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LCRS2- RDA > RDA > Flashcards

RDA Flashcards

1
Q

How man Carnegie Stages of Human Development are there?

A

1-23

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2
Q

What percentage of identifiable structures of the adult body have appeared by Carnegie stage 23?

A

90 percent

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3
Q

What is PF?

A

Post-fertilisation

Approx. 2 weeks less than gestational age, GA

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4
Q

What is oxygen tension in the fetus and placenta in the first trimester?

A

Before week 3= 3%

By week 10 PF= 8%

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5
Q

What happens in the 3rd week of pregnancy?

A

Formation of trilaminar disc (mesoderm), CNS and somites
Blood vessel initiation
Initiation of placental villi
(3mm)

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6
Q

What happens in the 4th week of pregnancy?

A 
Closure of neural tube
Heart, face, arm initiated
Umbilical cord
elaboration of placental villi 
(4mm)
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7
Q

What happens in the 5th week of pregnancy?

A

Face and limbs continue

5-8mm

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8
Q

What happens in the 6th week of pregnancy?

A

Face, ears, hands, feet, liver, bladder, gut, pancreas

10-14mm

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9
Q

What happens in the 7th week of pregnancy?

A

Face, ears, fingers, toes

17-22mm

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10
Q

What happens in the 8th week of pregnancy?

A

Lungs, liver, kidneys
Placental elaboration continues, development of villi
Placental endocrinology becomes dominant
Cytotrophoblast plugs in spiral arteries lost over next 2 weeks
(28-30mm)

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11
Q

How much does a fetus weigh by the end of week 12?

A

50g

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12
Q

How much does a fetus weigh by the end of week 28?

A

1050g

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13
Q

How much does a fetus weigh by the end of week 40?

A

2100g

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14
Q

When does most growth in the fetus occur?

A

Mostly 2nd and 3d trimester

Before 2nd= 50g, after 3rd= 2100g

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15
Q

How can you see changes in the first 4 weeks PF?

A

Microscopy

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16
Q

What size is a blastocyst at 9 days?

A

0.1cm

Early stage of implantation

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17
Q

What size is an embryo at 5-6 weeks?

A

1cm

Can see yolk sac (very red area= liver)

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18
Q

What size is a 3 month old fetus?

A

7cm

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19
Q

What is the conceptus?

A

Everything produced from fertilised egg

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20
Q

When is the embryonic genome activated?

A

Between Day 2 and 3

Between 4 and 8 cells

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21
Q

When do you call a fertilised egg an embryo?

A

After week 1

Expanded blastocyst has hatched

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22
Q

How do cells proliferate in the embryo?

A

Changes in response to GFs
Changes in receptor expression
May be due to changes in cell survival
All paracrine or autocrine regulation (embryo doesn’t have blood vessels so can’t have endocrine processes)

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23
Q

How do chemo-attractants cause movement in embryos?

A

Local production

Paracrine effects

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24
Q

What are cognate receptors expressed on?

A

Target cells

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25
Q

Why are proteases and inhibitors important in movement in embryos?

A

Production and activation of movement

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26
Q

Why is the ECM important in movement of embryos?

A

Re-modelling of tissues

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27
Q

How does differentiation happen in embryo movement?

A

Paracrine regulation
Receptor expression (necessary in target cells)
Loss of proliferation (not necessarily)

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28
Q

What controls cell loss in an embryo? Give examples of this

A

Apoptosis
Controlled mainly by paracrine factors
Stops webbing between digits and loses tail

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29
Q

How do concentration effects affect regulation of cells?

A

Cells are exposed to different combinations of regulators
Leads to different responses

Gradients of factors important
Temporal changes in factors or responses to them

E.g. limb bud from proliferation in 3 dimensions causing finger-like projection

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30
Q

What kind of cell regulators operate on embryos?

A

Proliferation
Differentiation
Chemo-attraction

Can operate individual or together

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31
Q

What are main models of embryos?

A 
Chicks= limb, mainly wing
Fish= eye
Mouse= KO or KI, tissue specificity

Gene families involved in development are same in many species

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32
Q

Give an example of genes having a similar effect in animals and in humans?

A

Piebaldism in mouse and boy (mutation of KIT receptor)

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33
Q

What do Hox genes do?

A

Establish A-P axis
Differences in the vertebrae
CNS divisions
Pattern the limbs

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34
Q

What controls Hox genes?

A 
Retinoic acid (derivative of vitamin A)
Environment important (especially mothers health and diet)
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35
Q

Describe the bilaminar disc 9 days PF

A

Found within decidualising endometrium

(TOP TO BOTTOM)
Syncytiotrophoblast 
Amnion 
Bilaminar embryonic disc= epiblasts and hypoblasts
Yolk sac
Cytotrophoblast
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36
Q

What happens in gastrulation (day 15/16)?

A

Forms a 3 layer embyro

Becomes elongated
Buccopharyngeal membrane (prechordal plate) at head end
Primitive streak at other end
Surrounded by cut edge of amnion and then wall of yolk sac around

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37
Q

What is the primitive streak? What happens in gastrulation

A

Depression where epiblast cells are proliferating and then undergo differentiation

These then move into layer between epiblast and hypoblast

Form germ layer

Proliferation, differentiation, movement and apoptosis happen at same time

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38
Q

What happens to mesoderm cells that bump into the hypoblast (rather than forming germ layer)?

A

Form exoderm (possibly)

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39
Q

What are the 3 germ layers?

A

Ectoderm (epiblast)
Mesoderm
Endoderm (hypoblast)

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40
Q

What is the fate of the germ layers?

A

Endoderm-> gut, liver, lungs
Mesoderm-> skeleton, muscle, kidney, heart, blood
Ectoderm-> skin, nervous system

Very few tissues are just one type

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41
Q

What happens in neurulation?

A

By 21 days

Neural plate forms with notochordal process in it
Primitive streak lengthens and develops
Newly added cells to both

Oropharyngeal membrane at top
Cloacal membrane at bottom

Notochord deep to neural groove
Surrounded by neural fold which close
Somite around neural groove

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42
Q

What is the relationship between the developing umbilical cord and yolk sac?

A

Between 21 and 28 days= closure of body cavity

Developing umbilical cord is directly adjacent to yolk sac

Gap in body wall for this= belly button

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43
Q

What kinds of folding occur between day 17 and 28?

A

Head to tail folding and lateral folding

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44
Q

When does a fetus start looking human?

A

By day 56

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45
Q

When does CNS development begin?

A

Week 3

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46
Q

When does heart development begin?

A

Week 3

Starts outside main embryo

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47
Q

When does limb development start?

A

Week 4

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48
Q

When does the urogenital system development start?

A

Week 3

Link between urinary and gonadal/tubular systems linked

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49
Q

When do the lungs start to develop?

A

Week 3

Continues during rest of pregnancy and after birth

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50
Q

When does face development start?

A

Week 4

Throughout first trimester

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51
Q

How does the CNS develop?

A

22 days= fusion of tissues
Somites attach
Neural fold surrounded by otic placode, then pericardial bulge (anterior end), then amnion edge

23 days= elaboration
Anterior neuropore forms
Posterior neuropore forms

25 days
Pharyngeal arches start to form
Yolk sac develops

28 days
Lens
Otic placode
Pharyngeal arches develop
Limb ridges begin
Heart bulge forms
Umbilical cord forms
Closure of neuropores
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52
Q

What causes spina bifida?

A

If posterior neuropore doesn’t close (failure of caudal fusion)
Should close by 28 days
Faulty neurulation

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53
Q

What happens in spina bifida?

A

Range of effects
Depends on type and severity

Neurogenic bowel/bladder incontinence
Lower limb paralysis
Fractures 
Joint contractures
Developmental deformities
Learning impairment
Hydrocephalus and meningitis

Surgery helps anatomical, but not functional problems

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54
Q

What are the types of spina bifida?

A

Spina bifida occulta= doesn’t go through skin, patch of hair

Meningocele= spinal cord protrudes through child’s back (meninges don’t)

Myelomeningocele= spinal cord and meninges protrude through child’s back

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55
Q

How often do anencephaly and spina bifida occur?

A 
SB= 1-2 per 1,000 pregnancies
A= 1-8 per 10,000

Anencephaly more severe but less common than spina bifida (particularly in female babies)

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56
Q

When should folic acid be given to avoid spina bifida and anencephaly?

A

Before pregnancy
Problem present within 4 weeks of fertilisation

Less sure about effects of FA on A than on SB

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57
Q

What causes anencephaly and what happens?

A

Literally ‘lack of head’
Caused by anterior neuropore not closing (failure of rostral fusion)
Under-developed brain
Abnormally developed skull line

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58
Q

How does the heart develop?

A

Between week 2 and 7

Cardiogenic area with primitive blood vessels around day 18

Initial formation of the heart as a muscular tube, which can pump blood

  • Heart tube fusion
  • Heart tube begins to beat

A complex pattern of folding forms the basic structure of the heart (LOOPING)
- C-shaped loop and S-shaped loop

Separation into the four main chambers by septae and valves

Connection of specific arteries and veins to each chamber of the heart

  • Rotation of arteries and veins (connections between precursor tissues)
  • If under pressure-> bends and makes corkscrew shape

Closure of the ductus arteriosus and foramen ovale at birth convert the single-cycle flow of the fetus into a figure-of-eight loop
- Very limited blood to lung (don’t need lungs until birth)

Heart tube structures seen only near head end

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59
Q

What are the main changes in the heart after birth (vs before)?

A 
FETAL HEART 
Open ductus arteriosus
Open foramen ovale
Minimal blood to lungs (and deoxygenated blood from lungs)
Get oxygenated blood also from placenta

HEART AFTER BIRTH
Closed ductus arteriosus
Closed foramen ovale
All deoxygenated blood now flows to lungs

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60
Q

How do limbs develop?

A

Forelimb bud appears at d27/28
Hindlimb bud appears at d29

Grow rapidly out of lateral plate mesoderm

Fully formed by d56

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61
Q

What courses Achrondroplasia?

A

Gain of function mutation in FGFR3
Stops switch of cartilage to bone
Bones remain short

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62
Q

What does thalidomide cause?

A

Interferes with blood vessel development

Variable pattern typical
More common in boys
Affects upper limbs more
Can also cause deformed eyes and hearts, deformed alimentary and urinary tracts, blindness and deafness

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63
Q

What can thalidomide be used to treat?

A

Leprosy and some cancer treatments

Was used for morning sickness

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64
Q

What regulates limb development?

A

Sonic hedgehod (Shh)- zone of polarizing activity

Fibroblast-like growth factor-8 (Fgf8) in chick- apical ectodermal ridge

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65
Q

What is polydactyly?

A

Addition digits

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66
Q

How is the kidney developed?

A

Pronephros develops first (precursor tissue that directs formation of mesonephros)

Metanephros/permanent kidney appears by the 5th week

Develops from the metanephric mesoderm

Ureteric bud (outgrowth of cloaca) leads to collecting ducts of the permanent kidney 
- Bud penetrates metanephric tissue and gives rise to ureter, renal pelvis, calyces and collecting tubules

Newly formed collecting tubule is covered at its end by a metanephric tissue cap

Kidney ascent (by end of week 9)

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67
Q

What happens in kidney ascent?

A

Kidneys initially form near the tail of embryo
Vascular buds from the kidneys grow toward and invade the common iliac arteries
Kidney position changes relative to adrenal glands and gonads
Kidneys then send out new cranial branches and then induce the regression of the more caudal branches

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68
Q

How is the bladder formed?

A

Mostly endodermal (except the trigone, mesodermal) which develops from the mesonephric duct

Trigone signals filing of the bladder to the brain

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69
Q

What happens if development of the kidneys goes wrong?

A 
Renal agenesis
Abnormal shaped kidneys
Abnormal ureter
Pelvic or horseshoe shaped kidney (enlarged renal pelvis)
Bladder exstrophy
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70
Q

What is renal agenesis?

A

Early degeneration of ureteric bud
Unilateral (L more than R)
NB. bilateral= Potter’s syndrome (oligohydramnios)- baby doesn’t produce enough urine

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71
Q

How do gonads and other reproductive tissues developed?

A

Gonads arise from intermediate mesoderm within urogenital ridges of the embryo

Primordial germ cells are the precursors of all gametes

Genital ducts arise from paired mesonephric and paramesonephric ducts

  • Mesonephric ducts give rise to MALE genital ducts
  • Paramesonephric ducts give rise to FEMALE genital ducts

Differentiation happens after 7 weeks

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72
Q

What causes sexual differentiation?

A

The gonads and reproductive tracts are indifferent up until 7 weeks

Differentiation is determined largely by the presence or absence of SRY (on the Y chromosome)

SRY+= development proceeds along the male path (7 weeks onwards)
SRY-= development proceeds along the female path (9 weeks onwards)
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73
Q

How does the male reproductive tract develop?

A

SRY expression= gonad develops into a testic containing spermatogonia, Leydig cells and Sertoli cells

Leydig cells produce testosterone (support growth of mesonephric ducts)

Some testosterone converted to DHT which supports development of prostate gland, penis and scrotum

Sertoli cells produce anti-mullerian hormone (AMH) which induces regression of the paramesophric ducts

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74
Q

What do the following embryonic features lead to (in men)?

Ureteric bud
Mesonephric ducts
Urogenital sinus

A

Ureteric bud= ureter

Mesonephric ducts= rete testis, efferent ducts, epididymis, vas deferens, seminal vesicle, trigone of bladder

Urogenital sinus bladder (except trigone), prostate gland, bulbourethral gland, urethra

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75
Q

How does the female reproductive tract develop?

A

In absence of SRY, gonad develops into an ovary with oogonia and stromal cells

Since no testosterone= mesonephric (Woolfian) ducts regress
No AMH so Mullerian (paramesonephric) ducts persist and give rise to oviducts, uterus and upper third of vagina

Urogenital sinus contributes to formation of bulbourethral glands and lower 2 thirds of vagina

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76
Q

What do the following embryonic features lead to (in women)?

Ureteric bud
Paramesonephric ducts
Urogenital sinus

A

Ureteric bud= ureter

Paramesonephric ducts= oviducts, uterus and upper third of vagina

Urogenital sinus= bulbourethral glands and lower 2 thirds of vagina

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77
Q

What ducts are in male and female fetuses?

A

Male= mesonephric, Woolfian

Female= paramesonephric, Mullerian

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78
Q

When does hCG peak?

A

Week 8 after LMP

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79
Q

When do the testes descent?

A

Testes arise in lumbar region

Descent is due to tethering of the testes to the anterior body wall by the gubernaculum

Descend into pelvic cavity and through the inguinal canal to end up in the scrotum (due to growth and elongation of embryo and shortening of gubernaculum)

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80
Q

What happens if there are undescended testes?

A

Stuck in inguinal canal (don’t go through superficial inguinal ring)
Increased risk of cancers
Abnormal function

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81
Q

What happens to development of genitalia if there is no testosterone?

A

Female structures will form

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82
Q

What is hypospadia?

A

Structurally abnormal development of reproductive systems

Fusion of urethral folds is incomplete so urethra exits the penis other than at the tip

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83
Q

What Mullerian duct abnormalities are there?

A

Fusion of mullerian ducts is altered
Affect uterine structure
May affect fertility

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84
Q

What happens in Persistent Mullerian Duct syndrome?

A

Occurs in genetic males with mutations in AMH or the AMH receptor

Testosterone and DHT are produced leading to normal male external genitalia and male (Wolffian) genital ducts

No inhibition so the paramesonephric ducts persist i.e. there is a small uterus and paired fallopian tubes

The testes may lay either in what would be the normal position for ovaries (i.e. within the broad ligament) or one or both testes may descend into the scrotum

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85
Q

What is Androgen Insensitivity Syndrome?

A

Androgen insensitivity= testicular feminization

Occurs in genetic males (XY) with mutations in the androgen receptor (AR)

Androgens have no effect

Errors in production or sensitivity to testes hormones lead to a predominance of female characteristics under the influence of maternal and placental estrogens

Relatively normal female external genitalia (no functional androgens) but undescended testes

Mesonephric ducts are rudimentary or lacking due to loss of testosterone signaling

Normal production of MIS from Sertoli cells causes Mullerian duct regression, so no oviducts, uterus, or upper third of vagina

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86
Q

What is congenital adrenal hyperplasia?

A

Female homology to AIS

Genetic females with decreased or lacking 21-hydroxylase enzyme activity essential for cortisol synthesis

Leads to increased production of weak androgenic hormones from the adrenal gland which results in weak virilization of external genitalia
- Male features with enlarged clitoris and partial or complete fusion of labia majora

Internal genitalia are female
- Testes absent (no SRY)
- No mesonephric ducts
No AMH so Mullerian duct structures develop

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87
Q

How does the face develop?

A

Formation of face as two separate halves

5-10 weeks

Eyes move from side to front (front and inwards)

Medial nasal prominences merge

Facial symmetry especially attractive

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88
Q

What causes a cleft lip and palate?

A

Failure of tissues to fuse

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89
Q

Why is surgery to fix cleft lips and palates so successful?

A

Cells proliferate quickly
Heal very quick
Minimal scarring

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90
Q

What can be caused by a cleft lip and palate?

A

These disorders can result in feeding problems, speech problems, hearing problems, and frequent ear infections

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91
Q

How do lungs develop before birth?

A 
Conducting zone (weeks 3-16)
WEEKS 3-8
Embryonic= bronchi

WEEKS 5-17
Pseudoglandular= bronchioles then terminal bronchioles
Lobes begin to form

Transitional and respiratory zone (weeks 16-38)
WEEKS 16-27
Canalicular= respiratory bronchioles

WEEKS 24-36
Saccular= alveolar ducts (AND SURFACTANT)

WEEKS 26 and after birth
Alveolar= alveolar sac

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92
Q

What happens to lungs from 26 weeks to childhood?

A

Saccular period= 26 weeks to birth

Alveolar period= 8 months to childhood

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93
Q

What causes Respiratory distress syndrome (RDS)?

A 
Surfactant levels are low or absent
Alveoli collapse (surfactant normally keeps low surface tension in alveoli)
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94
Q

What is surfactant comprised of? How can it be produced artificially?

A

Lipids, proteins and glycoproteins

Know composition
Half life 5-10 hours

Can increase production in utero (1 injection of glucocorticoids)

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95
Q

Why is premature delivery dangerous for lungs?

A

Before 24 weeks, surfactant not produced

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96
Q

What are teteratogens?

A

Factors which dysregulate patterning

Cause congenital anomalies defects in development (affect normal patterning and lead to maldevelopment)

Interfere with embryonic or fetal organogenesis, growth or cellular physiology

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97
Q

What factors can act as teratogens? When do they have their main effects?

A

Illegal drugs, medications, radiation, infections

Main effects in first trimester of pregnancy

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98
Q

When do most miscarriages occur?

A

Before 23 weeks of gestation

Mostly within 13 weeks

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99
Q

When is considered term?

A

37-41 weeks

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100
Q

What percentage of term babies are delivered by elective Caesarean?

A

25%

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101
Q

What are preterm babies?

A

Born 23-37 weeks of gestation

Either by labour or emergency Caesarean

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102
Q

What is the approximate size of a baby at term?

A

Head close to adult hand size
Body close to adult forearm size
Between 6-9 pounds

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103
Q

What happens in labour?

A

Cervical ripening and effacement (increasing)

Coordinated myometrial contractions (increasing)
- Fundally dominant

Rupture of fetal membranes

  • Fetal membrane remodelling
  • Lower segment relaxation

Delivery of infant

Delivery of placenta

Contraction of uterus

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104
Q

When does labour happen?

A

Latent stage approx 8 weeks e.g. Braxton hicks contractions (practise)

Labour 12-48 hours

  • PHASE 1= many hours (contractions, cervical changes
  • PHASE 2= hours (baby)
  • phase 3= 30 mins (placenta)
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105
Q

What can initiate preterm labour?

A 
Intrauterine infection
Intrauterine bleeding
Multiple pregnancy
Stress (maternal)
Others
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106
Q

What happens in cervical ripening and effacement in labour?

A 
Change from rigid to flexible structure
Remodelling (loss) of extracellular matrix
Recruitment of leukocytes (neutrophils)
Inflammatory process (PGE2, IL8)
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107
Q

What happens in co-ordinated myometrial contractions in labour?

A

Fundal dominance
Increased co-ordination of contractions
Increased power of contractions

Key mediators

  • PG F2α (E2) levels increased from fetal membranes
  • Oxytocin receptor increased
  • Contraction associated proteins
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108
Q

What happens in rupture of fetal membranes in labour?

A

Loss of strength due to changes in amnion basement component
Inflammatory changes, leukocyte recruitment
Modest in normal labour, exacerbated in preterm labour
Increased levels and activity of MMPs
Inflammatory process in fetal membranes

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109
Q

What is NFKB involved in?

A

A pro-inflammatory transcription factor

Involved in labour too (almost all pro-labour genes have NFKB binding domains in their promoters, seems to be key regulator)

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110
Q

How does inflammation relate to labour?

A

NFKB in both

Inflammatory changes are strongly linked with labour

NB. Differs in term and pretem labour
Activators of inflammation are readily linked with preterm labour (e.g. intrauterine infection)

PGE2 involved in term labour induction
CRH and PAF can upregulate inflammatory pathways in fetal membranes (and initiate labour)

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111
Q

What is the role of platelet-activating factor in the fetus?

A 
Part of lung surfactant
Surfactant proteins and complexes
Produced by maturing lung, before birth
Levels in amniotic fluid increase near term
Fetal signal of maturity
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112
Q

What happens to CRH in pregnancy?

A

CRH upregulated in maternal circulation and CRH binding proteins fall at end of pregnancy

Anything that increases CRH may predispose to labour (stress, multiple infants)

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113
Q

What can predispose to labour?

A

Increased CRH (stress, multiple infants)
Increased muscle contraction (stretch of uterus)
Activation of inflammatory cascades
Intrauterine infection, bleeding, twins

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114
Q

What is the role of progesterone in human pregnancy?

A

Needed to sustain pregnancy

Levels very high until after delivery of placenta

There is a mutually negative interaction between NFKB and progesterone

Can switch of many pathways involved in labour biochemistry

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115
Q

What does the progesterone receptor mediate?

A

PR-B mediates the main effects of progesterone via gene expression
PR-A is less able to mediate these effects
Ratio of PR-A : PR-B increases at term
Loss or change in PR may lead to ‘functional progesterone withdrawal’ (e.g. during labour)

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116
Q

What is development?

A

Increase in understanding, acquisition of new skills and more sophisticated responses and behaviour

Gain ability to respond and adapt to environment in a planned, organised and independent manner

Dynamic process

Bidirectional transactional process (between genetic and environmental factors)

Process by which child evolves from helpless infancy to independent adult

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117
Q

What are the ANTENATAL environmental causes of damage to brain development?

A

Early maternal infections e.g. rubella, toxoplasma, cytomegalovirus

Late maternal infections e.g. varicella, malaria, HIV

Toxins e.g. alcohol, pesticides, radiation, smoking

Drugs e.g. cytotoxics, antiepileptics

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118
Q

What are the POSTNATAL environmental causes of damage to brain development?

A

Infections e.g. meningitis, encephalitis, cytomegalovirus

Metabolic disorders e.g. hypoglycaemia, hyponatraemia or hypernatraemia, dehydration

Toxins e.g. lead, mercury, arsenic, chlorinated organic compounds, solvents

Trauma e.g. especially head injury

Severe understimulation, maltreatment or domestic violence

Malnutrition e.g. iron defiency, folate deficiency, vitamin D

Maternal mental health disorders (depression)

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119
Q

When are the periods of susceptibility to teratogens?

A

Greatest sensitivity= 3-8 weeks
Highest risk around week 5 (embryonic period)
Each organ will also have a period of peak sensitivity

Lethality may occur before 2 weeks

(Decreasing sensitivity= after 9 weeks, period of functional maturation)

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120
Q

What happens to the baby if the mother has rubella in the first trimester?

A

Congenital rubella in baby

Cataracts, glaucoma, heart defects, hearing loss, tooth abnormalities, pneuomonitis, splenomegaly, blueberry rash muffin or petechial, bone abnormalities, jaundice, hepatomegaly, virus in urine, microcephalus, intracerebral calcification, hydrocephalus, growth restriction

Lose red reflex

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121
Q

What happens to the baby if the mother has cytomegalovirus?

A

Microcephaly, visual impairment, intellectual disability, fetal death

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122
Q

What happens to the baby if the mother has herpes simplex virus?

A

Microphthalmia, microcephaly, retinal dysplasia

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123
Q

What happens to the baby if the mother has varicella virus?

A

Skin scarring, limb hypoplasia, intellectual disability, fetal dysplasia

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124
Q

What happens to the baby if the mother has toxoplasmosis?

A

Hydrocephalus, cerebral calcifications, microphthalmia

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125
Q

What happens to the baby if the mother has syphilis?

A

Intellectual disability, hearing loss

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126
Q

What medications can be dangerous for pregnant women?

A 
Valproic acid
Trimethadione
Lithium
SSRIs
Amphetamiines
Warfarin
ACE inibitors
Mycophenylate 
Alcohol
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127
Q

What does maternal valproic acid cause in babies?

A

Neural tube defects

Heart, craniofacial and limb anomalies

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128
Q

What does maternal alcohol cause in babies?

A 
Fetal alcohol syndrome (FAS)
Short palpebral fissures
Maxillary hypoplasia
Heart defects
Intellectual disability
Dysmorphic features
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129
Q

What maternal hormone conditions can lead to child developmental displays?

A

Androgenic agents
DES
Maternal diabetes
Maternal obesity

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130
Q

What does maternal diabetes cause in babies?

A

Various malformations
Heart and neural tube defects most common
Large for gestational age baby (uterus is too small, can get stuck and have hypoxia)

Particularly bad if uncontrolled during pregnancy

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131
Q

What can cause folate deficiency?

A

Nutritional

Inhibitors of folate synthesis

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132
Q

What are the domains of child development?

A

Gross motor
Vision and fine motor
Hearing, speech and language
Social, emotional and behavioural

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133
Q

What is a milestone? How are they estimated?

A

Acquisition of a key performance skill

Normal range of attainment varies widely

Estimations based on median age when half of a standard population of children achieve that level

Limit ages= age by which they should be reached

Correct for prematurity until age 2

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134
Q

What are the shared features of development between children?

A

Remarkably constant pattern

Varies in rate

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135
Q

How can you check gross motor and posture?

A 
Standing
Walking
Running
Kicking a ball
Climbing stairs
Peddling a tricycle
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136
Q

How does lying/sitting change in the first 8 months?

A

Newborn= lying down, limbs flexed, symmetrical posture
= marked head lag on pulling up

6-8 weeks= raises head to 45 degrees in prone

6 months= sits without support, round back

8 months= sits without support, straight back

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137
Q

How does crawling/standing change in the first 15 months?

A

8-9 months= crawling (commando crawl, on all fours or bottom shuffling)

10 months= cruises around furniture

12 months= walks unsteadily, broad gait hands apart

15 months= walks steadily

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138
Q

Why do babies have primitive reflexes?

A

Protective and survival value
Promote proper orientation
Promote postural support and balance

Should be present from birth to 4 or 6 months

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139
Q

Give examples of primitive reflexes

A 
Stepping
Moro
Grasp
Asymmetric tonic reflex
Rooting
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140
Q

What is the downward parachute reflex and when does it occur?

A

5 months

When held and rapidly lowered the infant extends and abducts both legs
Feet are plantigrade

141
Q

What is the sideward protective reflex and when does it occur?

A

6 months

Infant puts arms out to save if tilted off balance

142
Q

What is the forward protective reflex and when does it occur?

A

7 months

Arms and hands extend on forward descent to ground

143
Q

What is the backward protective reflex and when does it occur?

A

9 months

Backward protective extension of both arms when pushed backwards in sitting position

144
Q

What are the protective or righting responses?

A

Downward parachute reflex
Sideward protective reflex
Forward protective reflex
Backward protective reflex

145
Q

What is the moro reflex?

A

Almost drop the baby (back a few inches)

Baby should put arms to try and protect itself

146
Q

What is the asymmetric tonic reflex?

A

Turn baby to one side
They extend their limbs on that side
Fencing posture

147
Q

How can you study fine motor and vision in a child?

A

Looks at hand function and hand-eye coordination

Can also give some information of cognitive function:
Holding objects
Picking up objects
Pointing 
Waving
Throwing/catching
148
Q

What is object permanence?

A

Cognitive ability
Infant realizes that out of sign doesn’t mean object has disappeared
Happens around 8-9 months

149
Q

What happens to vision and fine motor over the first 5 years?

A

6 weeks= follows moving object or face by turning the head (relatively blind compared to adults)

4 months= reaches out for toys

4-6 months= grasps toys (palmar grasp)

7 months= transfers toys from one hand to another

10 months= mature pincer grip

16-18 months= makes marks with a crayon

14 months- 4 years= tower building (develops)

2-5 years= ability to draw without seeing how it’s done
Can copy 6 months earlier

150
Q

What happens if there is normal hearing in a baby?

A

Normal speech develops

Babbling
Words
Sentences
Social communication

Language is birectional

151
Q

How does speech develop over the first 3 years?

A

Newborn= startles to loud noises

3-4 months= vocalises alone or when spoken to (coos or laughs)

7 months= Manchester rattle test (turns to soft sounds out of sight)

7 months= At 7 months, sounds used indiscriminately

10 months= At 10 months, sounds used discriminately to parents

12 months= two to three words (other than dada and mama)

18 months= 6-10 words, shows two parts of the body

20-24 months= uses two or more words to make simple phrases

2.5-3 years= talks constantly in 3-4 word sentences

152
Q

What can you study to evaluate a child’s social behaviour and play?

A 
Looks at interaction with others and self care skills
Stranger awareness
Play
Feeding, toileting and dressing
Social interaction
153
Q

How does the social, behaviour and play of a child change in the first 3 years?

A

6 weeks= smiles responsively

6-8 months= puts food in mouth

10-12 months= waves bye-bye, plays peek-a-boo

12 months= drinks from a cup with two hands

18 months= holds spoon and gets food safely to mouth

18-24 months= symbolic play

2 years= dry by day, pulls off some clothing

2.5-3 years= parallel play, interactive play evolving, takes turn

154
Q

What are the key features of speech and language skills?

A

Vocalization
Words
Understanding
Imaginative play

155
Q

What are the key features of social skills?

A

Social interaction
Stranger reaction
Eating skills
Dressings

156
Q

What are the key features of gross motor skills?

A 
Position
Head tag
Sitting 
Walking 
Running
157
Q

What are the key features of fine motor skills?

A 
Uee of hands
Grasp and fine pincer
Bricks
Crayon
Puzzles
158
Q

What is a limit age of milestones?

A

Limit ages= latest age by which a child should have achieved a milestone

2 standard deviations from the mean

159
Q

When should children have their first steps?

A 
25% by 11 months
50% by 12 months
75% by 13 months
90% by 15 months
97.5% by 18 months
160
Q

When should a child walk independently?

A

18 months

161
Q

When should a child fix and follow visually?

A

3 months

162
Q

When should a child join words?

A

2 years

163
Q

When should a child engage in symbolic play?

A

2-2.5 years

164
Q

What is developmental delay?

A

Slow acquisition of skills

May be in one or more domains

165
Q

What is a development disorder?

A

Maldevelopment of a skill

166
Q

What is it called if:
1 domain is affected by delay
2 domains affected by delay

A

1 domain is affected by delay= domain-specific

2 domains affected by delay= global

167
Q

What is consonant delay?

A

All domains affected to same extent

168
Q

What is dissonant delay?

A

Domains affected to different extent (most delay starts dissonant, rate differs)

169
Q

What are the patterns of developmental delay?

A

Slow but steady
Plateau
Regresses

170
Q

What causes GLOBAL developmental delay?

A 
Idiopathic severe learning disability
DS
Other dysmorphic and chromosomal abnormalities
Meningitis
Trauma
FAS
Abuse and neglect
Neurodegenerative disorders
Neurocutaneous disorders
171
Q

What causes TALKING delay?

A 
Stammering
Hearing deficit
Maturational delay
Environmental factors
Learning disabilities
Autism
Language disorders
172
Q

What causes WALKING delay?

A

Maturational delay
Severe learning disabilities
Cerebral palsy
Duchenne muscular dystrophy

173
Q

How do children present with developmental problems?

A

Routine child health surveillance

Identified risk factors (such as prematurity)

Parents may be worried

Professionals in a nursery or day care setting concerned

Concerns may be detected opportunistically at health contacts

174
Q

What questions should be asked to identify and then treat a child with developmental problems?

A

Routine child health surveillance

Identified risk factors (such as prematurity)

Parents may be worried

Professionals in a nursery or day care setting concerned

Concerns may be detected opportunistically at health contacts

175
Q

What are the clinically approaches to treating developmental delay?

A

History= risk factors, reported milestones
Physical examination
Developmental assessment
Differential diagnosis and identification of co-morbidities
Targeted tests

176
Q

What needs to be considered in the history to study a developmental delay?

A 
ANTENATAL
Illnesses and infections
Medications
Drugs
Environmental exposure

BIRTH
Prematurity
Prolonged and complicated labour
NNU stay and problems

POSTNATAL
Illnesses and infections
Trauma

CONSANGUINITY

FAMILY AND SOCIAL HISTORY

MILESTONES
Developmental milestones from parents

177
Q

What needs to be considered in the physical exam to study a developmental delay?

A

Growth parameters= height, weight and head circumference

Dysmorphic features= face, limb, body proportions

Skin= neurocutaneous stigmata, injuries

Central nervous exam= power, tone, reflexes and any asymmetry

Systems exam e.g. cardiac= related to different syndromes and chromosomal abnormalities

Formal developmental assessment= SOGS II, Griffiths, Denver, Specialised

178
Q

What is SOGS II?

A

Schedule of growing skills assesment

Considers:
Passive postural skills
Active postural skills
Locomotor skills
Manipulative skills
179
Q

What is the Griffiths Mental Development?

A

Birth to 2 years (GMDS 0-2)

Used to measure the rate of development of infants and young children

180
Q

What is the Denver scale?

A

DDST is a widely used assessment

Examines the developmental progress of children from birth until the age of six devised

181
Q

What investigations can be used to consider for developmental delay?

A

Cytogenetic= chromosome karyotype, fragile x, DNA FISH analysis

Metabolic= thyroid function tests, LFTs, bone chemistry, urea and electrolytes, amino acids, creatine kinase, blood lactate etc.

Infection= congenital infection screen

Imaging= cranial ultrasound in newborn, CT and MRI, skeletal survey and bone age

Neurophysiology= EEG, EMG, nerve conduction studies, ERG, VEP

Histopathology and histochemistry= Nerve and muscle biopsy

Other= hearing, vision, cognitive assessment, therapy assessment, child psychiatry, dietician, nursery reports

182
Q

What is the Child Development Service?

A

Multidisciplinary (health professionals and social worker)

Multi-agency (health, social services, education, volunteers, parent support groups)

Coordinated service

Monitor children up to 25 years

Emphasises children’s needs within community

Often has nominated key worker for a child

183
Q

What is cerebral palsy?

A

Disorder of movement and posture due to a non-progressive lesion of motor pathways in the developing brain

The clinical manifestations emerge over time, reflecting the balance between normal and abnormal cerebral maturation

The most common cause of motor impairment in children

184
Q

What causes cerebral palsy?

A

80% of cases antenatal due to genetic syndromes and congenital infection

10% of cases are thought to be due to hypoxic-ischaemic injury at birth

10% are postnatal in origin (e.g. in meningitis, encephalitis, encephalopathy, head trauma, symptomatic hypoglycaemia, hyperbilirubinaemia)

185
Q

How does cerebral palsy present?

A

Abnormal limb tone and limb and/or trunk posture in infancy with delayed motor milestones may be accompanied by slowing of head growth

Feeding difficulties, with oromotor incoordination, slow feeding, gagging and vomiting
abnormal gait once walking is achieved

Asymmetric hand function before 12 months of age

Primitive reflexes may persist and become obligatory

186
Q

What are the classifications of cerebral palsy?

A

Spastic (70%)

Ataxic hypotonic (10%)

Dyskinetic (10%)

Mixed pattern (10%)

187
Q

What problems are associated with cerebral palsy?

A 
Learning difficulties 
Epilepsy
Squints 
Visual impairment from errors of refraction and cortical damage
Hearing impairment 
Speech and language disorders 
Behaviour disorders 
Feeding problems 
Joint contractures, hip subluxation, scoliosis
188
Q

What is autism spectrum disorder characterised by? When does it present and how does it happen?

A

Neurobiological disorder characterised by

  • Qualitative impairment of social interaction
  • Qualitative impairments in communication
  • Restricted, repetitive, and/or stereotyped patterns of behaviour, interests and activities

Boys>girls

Usually presents 2-4 years of age

Screening and diagnostic assessment tools are available

Intensive support required for child and family

Prognosis depends on severity

189
Q

What are the main features of autism?

A

IMPAIRED SOCIAL INTERACTION
Doesn’t seek comfort, share pleasure, form close friendships
Prefers own company
No interest in others
Gaze avoidance
Socially and emotionally inappropriate behaviour
Doesn’t appreciate that others have thoughts and feelings
Lack of appreciation of social cues

SPEECH AND LANGUAGE DISORDERS
Delayed development, may be severe
Limited use of gestures and facial expression
Formal pedantic language, monotonous voice
Impaired comprehension with over-literal interpretation of speech
Echoes questions, repeats instructions
Can have superficially good expressive speech

IMPOSITION OF ROUTINES WITH RITUALISTIC AND REPETITIVE BEHAVIOUR
On self and others, with violent temper tantrums
Unusual stereotypical movements e.g. gait and hand flapping
Concrete play
Poverty of imagination in play and general activities
Restriction in behaviour repertoire

CO-MORBIDITIES
General learning and attention difficulties
Seizures

190
Q

What are learning disability?

A

Classified as mild, moderate, severe and profound

May present:
As part of a recognizable syndrome
Failure to meet milestones
Dysmorphic features with associated problems

191
Q

What causes learning disabilities?

A 
Chromosome disorders
Identifiable syndromes
Cerebral palsy, infantile spasms, post-meningitis
Metabolic or degenerative diseases
Idiopathic (25%)
192
Q

How do you manage learning disabilities?

A 
Identify a possible cause
MDT
School= statementing required
Associated problems= vision, hearing, epilepsy
Specific diagnosis=specific problems
193
Q

How can education be affected by learning difficulties?

A

Education Acts= provide children with Special Educational Needs and Disability with additional support to integrate in mainstream schools

Early identification and intervention maximises progress and potential

Children identified are notified to the Local Education Authority (LEA)

194
Q

What is ADHD?

A

Attention Deficient Hyperactivity Disorder

A persistent pattern (> 6 months) of inattention with or without hyperactivity-impulsivity that

Interferes with functioning or development to a degree that is inconsistent with developmental level and that

Negatively impacts directly on social, academic and occupational activities

Are not solely a manifestation of oppositional behaviour, defiance, hostility or failure to understand tasks or instructions

Were present prior to age 12 years

Are present in two or more settings

195
Q

How can you assess ADHD?

A

Questionnaires (strengths and difficulties, Connors)

Exclude medical causes e.g. hyperthyroidism, iron deficiency anaemia

Hearing deficits

Identify risk factors and co-morbidities

196
Q

What is the SDQ?

A

Strengths and Difficulties Questionnaire

Brief behavioural screening questionnaire about 3-16 year olds

Exists in several versions to meet the needs of researchers, clinicians and educationalists

197
Q

What is the Connors questionnaire?

A

ADHD Connors test

Doctors can assess what type of behaviour has been observed by parents over time

198
Q

What is the recommended management for ADHD?

A 
Pyschotherapy
Family therapy
Medication e.g. methylphenidate, other
Co-morbidities e.g. medical management
Diet modification
CAMHS for more complex cases
199
Q

What are the main themes of development?

A

Physical
Cognitive
Emotional
Social

200
Q

What are the developmental stages of adolescence?

A

Early adolescence= 11-14
Middle adolescence= 14-17
Late adolescence= 18-21

201
Q

What are the gender differences in adolescence?

A

Girls grow taller earlier than boys
Girls start puberty earlier than boys
Girls are physically mature in general 2 years earlier

202
Q

Outline the pubertal changes in girls?

A

8-13 years= breast budding
8-14 years= growth of pubic hair
9.5-14 years= growth spurt (peaks 11-13.5)
10-16 years= menarche
10.5- 16.5 years= growth of underarm hair
11-15.5 years= change in body shape
12.5-16.5= adult breast size

203
Q

Outline the pubertal changes in boys?

A

10.5-17 years= growth of scrotum and testes
10.5-18 years= change in voice
11-15 years= lengthening of penis
11-14= growth of public hair
12-17 years= growth spurt (peaks 13-15)
11-17 years= change in body shape
13-18= growth of facial and underarm hair

204
Q

What are early maturing girls and late maturing boys are at higher risk of?

A 
Depression
Substance abuse
Disruptive behaviour/ delinquency
Eating Disorder
Bullying
205
Q

What happens in the brain during puberty?

A

Developmental curves peak at at 12 years (frontal and parietal lobes) and at 16 years (temporal lobes)

PFC increases in density of GM up to puberty and then after puberty decreases GM density

From puberty= increases density cortical WM

Dorsolateral PFC= late in reaching adult levels cortical thickness

Cellular changes too (synaptogenesis, axonal myelination and fine tune PFC and other cortical regions)

206
Q

What are the executive functions?

A 
Working memory
Cognitive flexibility
Selective attention
Planning
Inhibition and abstract reasoning
207
Q

What happens in the brain to cellular processes?

A

Synaptogenesis followed by pruning (synapse elimination)

Axonal myelination (speeds up nerve conduction)

Fine tune prefrontal cortex and other cortical regions

208
Q

What are Piaget’s 4 stages of cognitive development?

A

Birth-2 years= sensorimotor stage
- Infant constructs an understanding of the world by coordinating sensory experiences with physical actions

2-7 years= preoperational stage

  • Begins to represent the world with words and images
  • This reflects and increased symbolic thinking

7-11 years= concrete operational stage
- Child can now reason logically about concrete events and classify objects into different sets

11-15 through adulthood= formal operational stage
- The adolescent reasons in more abstract idealistic and logical ways

209
Q

What is Kohlberg’s theory of moral development?

A

Moral reasoning (basis for ethical behaviour), has 6 developmental stages, each capable of responding to moral dilemmas than its predecessor

Sequence is fixed,three broad stages

Many people never obtain highest level

Pre-conventional, conventional and post-conventional

210
Q

What are the stages of Kohlberg’s theory?

A

Level 1 and 2: PRE-CONVENTIONAL

  • Obedience and punishment orientation (how can I avoid punishment?)
  • Self-interest orientation (what’s in it for me?)

Level 3 and 4: CONVENTIONAL

  • Interpersonal accord and conformity (social norms)
  • Authority and social-order maintaining order morality (law and order morality)

Level 5 and 6: POST-CONVENTIONAL

  • Social contract orientation
  • Universal ethical principles (principle conscience)
211
Q

What influences self-concept?

A

Intellectual development leads to more complex self-concept
Pubertal and social changes leads to self concept
Adolescence leads to struggle to understand self

212
Q

What are the 8 dimension of self-concept according to Harter?

A 
Scholastic competence
Job competence
Athletic competence
Physical appearance
Social acceptance
Close friendships
Romantic appeal
Conduct
213
Q

What is the structure of self-concept according to Shavelson, 1976?

A

Need academic, social, emotional and physical

Academic and non-academic self- concept
Evolution of behaviour

214
Q

What are the clinical implications of good self-esteem?

A

70-80% adolescents

Self-confidence
Leadership

215
Q

What are the clinical implications of low self-esteem?

A

20-30% adolescents

Depression
Anxiety
Poor school performance
Social isolation
Feeling not respected
216
Q

What is important in identity formation in adolescence?

A

Search for identity important at this stage
Coincides with physical growth
Need for important life decisions
Resolution may be through “crisis”

217
Q

What are Erikson’s 8 life-span stages?

A

Trust vs mistrust (infancy, first year)
Autonomy vs shame and doubt (infancy, 1-3 years)
Initiative vs guilt (early childhood, 3-5 years)
Industry vs inferiority (middle and late childhood)
Identity vs confusion (adolescence 10-20 years)
Intimacy vs isolation (early adulthood, 20s and 30s)
Generativity vs stagnation (middle adulthood, 40s and 50s)
Integrity vs despair (late adulthood, 60s+)

218
Q

What is identity formation according to Marcia?

A

Identity diffusion= not yet experienced crisis, no commitment to cation/beliefs

Identity foreclosure= not yet experienced crisis, committed to goals, beliefs largely result of choices made by others

Moratorium= individual not resolved struggle over identity, actively searching to achieve identity

Identity achievement= individual experiences crisis, resolved on own terms

219
Q

What is identity associated with?

A 
Achievement
Moral reasoning
Career maturity
Social skills
Lower anxiety
220
Q

How do cultural minorities develop ethnic identity?

A

Integration= retain cultural traditions, develop and maintain relationships with mainstream culture

Assimilation= high involvement and relationships with mainstream culture, low maintenance cultural traditions

Separation= retains cultural traditions, low identification mainstream culture

Marginalisation= low both dimensions

221
Q

How do family relationships contribute to adolescence?

A

Development of autonomy and continuation close relationships

Social domains - adolescents and parents may have different views about who has final say depending on “domain” friendships, clothes, career etc.

Mid-adolescence: most intense negotiations

222
Q

How does conflict with parents affect adolescents?

A

Most adolescents report good relationships parents

Get on well with mother 86% and father 80%

High confiding to mothers

Disagreements around dress, music choice, leisure activities, time of coming home, tidying bedrooms

223
Q

What does family connectedness manifest as?

A

Joint activities, mealtimes etc.

High confiding

Parental surveillance: parents communicates with adolescent, knows where they are, etc.

224
Q

What are the benefits of family connectedness?

A

Associated with reduced risk behaviours (early and unprotected sex, drug, alcohol, cigarette consumption, fighting)

Higher adolescent self-esteem

225
Q

What happens in primary school (7-11 years) in friendships (peer development)?

A

Friends shared activities
Main goal- acceptance by same gender group
Prefer same gender friends
Loyalty build on earlier interactions

226
Q

What happens in 11-13 year olds in friendships (peer development)?

A

Expect genuineness, intimacy, self-disclosure, common interests
Emergence of cliques

227
Q

What happens in 13-16 year olds in friendships (peer development)?

A

Friendship goal= understanding self
Beginning cross gender relationships
Development of larger groups

228
Q

What happens in 16-18 year olds in friendships (peer development)?

A

Expects friends to provide emotional support

Increased dyadic romantic ties

229
Q

What happens to children rejected in friendships?

A

In less satisfying friendships

230
Q

What are the gender differences in peer development?

A 
Girls= close relationships, more confiding, more brittle
Boys= less intimate, less disclosing, friendships more embedded in larger circle
231
Q

What do parents have more influence than peers on?

A

Academic choices
Job preferences
Future aspirations

232
Q

What do peers have more influence than parents on?

A

Interpersonal style
Friendships selection
Fashion and entertainment

233
Q

How do parental and peer influences interact in marijuana consumption?

A

If friends don’t use and parents use= 17% use

If friends use and parents don’t= 56% use

If friends and parents use= 67% use

234
Q

What online opportunities are present to the digital generation?

A

Social networking
Peer contact
Obtain information/learning
IT expertise

235
Q

What online risks are present to the digital generation?

A 
Illegal
Unhealthy content e.g. self-harm or pro-anorexia
Cyber-bullying 
Abuse personal information
Amount of time online or sedentary
236
Q

What do adolescents usually use the internet for?

A

5-7 year olds= mostly playing games
8-11 year olds= mostly school work and homework
12-15 year olds= mainly school work, homework and social networking

237
Q

Why is school important in developing an adolescent’s behaviour?

A

Teacher effects expectancy and positive attitude

Classroom rules teach about structure, cooperation, competition

School ethos teaches about attainment and behaviour

238
Q

Who is most likely to do well in school?

A

5 or more A*-C grades

  • Higher if upper social class
  • Ethnic variation (chinese, indian, white, bangladeshi, pakistani, black)
239
Q

What is the ICD 10 criteria of anorexia nervosa?

A 
Body weight at least 15% below expected
Avoidance of 'fattening' foods
Psychopathology- morbid dread of fatness, aims for weight lower than premorbid or healthy
Endocrine disturbance
May be other weight loss behaviours
240
Q

List endocrines disturbances that may result from anorexia nervosa?

A

Amennorrea in women
Loss of sexual interest in men
Puberty may be delayed

241
Q

What is the ICD 10 criteria of bulimia nervosa?

A

Persistent preoccupation with eating and binges
Weight losing behaviours (purging by vomiting, laxatives, diuretics, stimulants, excessive exercise)
Psychopathology- morbid dread of fatness, aims for weight lower than premorbid or healthy

242
Q

What is the DSM 5 criteria of bulimia nervosa?

A

Recurrent episodes of binge eating
Sense of lack of control over eating during episode
Recurrent inappropriate compensatory behaviour to prevent weight gain (purging by vomiting, laxatives, diuretics, stimulants, excessive exercise)
Binge eating and compensatory behaviours both occur and last at least 1 week for 3 months
Self evaluation is unduly influenced by body shape and weight

243
Q

What happens if boys have early pubertal development?

A

Satisfaction related to height and musculature
Feel more attractive
More popular and relaxed
Advantages may persist e.g. better at sport

244
Q

How does puberty affect girl’s feelings about herself?

A

Associated with increased height and body fat (dissatisfaction related to weight and fat- being slim perceived as desirable)
Ambivalent attitude to menarche

245
Q

How does fashion and media influence girls during puberty?

A

Slimmer body shapes attractive (e.g. models, mannequins, magazines)
Hard to prove direction of causality

246
Q

True or false; girls ‘feeling fat’ decreases between ages 12 and 17?

A

False

Increases (and increase in dieting)

247
Q

True or false; boys ‘feeling fat’ decreases between ages 12 and 17?

A

False
Boys feel fattest around 14 years
Many want to gain weight (particularly by age 17)

248
Q

What race is most associated with seeing self as fat overweight in girls and boys?

A

GIRLS
White, asian, black

BOYS
White, asian (similar to white), black

249
Q

What are the best ways to predict that a girl may develop eating problems?

A

Earlier pubertal maturation and higher body fat

Concurrent psychological problem e.g. depression (7x)

Dieting over 6 months at severe level (16x) or moderate level (5x)

Family history (twin studies 50% heritable)

Personality (perfectionist, obsessional)

250
Q

Outline the epidemiology of anorexia nervosa

A

Female 10x more than men
Onset teenage usually
Dieting
More in certain subcultures e.g. ballet schools, Western affluence societies

251
Q

What are the possible mechanisms of distorted body image in AN?

A

Somatosensory cortex

252
Q

What are the possible mechanisms of increased anxiety in AN?

A

Amygdala

253
Q

What are the possible mechanisms of obsessional drive in AN?

A

Basal ganglia

254
Q

What are the possible mechanisms of enhanced sense of reward in AN?

A

Nucleus accumbens

255
Q

What are the possible mechanisms of visuo-spatial deficits in AN?

A

Parietal cortex

256
Q

What are the possible mechanisms of executive impairments in AN?

A

Frontal lobe

257
Q

What happens if you have weak central coherence in EDs?

A

Poorer global processing-> weak central coherence (limit ability to understand context or see big picture)

258
Q

What family factors are important in developing AN?

A

Parental negative attitudes to body fat and shape
Maternal dieting and eating disorders
Family interaction
Dissatisfaction with family life

259
Q

What adverse experiences are important in developing AN?

A

Sexual abuse
Death
Other adverse life events

260
Q

What sociocultural factors are important in developing AN?

A

Ethnic group (less in Afro-caribbeans in UK)
Institutions e.g. ballet school
Media (role unclear)
Anorexia in higher social class

261
Q

How does anorexia present?

A

Self starvation, weight loss, abnormal growth
Symptoms related to self starvation e.g. nausea, abdominal distension, fainting and dizziness
Selective eating e.g. fat avoidance
Other weight controlling strategies e.g. vomiting, exercising, laxatives
Low mood, irritability
Later may have withdrawal, poor concentration, sleep disturbance

262
Q

How do you assess a patient with AN?

A

Family interview (structure, EDs, illness, psych issues, siblings, parental authority in attitude to treatment)

Individual interview with child or adolescent
- Social adjustment

Physical exam and investigations

  • Eating and weight history
  • Psychosexual (menstruation and puberty)
  • Past medical histroy
  • Mental state exma

Data on growth

263
Q

What are the differential diagnose for AN?

A

PHYSICAL
GI disorder e.g. Crohns
Metabolic e.g. diabetes
Pituitary

PSYCHIATRIC
Bulimi nervosa
Depression
Psychosis 
OCD
264
Q

How is AN treated?

A

Admission for weight restoration in minority of cases

Family therapy

Nutritional counselling

CBT (to reduce weight preoccupations and challenge faulty cognitions)

265
Q

What does family therapy to treat AN include?

A

Parents supervise eating, ensure weight gain

Discussion of family relationships

Family life-cycle issues

Most adolescents are significantly helped by family treatments

Initially weight gain, then improvement in eating attitudes and mood

Family conflict reduces and warmth between parents increases, relationships become more harmonious

Important problems in treatment are drop-out, depression, poor treatment progress, low weight

266
Q

How does family therapy lead to a patient’s recovery?

A

Initial focus of adolescents= need to eat
(Parents and carers to supervise)

Adolescent gradually assumes more control of eating (graded improvement in social function)

Address other developmental, relationship and life cycle issues

267
Q

What is CBT?

A

Cognitive behavioural therapy
Can be individual, groups or self-help
Can be with other treatments (sequenced or concurrent)

Involves:
Psychoeducation
Self-monitoring
Behavioural goals
Modify abnormal cognitions
268
Q

What is the prognosis for AN?

A

Only can study the half that present for treatment

50% recover after 5 years
30% weight far below average
Many don’t have menstruation

76% recover after 15 years
30% developed binge eating

5-15% mortality after 20 years

269
Q

What kind of model is needed for AN?

A

Multifactorial
Psychosocial factors mediate between pubertal development and onset of unhealthy eating with weight controlling behaviours

270
Q

What developmental features characterise adolescence?

A

Cognitive and emotional
Family
Peers
Biology

271
Q

What cognitive and emotional changes happen in adolescence?

A

Emotional change (including increased intensity of mood states)

More abstract reasoning (sophisticated)

Ability to consider alternative outcomes, consequences, ambiguity (what if?)

Greater knowledge and awareness of the world

Identity (of self, family, ethnicity)

  • Autobiographical memory develops (can get sense of self across time)
  • Care about how others view them (reputation with peers)
272
Q

What family changes happen in adolescence?

A

Relationships transformed

Challenging rules

Discipline needs reasoning

Less confiding and intimacy in parents

Shift from time with family to autonomy and independence

273
Q

What peer changes happen in adolescence?

A

Peer activities and confiding

Sexual relationships

Peer group influences values and behaviour

Over time, peers become more important and take up more time

More exposure to other social factors e.g. media, experimentation

Tend to choose friends with similar values to our parents

274
Q

What biological changes affect behaviour in adolescence?

A

Puberty and endocrine changes

Physical growth

Brain maturation

275
Q

Who defines the following?
Anti-social behaviour
Delinquency or offending
Conduct disorder

A

Anti-social behaviour= defined by society

Delinquency or offending= defined by law

Conduct disorder= defined by psychiatry

276
Q

What is the ICD 10 definition of conduct disorder?

A

Repetitive and persistent (>6 months) pattern of dis-social, aggressive or defiant behaviour

Frequency and severity beyond age appropriate norms

(DSM 5 also says impaired everyday functioning- social, acadmeic or occupational)

277
Q

What behaviours are typical in conduct disorder?

A 
Oppositional behaviour, defiance
Tantrums
Excessive levels of fighting or bullying, assault 
Cruelty to animals
Running away from home
Truancy
Stealing
Destructiveness to property
Fire-setting
278
Q

What is cyberbullying?

A

Can be from one incidence (single posting can repeatedly injure individual)

Impact is often delayed

Anonymity and disinhibition can lead people to be more aggressive

Aggressors don’t receive communication from their victims that might otherwise moderate behaviour

Forms of cyber bullying evolved with technology

279
Q

What is the epidemiology of conduct disorder?

A

Higher in London (2x)

4% 5-10 year olds
6% 10-15 year olds

Higher in boys (2x)

Anti-social behaviour can be limited to adolescence of persist for life

Anti=social behaviour is increasing

280
Q

What factors are important int the aetiology of conduct disorder?

A

Individual child factors e.g. ADHD, Callous-Unempotional traits, physical or developmental healthy problems, difficulties at school or with friends

Family factors e.g. inadequate parenting, poor family communication, parental personality and mental health

School factors e.g. poor organisation, teacher satisfactors and cooperation, deviant peers,

Societal factors e.g. socioeconomic status, neighbourhood

281
Q

What are the risk factors for conduct disorder?

A

Interaction of factors (individual, family, school and society)

Cumulative factors

Protective factors insufficient

282
Q

What is the impact of conduct disorder?

A

Affects the individual child e.g. exclusion, imprisonment

Affects the family

Affects innocent victim (antisocial behaviour)

Huge financial costs to society

283
Q

How can you treat conduct disorder?

A 
Begin at early age
Deal with major modifiable risk factors
Treat comorbidity e.g. underlying hyperactivity, LD, depression
Parenting programmes
Cognitive problem-solving skills
Interventions at school
Multi-systemic therapy
284
Q

What do parenting programmes (for parents of children with CD) include?

A

Play and good times together

Praise and recognition for good behaviour

Clearly expressed expectations

Consistent and calm consequences for misbehaviour

Planning ahead to avoid trouble

285
Q

What is cognitive problem-solving skills training?

A

For adolescents with CD

Techniques to develop more accurate perceptions (people with CD may have distorted attributions of aggressions in other people)

Teaching problem-solving skills using range of options and their consequences

286
Q

What kind of interventions for conduct disorder are there?

A

Parenting programmes

Cognitive problem-solving skills training

Interventions at school

Multi-systemic therapy

287
Q

What interventions at school can help a child with conduct disorder?

A

Teaching teachers how to manage disruptive behaviour

Increasing reading ability

288
Q

What multi-systemic therapy can be used for conduct disorder?

A

Targets causes of youth anti-social behaviour

Intensive package to improve:
Parent-adolescent relationship
Parent skills and understanding
Decrease deviant peer associations
Enhance school and occupational performance
Develop support network for family
289
Q

What is the prognosis for conduct disorder?

A

40% of 7 and 8 year olds with CD become a convicted, reoffending criminal as teenagers

90% of recidivist juvenile delinquents had CD

Also predicts alcohol, drug dependence, unemployment and relationship difficulties

290
Q

How has the concept of depression changed?

A

Used to be yes or no (coding system categorically)

Now seen as more of spectrum

291
Q

True or false; increased symptoms leads to increased impairment in depression?

A

True

292
Q

What are the symptoms of depression disorder?

A

1 OR MORE OF THESE:
Persistent sadness or low mood
Loss of interests or pleasure (anhedonia)
Fatigue or low energy

ASSOCIATED WITH (at least 2 weeks, most days)
Disturbed sleep
Poor concentration, indecisiveness and libido
Low self confidence
Change in appetite and weight
Suicidal thoughts or acts
Agitation and slowing of movements
Guilt or self-blame
293
Q

How can you define the degree of depression?

A

<4 symptoms= not depressed
4 symptoms= mild depression
5-6 symptoms= moderate depression
7 or more symptoms= severe depression (with or without psychotic symptoms)

Symptoms pervasive, impairing and present for at least 2 weeks

294
Q

What are the associated problems of depression?

A

Increased risk of self-harm
Association with anxiety disorders, EDs and conduct problems
Familial aggregation (genetic and learning)

295
Q

How does childhood depression present?

A 
Persistent safness
Anhedonia
Boredom or irritability (functionally impairing)
Unresponsive to pleasurable activities
Functional impairment
296
Q

What are the 2 main types of pre-pubertal depression?

A 
1
More common
Co-morbid behavioural problems
Resembles children with conduct disorder
No increased risk of recurrence in adult life

2
Less common
Highly familial (multigenerational loading)
High rates of anxiety and bipolar disorder
Recurrences of depression in adolescence and adulthood

297
Q

How can you tell the difference between normal adolescent angst vs psychiatric disorder?

A

NORMAL
Mastering the tasks of development (social, physical, cognitive, emotional, moral)

PSYCHIATRIC
Symptoms lead to severe suffering and impairment
Personal, family, peers, education and work

298
Q

What is adolescent depressive disorder?

A

Irritability instead of sadness and low mood (especially in boys)
Somatic complaints and social withdrawal are common
Psychotic symptoms rare before mid-adolescence

299
Q

What are the outcomes over time for adolescent depressive disorder?

A

SHORT TERM
High rates of persistence and recurrence

LONG TERM
Significant continuity into adulthood
Impaired relationships and educated in adulthood

300
Q

What is the epidemiology of adolescent depressive disorder?

A

No different pre-puberty between girls and boys

By 15, F 2x as likely as M

Cumulative probability by late adolescence 10-20%

Rate of depressive disorders may be increasing over time

301
Q

What is the amine hypothesis?

A

In depression

Results for hypo-activity of monoamine neurotransmitter reward systems

302
Q

What are the factors contributing to cognition, emotion, mood and pain? What is the neurotransmitter that relates to this?

A

DA= Pleasure, drive, energy

NE= Vigilance

5-HT= Impulsivity

303
Q

What happens in puberty that contributes to depression?

A

Gonadal hormones increase which has a direct CNS effect (estradiol)

Low levels of estrogen in women associated with premenstrual syndrome, postnatal depression and post-menopausal depression

Changes in body shape can be negative experience (especially for girls)
- Timing important

304
Q

What happens in the brain that leads to cognitive and emotional changes in adolescence?

A

PFC= synaptic pruning, myelination, changes in GM and WM

Lots of new connections in the brain-> development of dopaminergic system

305
Q

How can mild depression be treated?

A

CBD (individual or group)

Interpersonal psychotherapy for adolescents

306
Q

How can moderate-severe depression be treated?

A

Anti-depressants e.g. SSRIs e.g. fluoxetine

Could be SSRI and CBT (combined therapy)

307
Q

What is the theory CBT is based on? How does CBT work?

A

Based on Beck theory that depressed individuals show distortions in their thinking and info processing
I.e. they emphasise the negative aspects and under-emphasise the positive (leads to depressed mood and maladaptive behaviours)

CBT aims to interrupt this cycle
I.e. change feelings and thoughts to change body sensations and behaviour

308
Q

What is interpersonal psychotherapy?

A

Conceptualises depression as occurring within an interpersonal matrix and tries to get rid of interpersonal stress
E.g. loss, role disputes, role transitions, interpersonal skills deficits, adjustment to single parent family

Starts by taking an interpersonal inventory of important relationships

Aims to replace conflictual, unfulfilling relationships with meaningful lower-conflict relationships

309
Q

Is TCA (ticyclic AD) beneficial for treating depressioni in adolescents?

A

No better than placebo

Can have efficacy with SSRIs especially fluoxetine (adolescents and younger adults seem to respond better to serotonergic agents)

E.g. March et al, 2004 TADS study

310
Q

What is the difference between biological and chronological age?

A

Biological= age organs etc. seem

Chronological= age

311
Q

What is life expectancy?

A

Statistical measure of how long a person can expect to live

Increasing in most countries

312
Q

What are the 2 key drivers of population ageing?

A

Falling fertility rates

People living longer

313
Q

Why do people age?

A

Programmed ageing

Damage to error theories

314
Q

What happens to cause programmed ageing?

A

Hayflick limit (cells in culture would only undergo a certain number of divisions and then stop)

Seems to be controlled by cell being able to count (organism can reach maturity and reproduce)

Evidence mixed

  • Some older people have more active telomerase which repairs telomeres
  • Possible role of insulin and IGF-1
315
Q

What are free radicals?

A

Oxidative stress due to reactive oxygen species exceeds antioxidant capacity

O-, H202, H-, NO-

316
Q

Where do most free radicals come from?

A

Mitochondria
- Contain own DNA, repair mechanisms less robust and eventually DNA damaged repair-> mitochondrion die-> cells die

Chronic inflammation and chronic infections

  • Macrophages
  • Peroxisomes
  • Cytochrome P45-

Lifestyle options

  • Smoking
  • Skin damage
  • Diet (best to have micronutrients, <1500)
317
Q

Should people take antioxidant multivitamins?

A

No

No evidence for cancer, CV disease, DM, ARMD, cataracts, AD

318
Q

How do free radicals cause DNA damage?

A

Frequent damage to DNA whilst it’s being transcribed-> DNA polymerase can’t repair all of it-> damage accumulates and contributes to missing proteins and cellular apparatus etc -> eventually to cell death

319
Q

How does protein glycation lead to oxidative stress?

A

Contributes to neurofibrilliary tangles

Involved in AD, atherosclerosis and cataracts

320
Q

What challenges does society face as a result of population ageing?

A

Outdated and ageist beliefs and assumptions
Working life and retirement balance
Medical system designed for single acute diseases
Extending healthy old age not just life expectancy
Inadequate or absent services
Lack of accessibility for people with disabilities

321
Q

What makes us age differently?

A

Genetic inheritance (and epigenetic factors)
Sex and ethnicity
Lifestyle (where? behaviour? access to health care? education? social position? wealth?)

322
Q

Why is it important to invest in healthy ageing?

A

Older people make contribution to society

Bring benefits to older people and returns for society as a whole

323
Q

What does social care comprise of?

A 
Financial assessment
Home carers
Sheltered housing
Care home= residential, nursing
Personal budgets
324
Q

What is frailty?

A

Loss of biological reserve across multiple organ systems
Leads to vulnerability to physiological decompensation and functional decline after a stressor event

Cycle involving weight loss, declined activity, decreased strength, decreased walking speed and falling energy and VO2 max

325
Q

What alters the presentation of disease with age?

A

Frailty

Non-specific presentations

326
Q

Summarise the difficulties in managing disease in older people?

A 
Multimorbidity
Polypharmacy
Iatrogneic harm
Compprehensive geriatric assessment
Rehabilition
327
Q

What does frailty lead to?

A

Increased risk of falls
Worsening disability
Care home admission
Death

328
Q

How can frailty be treated?

A

Exercise
Nutrition
Possibly drugs

Prevention is better than cure

329
Q

What are the non-specific presentations of frailty?

A 
Instability
Immobility
Incontinence
Intellectual impairment
Iatrogenic harm

Older people less likely to have common symptoms e.g. chest pain in ACS and pleuritic chest pain and haemoptysis in PE

More likely to have shortness of breath and syncope

330
Q

Define: multimorbidity

A

2 or more chronic conditions

Impact on one another
NB. Treatments may impact each other

331
Q

What are the negative effects of multi-morbidity?

A

Worse QoL so more likely to be depressed
Increased functional impairment
Burden of treatment
Polypharmacy

332
Q

Why do older people take more drugs?

A 
Comorbidities
Guidelines, QOF and NICE (almost always single disease, don’t take burden of treatment into account, don’t consider other conditions)
Undetected non adherence
Infrequent review
Poor communication
333
Q

What is polypharmacy associated with bad outcomes?

A

Falls
Increased length of stay
Delirium
Mortality

334
Q

What is iatrogenic harm?

A

Iatrogenesis refers to any effect on a person, resulting from any activity of one or more persons acting as healthcare professionals or promoting products or services as beneficial to health, that does not support a goal of the person affected

335
Q

What nosocomial conditions cause iatrogenic harm?

A 
Infections
Pressure sores
Constipation
Deconditioning
Delirium
Malnutrition
Incontinence
336
Q

Which drug is most likely to be the cause of a hospital admission?

A

NSAID 30%

Warfarin 10%
Antidepressant 7%
Opioid 6%
Digoxin 3%

337
Q

Why are older people at increased risk of hospital admission?

A 
Reduced physiological reserve
Impaired compensation mechanisms
Comorbidities
Polypharmacy
Cognitive impairment
338
Q

What is the CGA?

A

Comprehensive geriatric assessment

Medical, function, social and psychological assessment

Problem list and plan developed

CGA IN THE COMMUNITY
Reduce admissions to institutional care
Reduce falls
Most benefit in mild or moderate frailty

CGA FOR FRAIL INPATIENTS
Reduces inpatient mortality
Reduces functional and cognitive decline
Reduces admission to institutional care

339
Q

What is the aim of rehabilitation for the elderly?

A

To restore or improve functionality
Multidisciplinary
Rehabilitation alongside acute illness (preventing deconditioning)
Prehabilitation

340
Q

What do you look for on an MRI of an ageing brain to check cognition?

A

Grey matter reductions- mainly in size and number of connections between neurons (not in neuron numbers)

White matter reduction

341
Q

What are normal cognitive changes in older people?

A

Processing speed slows
Working memory slightly reduced
Simple attention ability preserved, but reduction in divided attention
Executive functions generally reduced

No change in non-Wdeclarative memory
No change in visuospatial abilities
No overall change in language (some reduction in verbal fluency)

342
Q

What is dementia?

A 
Decline in all cognitive functions, not just memory
Impairment of function
Progressive
Degenerative
Irreversible
343
Q

What can cause dementia?

A

HIV
Progressive multifocal leukencephalopathy (PML)
Post encephalitis
Neuro syphilis

Thiamine deficiency
Pellagra (niacin def)
Hypothyroidism
Alcohol

Huntingdon’s
Multiple sclerosis
Progressive supranuclear palsy (PSP)
Corticobasal degeneration (CBD)
Posterior cortical atrophy
Creutzfeld-Jakob disease (CJD)

Normal pressure hydrocephalus

344
Q

What is the difference between dementia and delirium?

A 
DEMENTIA
Chronic (months-years)
Gradual progression
No change in conscious level
Irreversible
DELIRIUM
Acute (hours-days)
Fluctuating
Main problem with alertness and attention
Usually reversible
Usually precipitated by something
People with dementia are at higher risk
345
Q

What cognitive assessments are used e.g. looking for dementia?

A

SCREENING
AMT
4AT

DIAGNOSTIC AND MONITORING
Mini Mental State Examination (MMSE)
Montreal Cognitive Assessment (MOCA)
Addenbrooke’s Cognitive Examination (ACE)

346
Q

What is AMT?

A

Abbreviated mental test

10 questions:
DOB
Age
Current place
Year
Time (to nearest hour)
Dates of WW2
Monarch or PM
Count 20-1
Recognise 2 people
Remember 3-item address (“42 West Street”)

Score out of 10 (no half points)
>8 is normal

347
Q

What are the problems with AMT?

A

Very orientation focused (orientation can be well preserved in some forms of dementia)
Assumes cultural knowledge and interest (WW2, PM)
Assumes numeracy
Monarch or PM could give different results
No time limit on 20-1 (can count very slowly, shows processing time)
Person recognition can be difficult in hospital

348
Q

What are the problems with cognitive assessments?

A

Most assumes some basic cultural knowledge
Most assume numeracy and literacy
Depression can masquerade as dementia
Ceiling effects in highly educated/intelligent

Interpret them in context

LCRS2- RDA (1 decks)

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