN UPPER LIP, SMALLER JAW, DEFECT IN THE OPENING OF THE EYES..)
  • ALTERATIONS OF THE CNS; MICROENCEPHALY, MENTAL RETARDATION, IMPAIRED LANGUAGE, MOTOR AND FINE SKILLS, HYPERACTIVITY AND SEIZURES
  • CARDIAC ISSUES; HEART MURMUR
  • SKELETAL ISSUES; ALTERATIONS OF HAND ANATOMY
  • RENAL ISSUES
  • VISION PROBLEMS; ALTERATIONS OF THE OPTIC NERVE
25
Q

PATHOPHYSIOLOGY OF THE FETAL ALCOHOL SYNDROME (FAS):

A
  • ALCOHOL DOESN’T NEED TRANSPORTERS TO TRAVEL THROUGH MEMBRANES SO IT PASSES THROUGH THE PLACENTA FREELY
  • ALCOHOL ACCUMULATES IN THE AMNIOTIC FLUID AND GOES INTO THE FETUS’ LIVER
  • THE FETUS LACKS ENZYMES FOR ALCOHOL DEGRADATION SO IT ACCUMULATES INSIDE ITS BODY
  • THIS HAS HARMFUL EFFECTS ON CARBOHYDRATE, PROTEIN AND FAT METABOLISM
  • ALCOHOL WILL IMPAIR PLACENTA FUNCTION AND REDUCE TRANSFER OF NUTRIENTS + REDUCE THE ABILITY OF THE FETUS TO RECEIVE OXYGEN
26
Q

DIAGNOSIS OF FETAL ALCOHOL SYNDROME?

A

THE ALCOHOL WILL COMBINE WITH FATTY ACIDS AND FORM FATTY ACID ETHYL ESTERS WHICH ARE DETECTED IN THE MECONIUM (1ST STOOL) OF THE NEWBORN AND SERVES AS A DIAGNOSIS

27
Q

WHAT IS MECONIUM?

A

1ST STOOL OF THE NEWBORN

28
Q

IMPACT OF FETAL ALCOHOL SYNDROME PER TRIMESTER?

A

1ST: BRAIN ORGANIZATION AFFECTED
2ND: CLINICAL FEATURES, E.G. FACIAL FEATURES
3RD: HIPPOCAMPUS PARTICULARLY AFFECTED

29
Q

FETAL RESPONSE TO UNDERNUTRITION:

A
  • IMMEDIATE RESPONSE IS USE OF PROTEIN TO PROVIDE ENERGY INSTEAD OF ACTING AS BUILDING BLOCKS OF TISSUES
  • IF UNDERNUTRITION IS PROLONGED, THE FETUS CHANGES ITS METABOLIC RATE
  • DURING UNDERNUTRITION, STRESS HORMONES INCREASE AND HIGH CHOLESTEROL WILL IMPAIR CELL DIFFERENTIATION
  • FETAL GROWTH SLOWED DOWN AND CHILDREN BORN WITH LOWER BIRTH WEIGHT; INTRA UTERINE GROWTH RESTRICTION
30
Q

2 TYPES OF IUGR (INTRA UTERINE GROWTH RESTRICTION):

A

SYMMETRICAL AND ASYMMETRICAL

31
Q

SYMMETRICAL IUGR:

A
  • 20% OF CASES
  • ONSET EARLY IN GESTATION
  • THE ENTIRE BODY PROPORTIONAL, JUST SMALLER
  • PROGNOSIS POOR, HIGH DEATH RATES
  • CAN BE GENETIC OR DUE TO AN INFECTION
32
Q

ASYMMETRICAL IUGR:

A
  • 80% OF CASES
  • DIRECT CONSEQUENCE OF NUTRIENT DEFICIENCIES WITH ALTERATIONS OF UTERINE ENVIRONMENT
  • UNPROPORTIONAL BODY; LARGE HEAD, SMALL ABDOMEN
  • HIGHER DEATH RATES THAN NORMAL BABIES, BUT MOST SURVIVE
33
Q

TERM USED FOR BABIES THAT ARE SMALL AT BIRTH BUT APPROPRIATE:

A

CONSTITUTIONALLY SMALL

34
Q

WHAT EXACTLY IS DEFINED AS IUGR?

A

DEVIATION FROM NORMAL/EXPECTED FETAL GROWTH; BABIES CALLED SMALL FOR GESTATIONAL AGE (SGA)

    • BIRTH WEIGHT BEING LESS THAN 10TH PERCENTILE AS PER GESTATIONAL AGE
  • – NORMAL BABY: BETWEEN 1OTH AND 90TH CENTILE FOR GESTATIONAL AGE
35
Q

WHAT IS THE MOST PROBABLE CAUSE OF LATER HEALTH COMPLICATIONS RELATED TO IUGR?

A

CHANGES IN THE HPA AXIS (BECAUSE OF INTRAUTERINE STRESS)

36
Q

WHICH MEDICAL COMPLICATIONS IS IUGR RELATED TO?

A

LOW COGNITIVE SCORES, POOR SOCIAL SKILLS, IMPAIRED MOTOR SKILLS, BEHAVIOURAL PROBLEMS LIKE ADHS AND AUTISM, HIGHER RISK FOR NEURODEGENERATIVE DISEASES, IMMUNE FUNCTION PROBLEMS, CANCERS, METABOLIC DISORDERS (T2D, OBESITY..)

37
Q

FETAL RESPONSE TO OVERNUTRITION:

A
  • OBESE MOTHERS OFTEN HAVE IMPAIRED INSULIN FUNCTION
  • EXCESSIVE INSULIN WILL SEND TOO STRONG GROWTH SIGNALS TO THE FETUS
  • FETUS HAVE INCREASED ADIPOSE TISSUE AND GLYCOGEN STORES
38
Q

WHAT IS MACROSOMIA?

A

VERY HIGH BIRTH WEIGHT (MORE THAN 4KG, REGARDLESS OF GESTATIONAL AGE)

39
Q

HOW MANY BABIES WORLDWIDE ARE MACROSOMIC?

A

CCA 9%

40
Q

LONG TERM RISKS OF OVERNUTRITION DURING FETAL DEVELOPMENT?

A

METABOLIC SYNDROME, OBESITY, CVD, CANCER, NEURODEGENERATIVE DISEASE

41
Q

RISKS AT BIRTH OF BABIES LARGE FOR GESTATIONAL AGE?

A

HIGHER DEATH RATES, BIRTH TRAUMA, BIRTH HYPOGLYCEMIA (AKA ‘REBOUND SYNDROME’)

42
Q

EXPLANATION OF ‘REBOUND SYNDROME’ AKA BIRTH HYPOGLYCEMIA IN FETUSES WHO WERE EXPOSED TO OVERNUTRITION DURING DEVELOPMENT?

A

BECAUSE THE GLUCOSE AROUND THE FETUS WAS TOO HIGH, WHEN IT LEAVES THE WOMB, THE FETUS’ PANCREAS SENSES THIS AND RELEASES HUGE AMOUNTS OF INSULIN WHICH MY LOWER THE GLUCOSE LEVELS TOO MUCH

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